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Inflammatory Bowel Disease
      #13950 - 07/14/03 01:51 PM
HeatherAdministrator

Reged: 12/09/02
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All articles concerning Inflammatory Bowel Diseases such as Crohn's and Ulcerative Colitis should be posted here.



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Chemo Drug Improves Crohn's Symptoms new
      #13995 - 07/14/03 04:09 PM
HeatherAdministrator

Reged: 12/09/02
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Chemo Drug Improves Crohn's Symptoms - Immune-Boosting Therapy Opposite of Standard Treatment

By Sid Kirchheimer
WebMD Medical News

Nov. 7, 2002 -- The painful and debilitating symptoms of Crohn's disease may be eased or even eliminated by a seemingly unlikely source -- a drug primarily used to boost immunity. A study shows Leukine to be a unique and promising new approach to treat the disease.


The irony: Crohn's has been thought to result from an overactive immune system, and traditional therapies have attempted to suppress -- not enhance -- immune activity.


Yet researchers discovered that the drug Leukine, which strengthens immune response by increasing the size and function of white blood cells, offered "significant improvement" in symptom relief for 12 of 15 Crohn's patients -- that's 80% -- who were part of the first study using this therapy.


Of those, eight went into remission, says researcher Joshua Korzenik, MD, of Washington University School of Medicine and a Crohn's specialist at Barnes-Jewish Hospital in St. Louis.


"It's a small study, but the outcome exceeded our expectations, especially since people were saying that the idea of stimulating immune systems that are already revved up is like throwing oil onto a raging fire," he tells WebMD. "While this treatment approach certainly isn't prime-time yet, we're extremely excited because it offers a different approach and new understanding to a disease that has defied explanation."


His findings, published in the Nov. 9 issue of The Lancet, are now the subject of a follow-up study at 30 sites throughout the U.S. If future findings are similarly promising, Leukine might be available for Crohn's patients within five years, says Korzenik. It is usually used in cancer patients who are undergoing chemotherapy.


Leukine could provide some relief to a baffling condition that plagues nearly 500,000 Americans, causing extreme pain, diarrhea, ulcers, and other inflammation in the intestines.


"What's particularly heinous about Crohn's is the typical onset occurs in the teens or early 20s, a time when people are establishing their self-identity," notes researcher Brian Dieckgraefe, MD, PhD, also at Washington University. "So, as if going through your teens isn't bad enough, these patients also have severe daily abdominal pain, diarrhea, intestinal ulcers and abscesses."


Therapy for Crohn's patients currently involves several immune-suppressing drugs, including steroids. But many cause side effects not experienced by the test subjects using Leukine, says Korzenik. Only one medication is specifically approved by the FDA to treat Crohn's -- Remicade, which is also used to treat rheumatoid arthritis.


"But Remicade requires continuous infusion, whereas Leukine is injected, so it's a lot easier to administer," notes Seymour Katz, MD, of New York University School of Medicine and a spokesman for the American College of Gastroenterology. "Does this mean that Leukine is the only answer for Crohn's? No. Does it offer some hope for Crohn's patients? Yes. Is this an exciting finding that brings a new approach to treatment? Absolutely."

© 2002 WebMD Inc. All rights reserved.

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Hormone replacement therapy prevents bone loss in patients with IBD new
      #14115 - 07/15/03 06:02 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Gut. 1993 Nov;34(11):1543-6.

Hormone replacement therapy prevents bone loss in patients with inflammatory bowel disease.

Clements D, Compston JE, Evans WD, Rhodes J.

Department of Medicine, University Hospital of Wales, Cardiff.

Patients with inflammatory bowel disease have an increased prevalence of osteoporosis, and suffer high rates of spinal bone loss. Hormone replacement therapy (HRT) is effective in the treatment and prevention of osteoporosis but has not been studied in patients with inflammatory bowel disease. A two year prospective study of HRT in inflammatory bowel disease was performed in 47 postmenopausal women aged 44 to 67 years with ulcerative colitis (25) or Crohn's disease (22). Patients had radial and spinal bone density measured annually by single photon absorptiometry and quantitative computed tomography respectively. The mean (95% confidence intervals) annual change in radial bone density was +1.42%/yr (+0.58 to +2.26; P < 0.005) and for spinal bone +2.60%/yr (+1.06 to +4.15; p < 0.005). There was no significant correlation between rates of change of bone density at the two sites, or between the rates of change and the initial bone density either in the radius or spine. Twelve patients were given prednisolone during the study, and their rates of change for spinal bone density were lower, but values were not statistically significantly different from those who did not receive corticosteroids. Changes in bone density for patients with ulcerative colitis and Crohn's disease were not significantly different. The change in bone density did not correlate with the patients' age or number of years after the menopause. It is concluded that HRT is effective in prevention of bone loss in postmenopausal women with inflammatory bowel disease.

PMID: 8244141 [PubMed - indexed for MEDLINE]

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A study of the menopause, smoking, and contraception in women with Crohn's disease. new
      #14117 - 07/15/03 06:05 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Q J Med. 1989 Jul;72(267):623-31.

A study of the menopause, smoking, and contraception in women with Crohn's disease.

Lichtarowicz A, Norman C, Calcraft B, Morris JS, Rhodes J, Mayberry J.

City Hospitals, Nottingham.

One hundred and ninety-six women with Crohn's disease from south-east Wales were asked to provide details of their menstrual cycles, age at menopause, history of surgery, smoking habits and use of oral contraceptives. One hundred and forty-six provided the information (response rate 77 per cent). Eighty-four were still menstruating, three were pregnant, 10 had undergone hysterectomy, one had a pharmacologically-induced menopause and 48 had had a physiological menopause. Of these 48 women, 33 were diagnosed as having Crohn's disease before the menopause. Twenty-five of these were smokers. The mean age at menopause was similar in smokers and non-smokers and in those diagnosed before and after the menopause. The mean age at menopause was between 46 and 47. A logistic analysis using the 'status quo' method showed that 50 per cent of women with Crohn's disease had the menopause at 47.6 years compared with 49.6 years in a group of healthy women from the same area. The two groups had similar smoking habits and it would seem that a premature menopause is associated with Crohn's disease.

PMID: 2608881 [PubMed - indexed for MEDLINE]
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Inflammatory Bowel Disease During Pregnancy. new
      #14124 - 07/15/03 06:20 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Curr Treat Options Gastroenterol. 2003 Jun;6(3):227-236.

Inflammatory Bowel Disease During Pregnancy.

Tilson RS, Friedman S.

Gastroenterology Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. sfriedman1@partners.org

Physicians treating patients with Crohn's disease and ulcerative colitis will often need to care for them throughout pregnancy and deal with the surrounding issues of fertility, childbirth, and sexuality. Patients often worry about continuing medications during pregnancy and feel particularly at risk for poor birth outcomes. However, because pregnancy outcomes are most closely tied to disease activity at the time of conception, patients who are in remission when they conceive will have the most successful pregnancies. The overriding principle in treating pregnant patients with inflammatory bowel disease (IBD) is continued and close surveillance of disease activity, with aggressive medical, and if indicated, surgical treatment. With few exceptions, medicines used to induce remission before pregnancy should be continued throughout pregnancy. Pregnant women with active IBD should be followed by a gastroenterologist with experience in the issues surrounding pregnancy, and by an obstetrician with access to a tertiary referral center. Properly treated and followed, patients with IBD can expect outcomes from their pregnancies that approximate those of patients without the disease.

PMID: 12744822 [PubMed - as supplied by publisher]
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Bacteria in Milk Linked to Crohn's Disease and Possibly IBS new
      #17056 - 08/12/03 11:55 AM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

M. avium Implicated in Crohn's Disease, Perhaps Also Irritable Bowel Syndrome

By Richard Woodman

LONDON (Reuters Health) Aug 06 - Researchers said on Wednesday they had found a "highly significant" link between Crohn's disease and a mycobacterium that can be passed to humans in milk.

Professor John Hermon-Taylor and his research team at St. George's Hospital Medical School in London said they had detected Mycobacterium avium paratuberculosis (MAP) bacteria in 92% of ileocolonic biopsy specimens from patients with Crohn's disease but in only 26% of patients in a control group.

"The rate of detection of MAP in individuals with Crohn's disease is highly significant and implicates this pathogen in disease causation," they write in the July issue of the Journal of Clinical Microbiology.

"The problems caused by the MAP bug are a public health tragedy", said Dr. Hermon-Taylor, who has sent a copy of the paper to Britain's Chief Medical Officer, Liam Donaldson.

The study was backed by the medical charity Action Research, which said previous findings showed live MAP bacteria is present in 2% of retail pasteurised milk cartons.

"The discovery that the MAP bug is present in the vast majority of Crohn's sufferers means it is almost certainly causing the intestinal inflammation," the charity said in a statement.

It added: "Action Research does not recommend that anyone stops drinking milk. However, for those individuals with Crohn's disease or their close relatives, who may feel particularly at risk, it may be sensible to start drinking UHT milk. As UHT involves higher pasteurisation temperatures, it is probable that MAP is destroyed."

The charity called for Crohn's disease to be made a reportable condition, for more stringent milk pasteurisation, for tests for MAP in dairy herds, and procedures for reducing MAP infection on farms.

Hermon-Taylor said an unexpected finding of the research showed that patients with irritable bowel syndrome (IBS) were also infected with the MAP bug.

"In animals, MAP inflames the nerves of the gut," he said. "Recent work from Sweden shows that people with IBS also have inflamed gut nerves. There is a real chance that the MAP bug may be inflaming people's gut nerves and causing IBS."

J Clin Microbiol 2003;41:2915-2923.

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Familial Occurrence of Inflammatory Bowel Disease in Celiac Disease new
      #20915 - 09/16/03 03:30 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Familial Occurrence of Inflammatory Bowel Disease in Celiac Disease

Inflammatory Bowel Diseases 2003; 9(5):321-323

Mario Cottone; Ciro Marrone; Angelo Casà; Lorenzo Oliva; Ambrogio Orlando; Emma Calabrese; Giuseppe Martorana; Luigi Pagliaro

Background:
The authors have previously reported a possible increased risk of the familial occurrence of Crohn's disease in patients with celiac disease.

Aim:
The aim of the current study was to evaluate in a case-control study the familial occurrence of inflammatory bowel disease (IBD) in first-degree relatives of patients with celiac disease.

Methods:
One hundred eleven consecutive patients with biopsy-proven celiac disease were interviewed to ascertain whether IBD was present in first-degree relatives. The number of relatives, their ages, and possible IBD status were collected in a questionnaire. When a diagnosis of familial IBD was reported, the diagnosis was checked in the hospital records. Two hundred twenty-two controls matched for age and sex (111 from the general population and 111 from orthopedic wards) were also interviewed regarding the possible occurrence of IBD in first-degree relatives. The &#967;2 test was used to evaluate the difference in proportion of familial occurrence of IBD among individuals with celiac disease and controls.

Results:
Among 600 first-degree relatives of patients with celiac disease, 10 cases of IBD were identified among first-degree relatives (7 cases of ulcerative colitis and 3 cases of Crohn's disease), whereas only 1 case of IBD was identified among the 1,196 first-degree relatives of control patients (p < 0.01). When ulcerative colitis and Crohn's disease were analyzed separately, only the prevalence of ulcerative colitis was statistically significant (p &#8804; 0.02).

Conclusions:
This case-control study shows that there is a significantly increased prevalence of familial ulcerative colitis in patients with celiac disease. There was no significant increase in the prevalence of Crohn's disease in patients with celiac disease. The possible role of this association is discussed.

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Indeterminate Colitis new
      #20916 - 09/16/03 03:33 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Inflammatory Bowel Diseases 2003; 9(5):324-331

Indeterminate Colitis

Karel Geboes; Gert De Hertogh

Summary:
A diagnosis of Crohn's disease (CD) and ulcerative colitis (UC) is based on a combination of clinical, histologic, endoscopic, and radiologic data. The distinction between UC and CD can be difficult because of the lack of a differentiating single gold standard. Indeterminate colitis (IC) was introduced by pathologists for the diagnosis of surgical colectomy specimens showing an overlap between the features of UC and CD. The diagnosis of IC was based on macroscopic and microscopic features. The term indeterminate colitis is in recent years more widely applied to include all cases with endoscopic, radiographic, and histologic evidence of chronic inflammatory bowel disease confined to the colon, but without fulfilment of diagnostic criteria for UC and CD. As for UC and CD, the diagnosis of IC has therefore become a clinicopathologic diagnosis. IC is generally considered to be a temporary diagnosis. The clinical characteristics of patients with IC are, however, somewhat different from the characteristics of those with UC. Furthermore, serologic markers such as perinuclear antineutrophil cytoplasmic antibody and anti-Saccharomyces cerevisiae, which are strongly linked with UC and CD, are both negative in a subset of patients with IC. Therefore, the possibility that IC could be a separate entity must be investigated.

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Detection of Pulmonary Involvement in Inflammatory Bowel Disease new
      #22104 - 09/30/03 01:20 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Journal of Clinical Gastroenterology 2003; 37(4):292-298

Pulmonary Function Tests and High-Resolution CT in the Detection of Pulmonary Involvement in Inflammatory Bowel Disease

Necla Songur, MD; Yildiran Songur, MD; Meric Tuzun, MD; Ibrahim Dogan, MD; Dilek Tuzun, MD; Arzu Ensari, MD; Baki Hekimoglu, MD

Goals:
To assess the pulmonary involvement detected by pulmonary function tests (PFT) and high-resolution computed tomography (HRCT) in inflammatory bowel disease (IBD) patients and to investigate the relationship of the pulmonary abnormalities with respiratory symptoms and bowel disease activity.

Methods:
23 patients with ulcerative colitis, 13 patients with Crohn disease and 14 control subjects took part in this prospective, controlled study. In all patients, detailed clinical information was obtained and extent and activity of the bowel disease were established. Each patient underwent PFT and HRCT scanning.

Results:
A pulmonary function abnormality was present in 21 of 36 patients. In IBD patients, DLCO were significantly lower, but RV/TLC was significantly higher than those of controls. HRCT revealed air trapping, fibrosis, emphysema, bronchiectasis and alveolitis in 19 patients. One-third of the patients with PFT abnormality, and 42% of the patients with HRCT abnormality were respiratory symptom free. Approximately 80% of the patients with pulmonary involvement had active bowel disease.

Conclusions:
Pulmonary involvement is common in patients with IBD. A high degree of suspicion is necessary to detect the pulmonary abnormality in IBD, because considerably large proportions of the symptom free patients have abnormal findings on HRCT and PFT.

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Colonoscopy Prep new
      #23729 - 10/17/03 12:05 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

The following is an excerpt from Jill Sklar's book, The First Year Crohn's Disease and Ulcerative Colitis (Marlowe 2002), which is available here on helpforibs.com or at any major bookstore. Jill hereby gives this as her contribution to humanity:

Colonoscopy
The colonoscopy is a very versatile and useful procedure that is used for many purposes including examining for cancer, locating and excising polyps and securing biopsies that can be later examined for CD or UC. In the past, it was done on patients who were fully awake but less sadistic methods are used now, leaving most patients to ask if the procedure has started when it is already done.

As you probably have heard, the worst part is the prep, an amazing statement given that there are at least a half a dozen ways that the prep is done. The goal of the preps is to strip away any fecal matter from the intestines, thus thoroughly cleansing the intestinal walls for a better view for the endoscopist. All of the preps involve ingesting a substance that then causes intense peristaltic waves and quick evacuation of the bowels, usually taking one to three hours.

Perhaps one of the older preparation ways is the use of a product called Go-Litely, which should probably be named Go Hard and Hurtfully. This involves drinking a glass of barely palatable salty liquid every few minutes until the only thing coming out of you resembles water; a gallon is the usual amount prescribed. A variation of that is Nu-Litely, a less salty, less cumbersome but no more palatable concoction that works in the same manner. Some doctors prescribe different mixes of castor oil, citrate magnesium, Ducolax tablets or suppositories and Fleets enemas to be taken at various times in the two days leading up to the big day. Another relatively new product is Fleets phosphosoda, an intensely briny tasting liquid. The label says that the patient can mix three tablespoons of the liquid with three ounces of water; for a usual colonoscopy prep, a dose the night before and another the morning of the test usually does the trick. The X prep is similar in that it involves drinking about two doses of two ounces of the nasty tasting prep liquid. Finally, the newest prep, Visicol, allows the patient to skip the bad taste by swallowing pills chased with an eight-ounce glass of clear liquid. On the day before the test and the morning of the test, the patient has to swallow three pills every 15 minutes over an hour and a half, with the last dose being two pills; the total of pills swallowed is 40.

There are drawbacks to every prep, chiefly swallowing things that will make you feel queasy. Because this prep is primarily done at home there are a few things you can do to make it more comfortable for yourself. Remember, these are tips and suggestions; I am not a doctor and although I have survived this test more times than any doctor I know, you should always follow the directives that your doctor gives to you regarding medication and bowel cleansing solutions.

We'll start with a shopping list. Since you will be headed to the store to pick up the bottles and boxes of prep materials, pick up the following as you will need them if you don't already have them:

1.Kleenex brand Cottonelle toilet paper infused with both aloe and vitamin E or a box of baby wipes infused with aloe (the quilted wipes provide that extra degree of comfort but may not be advisable if you have a septic system).

2. Hemorrhoidal cream such as Anusol HC or any other one with HC on the label. The HC stands for hydrocortisone, a topical steroid that helps reduce swelling and itching.

3. KY Jelly or Vaseline.

4. Plenty of reading material. I prefer to read magazines that I never read as it certainly provides a diversion so I pick up such paragons of journalism such as The National Enquirer, The Star, The Sun or the Weekly World News. Any other reading material that you would consider fun or distracting is a plus here as well.

5. Scented candles or fragrant bath oil in a pleasing, relaxing scent.

6. A heating pad or hot water bottle.

7. Lots of your favorite clear liquid food items (avoid all with red or purple dyes as the dye can mistaken for inflammation) such as Canada Dry, Jell-O, Italian ice, popsicles, chicken or beef broth. Also, be sure to pick up some electrolyte containing liquids such as Gatorade or Pedialyte.

First, I have a little rule of what ever goes in must come out, kind of like Newton's law but with a little digestive twist – call it Jill's law. The older preps used to dictate a diet devoid of roughage and fat followed for three days before the test, with a clear liquid diet on the last day. Why? Because these things tend to hang out in the colon the longest. With less in there, it made the prep a little easier. People were told to eat baked chicken, baked fish or scrambled egg whites for protein; oils or fats less than two tablespoons for the whole day, which meant no cheese, egg yolks or fried foods; doses of soluble fiber such as plain pasta, white rice, baked potatoes and white bread; sweets like angel food cake or vanilla wafers; and plenty of clear liquids such as broth, weak tea or coffee without cream, soda pop and clear juices such as apple juice or white grape juice. The last part, the clear liquids, was all a person could have the day before. But some doctors theorized that the newer preps could do the job without the diet, still stripping everything in their path.

I, however, still believe in the old diet. As a patient who has more colonoscopies than I care to remember, the diet helps to eliminate the bulk of the feces prior to prep, leaving less to evacuate. It also makes the liquid fast easier to tolerate for me. I also add a Ducolax tablet two nights before the blessed event to help get some of the heavy lifting out of the way first. My feeling is that if I can get the prep done in one dose, I have eliminated some of the misery. I also add clear electrolyte beverages like Gatorade or Pedialyte to the diet, sipping them almost constantly in the two days before the test. This will help to boost some of your electrolyte levels as many electrolytes are lost during the prep, leaving some people to feel cold, shaky and faint. I am not a fan of Gatorade but I love the Pedialyte as it tastes almost like Kool-Aid. I mix a bit of the orange flavor with Canada Dry ginger ale and crushed ice, a sort-of pre-colonoscopy cocktail.

For swallowing the nasty prep liquids, the rules for swallowing yucky things apply again; only this time, you may have more options than you do in a hospital setting. With the Go-Litely and Nu-Litely, you can add a little Crystal Lite for a bit of flavor. Lemons or limes dipped in sugar and tucked into the cheek counterbalance the salty flavor as well as can hard candy. Some people also swear by having the liquid as cold as possible. If you do this, be aware that you might have a sudden, sharp headache more commonly known as brain freeze.

Do not stray away from the bathroom. In fact, have it as stocked as it can be. You will need KY Jelly or Vaseline, the hemorrhoidal cream, the special toilet paper or baby wipes, reading material, bedtime clothing, a bath towel, the aromatherapy tools and anything else you can think of to add to your comfort. One friend of mine hauls in her television for the event.

You may feel somewhat nauseous and this is natural. Use cold cloths on your forehead or splash cold water on your face to fend off vomiting. Pacing helps as well but don't go too far from the bathroom because soon you will have an urge to go that you have never known before.

Before you begin to empty out, it helps a bit to coat your anus with the KY Jelly or Vaseline. The velocity of which your intestinal contents exit pared with the volume of the intestinal contents and the fact that some unabsorbed digestive enzymes will find their way out can make for a very sore anus and rectum. To ward this off a bit, it helps to thoroughly coat the anus and anal canal with the petroleum products. As the emptying begins, use the gentle wipes and flush often.

As the bowel evacuation subsides, you may feel cold and weak with muscle cramps. At this time, I usually draw a hot bath filled with scented bath crystals or oils and surround it with scented candles. This is soothing. If I still feel the urge to go, I am two steps from the toilet and a bath towel is always nearby. Before getting into my nightgown, I use a little soothing hemorrhoidal cream.

Following the first part of the prep, most doctors allow their patients to continue drinking clear liquids until midnight. This is important as the bowel cleanse solutions often draw in water from the body; paired with the diarrhea during the prep, this can make you dehydrated. Try to shoot for at least 24 ounces if you can. Also, if you are particularly nervous, a glass or white wine or a shot of vodka both count as clear liquids in my book and can help you to sleep.

On the day of the test, you will be asked to disrobe. Women may have to take a pregnancy test. An IV will be inserted in your arm before you are wheeled into the endoscopy suite. Draping will cover your body and your doctor will place a sedative in your IV. Usually, the painkiller Demerol is used with the sedative Valium and Versed, a short-term amnesia drug. Another option is to use a short-term anesthesia, administered by an anesthesiologist. While you are out, your doctor will insert the endoscopic tool and examine the colon, taking biopsies as well.

The next thing you should remember is waking up in recovery. You may be given juice to drink. When you are able to stand up, you can get dressed. The doctor who performed the test will discuss his or her findings with you and with the person who drove you to the test before you are allowed to leave. You may be woozy the rest of the day but you should recover by the next day.

If you experience sharp pain or a lot of bleeding, you should call the doctor. Rarely, a perforation of the intestines can occur.




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Environmental Factors May Play a Role in the Pathogenesis of IBD new
      #29622 - 12/01/03 05:56 PM
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Environmental Factors May Play a Role in the Pathogenesis of IBD

NEW YORK (Reuters Health) Nov 14 - The clinical spectrum of inflammatory bowel disease (IBD) is evolving, results of a study published in the October issue of the Journal of Pediatrics suggest. The findings point to changing environmental factors as contributors to the pathogenesis of the disease

In a population-based study, Dr. Subra Kugathasan, of the Medical College of Wisconsin, Milwaukee, and colleagues examined the incidence of pediatric IBD and defined clinical characteristics of the disease. Demographic and clinical data on all new cases of IBD in Wisconsin over a 2-year period were prospectively analyzed.

The overall incidence of IBD in children was 7.05 per 100,000, according to the researchers. The incidences of Crohn's disease (CD) and ulcerative colitis (UC) were 4.56 and 2.14 per 100,000, respectively.

The mean ages of diagnosis for IBD, CD, and UC were 12.5 years, 13.5 years, and 11.8 years, respectively.

The IBD incidence rates were similar among all ethnic groups, as well as among children from sparsely versus densely populated regions. Only 11% of the newly diagnoses IBD cases had first- or second-degree relatives with a history of the disease.

The lack of family history and the higher incidence of Crohn's disease than ulcerative colitis suggest to the investigators that new environmental factors are involved.

Also, they point out, the incidence of IBD in children they documented is the highest ever reported.

"A parallel phenomenon is the dramatic increase in asthma during the same period in the West," Dr. Kugathasan and colleagues note. "The concomitant emergence of chronic inflammation in the lung and gut also supports the concept that changing environmental factors play a pivotal role in the increased frequency of these disorders in children."

J Pediatr 2203;143:525-531.

http://www.medscape.com/viewarticle/464442?mpid=21407

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Increased Anal Resting Pressure and Rectal Sensitivity in Crohn's Disease new
      #32150 - 12/16/03 11:59 AM
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Diseases of the Colon & Rectum 2003; 46(12):1685-1689

Increased Anal Resting Pressure and Rectal Sensitivity in Crohn's Disease

Peter Andersson, M.D., Ph.D. *; Gunnar Olaison, M.D., Ph.D. *; Olof Hallböök, M.D., Ph.D. *; Bernt Boeryd, M.D., Ph.D. †; Rune Sjödahl, M.D., Ph.D., F.R.C.S. *

PURPOSE:
Anal pathology occurs in 20 to 80 percent of patients with Crohn's disease in which abscesses, fistulas, and fissures account for considerable morbidity. The etiology is not clearly defined, but altered anorectal pressures may play a role. This study was designed to investigate anorectal physiologic conditions in patients with Crohn's disease compared with healthy controls.

METHODS:
Twenty patients with Crohn's disease located in the ileum (n = 9) or the colon (n = 11) without macroscopic proctitis or perianal disease were included. All were subjected to rectal examination, anorectal manometry, manovolumetry, and rectoscopy. Comparison was made with a reference group of 173 healthy controls of whom 128 underwent anorectal manometry, 29 manovolumetry, and 16 both examinations.

RESULTS:
Maximum resting pressure and resting pressure area were higher in patients than in controls (P = 0.017 and P = 0.011, respectively), whereas maximum squeeze pressure and squeeze pressure area were similar. Rectal sensitivity was increased in patients expressed as lower values both for volume and pressure for urge (P = 0.013 and P = 0.014, respectively) as well as maximum tolerable pressure (P = 0.025).

CONCLUSIONS:
This study demonstrates how patients with Crohn's disease without macroscopic proctitis have increased anal pressures in conjunction with increased rectal sensitivity. This may contribute to later development of anal pathology, because increased intra-anal pressures may compromise anal circulation, causing fissures, and also discharging of fecal matter into the perirectal tracts, which may have a role in infection and fistula development.

http://ipsapp003.lwwonline.com/content/getfile/164/91/18/abstract.htm


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Bone Disease and Intestinal Problems May Share a Common Cause new
      #35699 - 01/07/04 11:47 AM
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By Megan Rauscher

NEW YORK (Reuters Health) Dec 26 - Scientists have evidence in mice that osteoporosis-like bone disorders and inflammatory intestinal disorders are both caused by abnormal regulation of a common protein.

Dr. Simon R. Carding from the University of Leeds in England and colleagues report their study in the December issue of the journal Immunity. "Autoimmune associated bone disease and intestinal inflammation are closely linked with deregulation and hyperactivation of autoreactive CD4 T cells," they write. "How these T cells are activated and mediate disease is not clear."

Mice engineered to lack a key regulator of CD4 T cells have overactive T cells and spontaneously develop ulcerative colitis and osteopenia, the scientists explain. Dr. Carding and colleagues' experiments indicate that this is caused by increased production of the ligand for receptor activator of NFkB (RANKL).

"We find that the hyperactive CD4 T cells produce too much of this protein, which then contributes to bone breakdown and bowel inflammation," Dr. Carding said.

Treating mice with exogenous recombinant osteoprotegerin -- a protein that interferes with RANKLs binding to its receptor -- reversed bone loss and improved colitis.

"This study shows that some bone diseases and intestinal problems may share a common cause," Dr. Carding told Reuters Health. "If similar mechanisms occur in humans, then osteoprotegerin might prove a useful treatment for intestinal disorders such as ulcerative colitis and Crohn's disease," he said, which are both often accompanied by bone loss.

Immunity 2003;19:849-861.

http://www.medscape.com/viewarticle/466447?mpid=23090

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Once-Daily Probiotic Treatment Maintains Remission in Ulcerative Colitis patients with Pouchitis new
      #41041 - 01/26/04 03:33 PM
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Once-Daily Probiotic Treatment Maintains Remission in Ulcerative Colitis Patients with Pouchitis


Mindy Hung


Jan. 7, 2004 — Once-daily high-dose probiotic therapy (VSL#3) sustains antibiotic-introduced remission in ulcerative colitis patients with pouchitis, according to a randomized, double-blind study published in the January issue of Gut.

"In parallel with clinical, endoscopic, and histological remission, a high level of QOL [quality of life] was maintained with this therapy," Toshiki Mimura, MD, and colleagues from St. Mark's Hospital in London, U.K., report.

Investigators drew 36 patients with recurrent (occurrence at least twice in the previous year) or refractory (requiring continuous use of antibiotics) pouchitis from St. Mark's Hospital and a center in Bologna, Italy.

All patients had a Pouchitis Disease Activity Index (PDAI) score of 7 or higher, with zero being no inflammation and 18 being the worst. Researchers induced remission in all patients with a four-week course of the antibiotics metronidazole (400 mg or 500 mg twice daily) and ciprofloxacin (500 mg twice daily).

Twenty patients were randomized to receive placebo, while 16 patients received 6g VSL#3 (3-g sachets containing 300 billion bacteria/g, made up of four strains of lactobacilli, three strains of bifidobacteria, and one strain of Streptococcus salivarius subsp thermophilus) once daily for one year or until relapse.

The researchers conducted physical examination prior to randomization and every two months for 12 months, or until relapse, which was defined as an increase in clinical PDAI score of 2 or higher together with an increase in the endoscopic PDAI score of 3 or higher compared with baseline. Researchers performed endoscopic and histological evaluations before randomization, at two months, and at 12 months.

The primary end point was a cumulative maintained remission rate at 12 months. Health-related QOL, a secondary outcome, was assessed at study entry, every two months, and at the time of relapse using the inflammatory bowel disease questionnaire (IBDQ).

Researchers evaluated the other secondary outcome, patient satisfaction with the treatment at study entry, every two months and at the time of relapse. Subjects chose their answer from the following options: (1) very dissatisfied, unhappy most of the time; (2) generally dissatisfied, unhappy; (3) neither dissatisfied nor satisfied; (4) generally satisfied, pleased; (5) very satisfied, happy most of the time.

Researchers confirmed the presence of viable probiotic bacteria in the stool of patients in the active group via stool analysis of a subgroup of 12 patients receiving active treatment or placebo at the beginning of treatment and after 60 days.

The median compliance rate was 96% in the VSL#3 group and 97% in the placebo group.

Seventeen patients (85%) in the VSL#3 group maintained remission at one year, while in the placebo group, one patient (6%) maintained remission (P < .0001). Two patients in the VSL#3 group relapsed at month two and month eight while one patient dropped out due to acute gastroenteritis-like symptoms.

The IBDQ score remained high in the VSL#3 group (P = .30) but deteriorated in the placebo group (P = .0005) over the year.

In terms of patient satisfaction, the investigators did not find a significant difference at entry between the two groups (median, 4 vs. 4 points; P = .26) but they differed significantly at the time of relapse or 12 months (4 points in the VSL#3 group vs. 2 points in the placebo group; P < .0001).

"This study has demonstrated that in patients with recurrent or refractory pouchitis who have achieved remission with intense antibiotic treatment, the probiotic therapy VSL#3 is highly effective in maintaining remission," write Dr. Mimura and colleagues.

This study was partially supported by VSL Pharmaceuticals, Inc.

Gut. 2004;53:108-114

Reviewed by Gary D. Vogin, MD


http://www.medscape.com/viewarticle/466792

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5-ASA Therapy for Inflammatory Bowel Disease No Bar to Colon Cancer new
      #44152 - 02/10/04 01:29 PM
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5-ASA Therapy for Inflammatory Bowel Disease No Bar to Colon Cancer

NEW YORK (Reuters Health) Jan 28 - Contrary to previous reports, new study findings suggest that treatment with 5-aminosalicylate (5-ASA) does not prevent colorectal cancer in patients with inflammatory bowel disease.

In studies in the UK and Denmark, Dr. Charles N. Bernstein and colleagues from the University of Manitoba in Winnipeg, Canada note that 5-ASA use has been linked to a reduced risk of cancer in patients with ulcerative colitis and Cohn's disease. However, it is possible that patient selection bias may have influenced the results.

To investigate, the researchers report in December issue of The American Journal of Gastroenterology, that they compared 25 inflammatory bowel disease patients who were diagnosed with colon cancer in Manitoba between 1997 and 2000 and 348 matched patients who did not develop cancer.

The investigators suggest that the main advantage of this study was that "it is population-based and is not sampling only those subjects who present to referral centers,"

Among patients exposed to 5-ASA, the average duration of use and the daily dose were similar in each group. In fact, the researchers note that the cancer patients were more likely to have been exposed to 5-ASA than were comparison patients. However, the difference was not statistically significant.

The researchers conclude that 5-ASA does not reduce the risk of colon cancer in such patients. However, they add that further studies with a larger sample size and longer duration of use are needed to completely rule out an anti-cancer effect.

Am J Gastroenterol 2003;98:2784-2788.

http://www.medscape.com/viewarticle/467896?mpid=24237

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Elan Reports Successful Results of Antegren Trial for Crohn's Disease new
      #44153 - 02/10/04 01:30 PM
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Elan Reports Successful Results of Antegren Trial for Crohn's Disease

By Kevin Smith

DUBLIN (Reuters) Jan 29 - Irish pharmaceutical firm Elan Corp Plc raised market hopes for its much-vaunted experimental drug Antegren on Thursday after it announced successful results from a key clinical trial in Crohn's disease.

The data are "very significant for patients with Crohn's disease-- the safety aspects of the drug and its efficacy are very encouraging," Lars Ekman, Elan's head of research and development, told Reuters in a telephone interview.

"This is a big step forward, a major breakthrough," he said.

Elan is pinning its future on Antegren, principally as a treatment for MS. Data from phase III studies of Antegren's effect on MS are expected by late 2004 or early 2005.

The results of the phase III trial on Crohn's disease showed no recurrence of the disease during a 6-month course of the drug, Elan said.

There was a significant treatment difference of more than 30% in patients taking the drug compared with those taking a placebo, and no difference in the rate of side effects, it said.

The result is a boost for Elan after a trial last summer of the drug's effects on the initial phase of a Crohn's attack failed to show any difference between the drug and the placebo. The latest trial showed the drug to be effective in the longer-term treatment of the disease.

(Additional reporting by Ben Hirschler in London)

http://www.medscape.com/viewarticle/468001?mpid=24237

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Data links Crohn's disease and antibiotics new
      #46423 - 02/24/04 02:07 PM
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Data link Crohn's disease, antibiotics - But it is unclear whether antibiotic use is a disease trigger or a result of patients seeking symptom relief.

By Victoria Stagg Elliott, AMNews staff. March 1, 2004.


--------------------------------------------------------------------------------

Use of antibiotics is a potential risk factor for the development of Crohn's disease, according to a paper published in the February issue of the journal Gut.

Researchers at England's University of Nottingham and Cambridge University analyzed the British General Practice Research Database for information about antibiotic use of those with and without the disease. The database includes information about diagnosing and prescribing practices of 5% of the nation's physicians and is considered to be one of the world's largest computerized databases of longitudinal anonymous patient medical records from this setting.

The researchers found that those with Crohn's received twice as many prescriptions over a five-year period and were 30% more likely to have been prescribed antibiotics.

Although Crohn's disease is primarily regarded as a genetic condition, researchers have been hunting for environmental reasons why the disease has increased significantly over the past few decades. Antibiotics are just one of many environmental triggers being scrutinized, along with factors such as appendectomies, the birth control pill, and smoking.

"Finding the environmental trigger is the million dollar question," said Subra Kugaphasan, MD, a pediatric gastroenterologist at the Medical College of Wisconsin in Milwaukee.

Researchers conceded that antibiotic use may be due in part to patients hunting for relief from symptoms before receiving a definitive diagnosis.

"Our data provide some support for antibiotic exposure playing a role, but we now need other studies particularly in children and looking at antibiotic use early in life," said Dr. Richard Logan one of the authors and a professor of clinical epidemiology at the University of Nottingham.

Experts said that although the study was provocative, the numbers did not seem strong enough to draw its conclusion even if they did reach statistical significance. Experts did say that studies like this should give physicians additional pause when it comes to prescribing antibiotics.

"Here is another condition that should make all physicians circumspect with regard to the application of antibiotics unless it's truly indicated," said Marvin L. Corman, MD, vice chair of surgery at North Shore-Long Island Jewish Medical Center in New York.

--------------------------------------------------------------------------------


ADDITIONAL INFORMATION:

Which comes first?

Objective: To determine if antibiotic use is linked to the development of Crohn's disease.

Participants: Patients with and without Crohn's who had five years' worth of data in Britain's General Practice Research Database.

Method: Data were extracted based on smoking status, drug prescriptions, age and sex. Logistic regression was used to investigate the relationship between Crohn's and antibiotic use.

Results: Seventy-one percent of those with Crohn's had used antibiotics in the previous five years, compared to 58% of controls. Those with the disease had twice as many antibiotic prescriptions than those without.

Conclusion: There is a statistically significant association between antibiotic use and Crohn's disease, although it is unclear whether this is the cause of the disease or a result of seeking treatment for symptoms.

Source: Gut, February

--------------------------------------------------------------------------------

Weblink
"Antibiotic use and the development of Crohn's disease," Gut, February (gut.bmjjournals.com/cgi/content/abstract/53/2/246)

Facts about Crohn's from the National Digestive Diseases Information Clearing House (digestive.niddk.nih.gov/ddiseases/pubs/crohns)


--------------------------------------------------------------------------------

Copyright 2004 American Medical Association. All rights reserved.

http://www.ama-assn.org/amednews/2004/03/01/hlsc0301.htm

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Faulty Gene for Crohn's Disease Found new
      #60852 - 04/13/04 03:19 PM
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Faulty gene for bowel disease found

By ANDRÉ PICARD
From Monday's Globe and Mail

Canadian researchers have isolated a gene that predisposes people to Crohn's disease, a painful disorder that strikes young people and that has sharply increased in frequency in recent years.

The discovery will have an immediate impact, allowing researchers to distinguish more readily between Crohn's and colitis, both inflammatory bowel diseases.

"The diagnostic benefits will be immediate," said Katherine Siminovitch, a professor of medicine at the University of Toronto. "That's important because you really want to catch these diseases in the early stages . . . then you can start a therapy that might put patients in remission and even eradicate the disease."

Dr. Siminovitch said, however, that development of new drugs based on this genetic finding is a long-term prospect; new treatments are probably a decade away.

The research, published in today's edition of the medical journal Nature Genetics, is nonetheless welcomed by people suffering from Crohn's disease.

"This is an exciting event for us," said Michael Howarth, executive director of the Crohn's and Colitis Foundation of Canada.

"It's important because it's one more piece in the puzzle. Finding the cure is not likely going to be one big event, but come about by finding out a little more every year."

More than 150,000 Canadians suffer from inflammatory bowel disease.

It most often strikes between the ages of 15-25, though a growing number of people are being diagnosed in their late 50s.

Crohn's and colitis affect the digestive system and cause the intestinal tissue to become inflamed, form sores and bleed easily, leading to problems eating, bloody diarrhea and excruciating pain.

Most sufferers experience periods of remission and flare-ups of the disease, often requiring long-term medication, hospitalization or surgery.

Jessica Grossman, 14, of Toronto, was diagnosed as having Crohn's five years ago. Since then, she has suffered greatly, enduring a number of drug treatments, all of which had severe side effects but none of which worked, and then surgery to remove her colon.

"It makes me happy to know they did this research because I don't want other people to go through what I did," Jessica said in an interview. She is currently in remission and remarkably healthy and active.

But Jonathan Grossman, Jessica's father, said he is excited by the new finding.

"We're quite cognizant of the fact that Crohn's doesn't just go away, so we really hope this will result in new treatments," he said.

"Anything that alleviates the suffering of people with Crohn's would be a godsend."

Inflammatory bowel disease does not have a single cause but is believed to result from a combination of genetic and environmental factors, such as diet and exposure to disease. (When the body fights off disease, there is inflammation, and these diseases have their roots in inflammation gone awry.) The newly isolated gene is located on Chromosome 5.

It produces a protein that sits on the cell surface and regulates how substances enter and leave the cell. In a majority of Crohn's disease patients, this protein functions improperly and allows in toxins.

Three years ago, French researchers discovered another abnormality, on Chromosome 16, that predisposes people to Crohn's.

Dr. Siminovitch, who is also the founding scientist of Ellipsis Biotherapeutics Corp., said a person with both genetic abnormalities has a tenfold risk of developing Crohn's disease.

She and her fellow researchers are now working on the development of a chemical that would alter the protein to restore its normal function. That chemical would become the basis of new drugs. The problem with drugs now being used to treat Crohn's is that they are non-specific, and as a result have a lot of side effects.

Dr. Siminovitch said the findings could also shed light on the basic causes of chronic inflammation.

From www.globeandmail.com


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Pipeline Treatments, Novel Procedures Offer New Options for GI Diseases new
      #76353 - 06/04/04 06:41 PM
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CONTACT: Tuesday, May 18, 3:00 pm CDT Kellie Hanzak, 202-955-6222 khanzak@spectrumscience.com Jessica Willocks, 301-941-2625 jwillocks@gastro.org

In New Orleans: Morial Convention Center 504-670-6420

RESEARCH HONES IN ON THERAPIES AND DIAGNOSIS OF BOWEL DISEASES

Pipeline Treatments, Novel Procedures Offer New Options for GI Diseases

New Orleans, LA – Inflammatory bowel diseases collectively cause significant lifestyle sacrifices and suffering and millions of dollars in related health care costs every year, partially due to a lack of effective diagnostic procedures and therapies. In new studies presented today at Digestive Disease Week in New Orleans, researchers show evidence of accurate and effective new methods for diagnosis, as well as improved treatment options, for sufferers of ulcerative colitis and Crohn's diseases.

Digestive Disease Week (DDW) is the largest international gathering of physicians, researchers and academics in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery.

"We are pleased to see more attention directed toward improving the lives of people suffering from inflammatory bowel diseases," said Jim Lewis, M.D., of the University of Pennsylvania. "For too long, the rate of discovery was slow. Now we are seeing more answers for the millions of sufferers."

Capsule Endoscopy in IBD: Findings and Effects on Clinical Outcomes (Abstract 105669*)

The M2A video capsule or "camera pill" allows gastroenterologists their best view yet of the small bowel, assisting in the diagnosis of inflammatory bowel disease. Until now, studies have not analyzed the influence of capsule endoscopy on clinical decision-making and therapeutic outcomes in IBD.

According to research presented by scientists from Mount Sinai Medical Center, use of the video capsule improves clinical outcomes significantly.

2 – 2 – 2 Bowel Diseases

For the study, the team of researchers reviewed the results of capsule endoscopy in patients with IBD-related indications. A total of 65 patients met the inclusion criteria and fit in four categories: A) abnormal small bowel series, rule out Crohn's Disease (CD); B) abdominal pain, normal radiologic studies, rule out CD; C) known ulcerative or Crohn's colitis; normal small bowel series and persistent symptoms, rule out small bowel disease; and D) known CD, with persistent obscure bleeding.

Overall, for 20 of the 21 patients (95 percent) in whom major diagnostic findings were discovered using capsule endoscopy, therapeutic decisions based on the results led to clinical improvement in patient outcome. In groups A and B, an absence of small bowel findings in 30 of 32 patients helped rule out CD. Throughout an average follow-up of 19 months, no evidence of CD developed, leading to a negative predictive value for the capsule study of 100 percent in this setting. In groups C and D, researchers discovered positive diagnostic findings on capsule endoscopy in 18 of 33 patients.

"Based on our research, we believe that capsule endoscopy may play an important role in clinical diagnosis and therapeutic decisions in patients with IBD indications," said Peter Legnani, M.D., lead author of the study. "We hope that the ease of use of the capsule may encourage more patients to undergo screening to confirm diagnosis of IBD and receive appropriate treatment."

Basiliximab (anti-CD25) for the Treatment of Steroid Resistant Ulcerative Colitis (Abstract 104640*)

Steroid therapy is one of the most effective treatments for ulcerative colitis (UC), which causes inflammation and ulcers in the lining of the large intestine, but up to 30 percent of patients will have a poor response to steroids. These steroid-resistant individuals present a difficult clinical challenge to gastroenterologists, because few treatment options exist after steroids other than removal of the entire colon (colectomy).

Basiliximab (Simulect®), a novel monoclonal antibody, has potential as a new treatment option, according to research from Henry Wellcome Laboratories at the University of Bristol in England.

3 – 3 – 3 Bowel Diseases

Basiliximab has been proven effective as a steroid sensitizer in steroid resistant UC both in the lab and in humans. This uncontrolled pilot study examined an extended series of 30 steroid resistant UC patients treated with basiliximab. Twenty patients with moderately active disease and 10 patients with severe disease were treated with a single intravenous (IV) dose of basiliximab (40 mg) in addition to their standard steroid therapy to monitor for remission within eight weeks, defined by an Ulcerative Colitis Symptom Score (UCSS) of less than two.

A total of 24 out of the 30 patients (80%) improved their UCSS score, with 19 of 30 (63%) achieving full remission. In the moderate disease group, 14 of 20 patients (70%) achieved full remission, and an additional five of 20 (25%) showed an improvement. In the severe disease group, five of the 10 patients (50%) achieved remission, while five required colectomy. There were no infusion reactions.

"These studies show that the use of basiliximab can provide significant improvements or remission for patients with ulcerative colitis," said Tom Creed, M.D., lead author of the study. "We hope that a larger, controlled trial will confirm these results and help make this potentially valuable therapy available to patients who can benefit from it."

Randomized, Double-Blind, Placebo Controlled, Parallel Arm, Safety and Efficacy Trial of Once-Daily, Oral OPC-6535 in the Treatment of Active Ulcerative Colitis (Abstract 105516*)

For patients suffering from severe ulcerative colitis (UC), new treatments that are safe and have minimal side effects are desperately needed. In this randomized study, researchers at the University of Chicago examined the effectiveness and tolerability of the compound OPC-6535 to treat UC. OPC-6535 was administered orally in a once-daily 25 mg or 50 mg dose to subjects with a new or established diagnosis of UC, flare within 12 weeks, and Disease Activity Index (DAI) of four to 11 on a scale of 12. A total of 186 patients were given either OPC-6535 or placebo for eight weeks. Patients were permitted to take 5-ASA (aminosalicylic acid) if they were stable for 14 days before entry and subsequent study duration (approximately 75% of subjects); 5-ASA is a standard treatment for UC.

4 – 4 – 4 Bowel Diseases

ore than half (55%) of the 25 mg group and 48 percent of the 50 mg group showed clinical improvement. The average change in DAI was significantly greater in the 25 mg group and was nearly statistically significant in the 50 mg OPC-6535 group versus placebo. Improvement in physician global assessment was more noticeable in the 50 mg dosage group, as a significantly higher proportion of these patients achieved remission (DAI 0-1) compared to the other treatment groups.

Responses were uniformly greater in the subgroup of patients with more severe disease. No differences were observed between 5-ASA users and non-users. "Based on these results, we are confident that OPC-6535 could be an effective treatment option for patients with ulcerative colitis, particularly in those with moderately severe disease," said Stephen Hanauer, M.D., lead author of the study.

"Further clinical studies are needed to confirm the best dose, but we were pleased to see a positive response to higher doses, as the efficacy may be even greater." ### Digestive Disease Week (DDW) is the largest international gathering of physicians, researchers and academics in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery.

Jointly sponsored by the American Association for the Study of Liver Diseases (AASLD), the American Gastroenterological Association (AGA), the American Society for Gastrointestinal Endoscopy (ASGE) and the Society for Surgery of the Alimentary Tract (SSAT), DDW takes place May 15-20, 2004 in New Orleans, Louisiana. The meeting showcases approximately 5,000 abstracts and hundreds of lectures on the latest advances in GI research, medicine and technology. *Abstract numbers listed above correlate to abstract ID numbers listed on the DDW Web site, www.ddw.org. They do not coincide with program numbers as found in the printed DDW Program Guide.

http://www.ddw.org/media/newsReleases/IBDTherapies.pdf

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Parasite Therapy for Crohn's and Colitis? new
      #96565 - 08/08/04 03:00 PM
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Patrick B. Massey, M.D., Ph.D.,
"The Alternative Approach", Daily Herald, August 2, 2004

Is it possible that an intestinal parasite holds a key to the treatment and possible cure for Crohn's disease, ulcerative colitis and other inflammatory bowel diseases (IBD)? Research at the University of Iowa suggests that infection by specific intestinal parasites may reduce the pain and inflammation associated with these serious diseases.

Crohn's disease and ulcerative colitis are part of a group of chronic inflammatory diseases of the gastrointestinal tract. The cause is unknown.

Crohn's disease is characterized by fever, abdominal pain, diarrhea and fatigue. Symptoms of ulcerative colitis include bloody diarrhea, abdominal pain, fatigue, dehydration, anemia and weight loss. In the most severe cases, surgery may be necessary to remove the affected
parts of the bowel.

IBD is becoming more common and our success at ridding our bodies of parasites may be to blame. With sanitation, better food and medications, intestinal parasites are relatively rare in industrialized societies, and that is a good thing. However, by making our lives increasingly hygienic, we may have made ourselves more susceptible to auto-immune diseases like Crohn's and ulcerative
colitis.

A successful parasite is very good at avoiding detection by the host. Parasites that live in the intestines, such as whip worms, or in the blood, such as malaria, survive by manipulating the host's self defense mechanisms. They are able to depress the immune system in a way that limits detection and response. They are able to moderate the
immune response in a way that may also prevent IBD.

IBD is often treated with powerful medications that suppress the immune response. These medications have saved the lives of many people with life-threatening Crohn's disease and ulcerative colitis. However, as good as these medications are, the side effects can be severe and
limit their use.

Other options are needed. Research involving intestinal parasites by Dr. Robert Summers of the University of Iowa, supported by the National Institutes of Health, may provide clues for a more natural (and effective) treatment of IBD.

In his study, 29 patients with active Crohn's disease ingested the pig whip worm, Trichuris suis. This parasite cannot multiply in the human intestine and is not transmissible from human to human. These patients
consumed the parasite every three weeks for 24 weeks. At 12 weeks, the symptoms of Crohn's disease decreased by 75 percent - and for 62 percent of the patients, the disease went into remission. At 24 weeks, the remission rate was an incredible 72.4 percent. There were no complications or adverse reactions.

In another study at the University of Iowa, patients with ulcerative colitis had a 48 percent improvement after 12 weeks, again without complications.

These response and remission rates with the pig whip worm are similar to those seen with medication, but apparently without the complications often associated with the drugs.

Now, I do not recommend infecting yourself with intestinal parasites. However, the increases we are seeing in many of the chronic diseases - heart disease, cancer, IBD, asthma, arthritis and others - are directly related to our modern lifestyle. We need to find safer solutions.

I believe that in nature everything has an antidote and that studying nature will reveal the solutions to many chronic medical problems. Parasite therapy for IBD is a novel approach.

About the Author: Patrick B. Massey M.D. Ph.D. is Medical Director for Alternative & Complementary Medicine, Alexian Brothers Hospital Network.

Website: www.ALT-MED.org.
<http://www.ALT-MED.org>



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Diet May Influence Relapse in Ulcerative Colitis new
      #115476 - 10/24/04 07:50 PM
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Diet May Influence Relapse in Ulcerative Colitis


Laurie Barclay, MD


Sept. 20, 2004 — Potentially modifiable dietary factors, such as high meat or alcoholic beverage intake, may increase the likelihood of relapse for patients with ulcerative colitis (UC), according to the results of a prospective cohort study published in the September issue of Gut.

"The causes of relapses of UC are unknown," write Sarah L. Jowett, MRCP, from the University of Newcastle upon Tyne, U.K., and colleagues. "Dietary factors have been implicated in the pathogenesis of UC."

To determine the effect of customary diet on likelihood of relapse, 191 patients in remission were recruited from two district general hospitals and followed for one year. Relapse was defined using a validated disease activity index; a food frequency questionnaire determined nutrient intake; and multivariate logistic regression, controlling for nondietary factors, determined adjusted odds ratios for relapse.

Of the 191 patients, 96% completed the study, and 52% relapsed. Compared with the lowest tertile of meat consumption, the highest tertile was associated with triple the risk of relapse (odds ratio [OR], 3.2; 95% confidence interval [CI], 1.3 - 7.8. Intake of red and processed meat was an even greater risk factor (OR, 5.19; 95% CI, 2.1 - 12.9. The top tertile of intake for protein (OR, 3.00; 95% CI, 1.25 - 7.19) and alcohol (OR, 2.71; 95% CI, 1.1 - 6.67) also increased the likelihood of relapse, as did high intake of sulfur (OR, 2.76; 95% CI, 1.19 - 6.4) or sulphate (OR, 2.6 (95% CI, 1.08 - 6.3).

Contrary to commonly held beliefs, increased intake of milk or dairy products did not increase risk of relapse, and increased intake of dietary fiber did not appear to protect against relapse.

Study limitations include potential criticisms of the dietary assessment tool; assessment of habitual diet at only one time point for each individual; failure to perform sigmoidoscopy or analysis of stool samples; and incomplete data for sulfur and sulphate content of the diet.

"Potentially modifiable dietary factors, such as a high meat or alcoholic beverage intake, have been identified that are associated with an increased likelihood of relapse for UC patients," the authors write. "Further studies are needed to determine if it is the sulphur compounds within these foods that mediates the likelihood of relapse and if reducing their intake would reduce relapse frequency."

Northumbria Healthcare Trust funded Dr. Jowett.

In an accompanying commentary, Herbert Tilg, from University Hospital Innsbruck in Austria, and Arthur Kaser, from Brigham and Women's Hospital and Harvard Medical School in Boston, Massachusetts, note that the role of dietary factors in UC relapse may be mediated by hydrogen sulfide production.

"This provocative and clinically important report by Jowett et al reopens the topic of diet and relapsing UC," Drs. Tilg and Kaser write. "The findings are well taken and may offer a new perspective for potential intervention by practical lifestyle modifications, and as such are eagerly awaited by our patients. Despite this excitement, interventional studies are now needed, setting the scene for specific dietary recommendations and for further defining the role of sulphur/sulphate which may even lead to novel therapies."

Gut. 2004;53:1399-1401, 1479-1484

Reviewed by Michael W. Smith, MD

http://www.medscape.com/viewarticle/489613?src=mp

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Increased Incidence of Inflammatory Bowel Disease: The Price of the Decline of Infectious Burden? new
      #125865 - 11/28/04 02:58 PM
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From Current Opinion in Gastroenterology

Increased Incidence of Inflammatory Bowel Disease: The Price of the Decline of Infectious Burden?

Posted 11/11/2004

Hélène Feillet; Jean-François Bach

Abstract and Introduction
Abstract
Purpose of Review: It is now apparent that the increase in the incidence of autoimmune and allergic diseases in Western countries is explained by the decrease in infections. The question is posed to determine whether a similar explanation can be proposed for the increased incidence of inflammatory bowel disease.
Recent Findings: Studies performed in murine experimental models of inflammatory bowel disease have shown that colitis onset can be prevented by bacteria, bacterial extracts, or helminths. Particular interest was given to probiotics (either live or killed), which protect from disease in a toll-like receptor 9 dependent fashion. This protective effect involves regulatory cytokines as indicated by in vitro studies on human inflamed colonic cells. At the clinical level, there is strong suggestion but still limited proof that probiotics improve inflammatory bowel disease through immunoregulatory mechanisms.
Summary: Converging clinical and experimental data strongly suggest the protective nonspecific role of infections on inflammatory bowel disease independently from the triggering role of some specific bacteria. The extension to inflammatory bowel disease of the hygiene hypothesis opens new therapeutic perspectives including the revisiting of probiotics and other forms of exposure to bacteria or parasite components.

Introduction
Converging epidemiologic data reveal a steady increase in the incidence of inflammatory bowel disease (IBD) during the last half of the twentieth century, even if a plateau has now been reached in some high-incidence areas such as northern Europe and North America.[1*,2] This increase in incidence is real but should be qualified in terms of the improvement of disease awareness and diagnosis. During the same period, an obvious trend towards the decline of infectious diseases was noted.[3]

As has been previously done for allergic and autoimmune diseases, it was tempting to hypothesize a causal relation between these two observations (according to the hygiene hypothesis). Because of decreased solicitation by infectious agents, the immune system mounts immunopathologic responses against various antigens (autoantigens, allergens, and antigens from some specific pathogens), giving rise to immune disorders.




--------------------------------------------------------------------------------

Hélène Feillet and Jean-François Bach, Necker Hospital, Paris, France

Curr Opin Gastroenterol 20(6):560-564, 2004. © 2004 Lippincott Williams & Wilkins

Section 1 of 7 Next Page: Suggestive Epidemiological Data
To view this whole article, follow the link:

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Probiotics Prove Just As Effective As a Popular Prescription Drug for Ulcerative Colitis new
      #131903 - 12/20/04 01:37 PM
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12.10.04 -- Probiotics Prove Just As Effective As a Popular Prescription Drug for Ulcerative Colitis


By Greg Arnold, DC, CSCS, October 21, 2004, abstracted from "Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine" in the November 2004 issue of Gut

Inflammatory bowel disease (IBD) includes a number of chronic, relapsing inflammatory disorders involving the gastrointestinal tract. It is estimated that more than 600,000 people in the United States have some form of inflammatory bowel disease.1 Classically, inflammatory bowel disease includes ulcerative colitis and Crohn's disease.

Ulcerative colitis (UC) presents as inflammation extending throughout the entire colon. Research increasingly suggests that the inflammation associated with UC and IBD is related to an overabundance of "bad" bacteria and a deficiency of "good bacteria" known as probiotics.(2, 3) Now a new study4 has found probiotics act just as well as prescription drugs in helping relapses in UC.

Researchers studied 327 IBD patients, with 162 receiving 200 mg Escherichia Coli Nissle once daily while 165 received 500 mg mesalazine, a prescription drug regarded as the "gold standard" for treating IBD, three times daily for one year. Patients were assessed were regularly assessed for signs of relapse using the Rachmilewitz clinical and endoscopic activity indices, and according to histology at the end of the study.

Compared to the relapses of patients on mesalazine (38/112 = 33.9 percent), the probiotic group had a similar percentage of relapse (40/110 = 36.4 percent). "The probiotic drug E. coli Nissle 1917 shows efficacy and safety in maintaining remission equivalent to the gold standard mesalazine in patients with UC" and that these results re-emphasize "the pathogenetic significance of the enteric flora."

Although both groups tolerated their treatment well with no reported adverse side effects, a note of caution should be raised about mesalazine, since it has been the subject of research regarding dangerous side effects that include pancreas and kidney damage,5 making probiotics all the more reasonable as an effective option for UC.

Reference:
1 Botoman VA. Management of inflammatory bowel disease. Am Fam Physician. 1998 Jan 1;57(1):57-68, 71-2

2 Kanauchi, O. Modification of intestinal flora in the treatment of inflammatory bowel disease. Curr Pharm Des. 2003;9(4):333-46

3 Linskins, RK. The bacterial flora in inflammatory bowel disease: current insights in pathogenesis and the influence of antibiotics and probiotics. Scand J Gastroenterol Suppl. 2001(234):29-40

4 Kruis S. Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine. Gut 2004 Nov; 53(11): 1617-23

5 Sulphasalazine and mesalazine: serious adverse reactions re-evaluated on the basis of suspected adverse reaction reports to the Committee on Safety of Medicines. Gut 2002 Oct; 51(4): 536-9

http://www.nowfoods.com/?action=itemdetail&item_id=42683

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Calming Crohn's Disease with Fish Oil and Antioxidants new
      #136195 - 01/07/05 04:55 PM
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Calming Crohn's Disease with Fish Oil and Antioxidants


By Sheila Russell, Ph.D. Abstracted from "Fish oil and antioxidants alter the composition and function of circulating mononuclear cells in Crohn disease" in the American Journal of Clinical Nutrition 2004;80:1137-44.

Crohn's disease is an inflammatory disease that can affect any area within the gut, including the intestines, stomach, esophagus, and the mouth. This disease can manifest itself at any age, from young childhood to advanced age. Crohn's disease occurs in whites at a rate of 2-5 times than that of non-whites3 and tends to run in some families.

The exact cause of this disease is unknown, and persons afflicted with Crohn's must also contend with two very common complications: malnutrition1 and bone loss.2 The development of malnutrition is due to poor absorption in the diseased area. The cause of bone loss is believed to be part of the inflammatory process. Researchers believe that immune cells present within the diseased area become activated. Then some of these activated cells migrate into the circulation where they cause additional sites of inflammation, such as in the bone, causing bone resorption. Therefore, treatments for this disease need to be able to combat the inflammation, not only in the gut, but also in the bones.

Supplementing with fish oil and antioxidants may be one way to prevent inflammatory cells from forming in the gut and to decreasing the overall tendency of circulating defense cells to cause inflammation. Based on a previous report showing that fish oil could inhibits Crohn's disease relapse in some patients with inactive disease,4 researchers wanted to know if fish oil along with antioxidants could work in patients with active Crohn's disease. Therefore, they conducted a study involving 62 adults with Crohn's disease.

Subjects received, either a fish oil supplement (2.7 g EPA and DHA) and an antioxidant supplement (200 mcg selenium, 3 mg manganese, 30 mg vitamin E, 450 mcg vitamin A and 90 mg vitamin C), or a placebo daily for 24 weeks. Blood samples were drawn to evaluate the effectiveness of the dietary supplements. Researchers analyzed the circulating defense cells to measure changes in the amounts and types of chemicals these cells were producing.

Results from the study showed that in subjects who consumed the fish oil and antioxidants, circulating defense cell contained more EPA and DHA. Circulating defense cells were also producing less inflammatory chemicals. These results are promising and demonstrate that alterations in the consumption of the type of fats in the diet can affect the state of the inflammatory cells. Now, whether or not these alterations within the circulating cells would lead to disease remission is unknown at this time. Additional clinical testing is required in persons with Crohn's disease before the benefits of this regiment can be determined.

Reference:

1 Harries AD, Jones LA, Heatley RV, Rhodes J. Malnutrition in inflammatory bowel disease: an anthropometric study. Hum Nutr Clin Nutr 1982;36:307-13

2 Bjarnason I, Macpherson A, mackintosh C, Buxton-Thomas M, Forgacs I, Moniz C. Reduced bone density in patients with inflammatory bowel disease. Gut 1997;40:228-33

3 Crawford JM. The gastrointestinal tract. in Robbins Pathologic Basis of Disease, 5th ed. eds. Cotran RS, Kumar V, Ribbing SL. W.B. Saunders Co. Philadelphia 1994, pg 801

4 Belluzzi A, Brignola C, Campieri M, Pera A, Boschi S, Miglioli M. Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease. N Engl J Med 1996;334:1557-41


http://www.nowfoods.com/?action=itemdetail&item_id=42749&TPL_NAME=printview.tpl&CSPID=a39d6fefcfee85d6e3b5b0129922e23b

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Biotic Therapy Cuts Inflammation in Ulcerative Colitis new
      #152022 - 02/19/05 05:59 PM
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Biotic Therapy Cuts Inflammation in Ulcerative Colitis



By David Douglas

NEW YORK (Reuters Health) Feb 04 - Synbiotic therapy, involving prebiotic and probiotic agents, reduces chronic inflammation in patients with active ulcerative colitis, Scottish researchers report in the February issue of Gut.

As lead investigator Dr. Elizabeth Furrie told Reuters Health, "Feeding twice daily with the synbiotic therapy for one month induced highly significant reduction in the inflammatory state of the colon that translated to clinical improvement. This therapy has demonstrated no side effects and can be taken in conjunction with conventional treatment."

Dr. Furrie and colleagues at the University of Dundee note that the immune response to normal commensal microorganisms is believed to be associated with such inflammatory processes in ulcerative colitis.

To see whether modulation of gut flora might alter the disease process, the researchers combined the probiotic Bifidobacterium longum and a prebiotic, the enriched inulin mixture Synergy 1 to provide a growth substrate.

In total, 18 patients with active ulcerative colitis were randomized in a double-blind fashion to 4 weeks of synbiotic therapy or to placebo.

Over this period, sigmoidoscopy scores on a 7-point scale fell in the active treatment group from 4.5 to 3.1. In placebo patients, there was an increase from 2.6 to 3.2.

In addition, mRNA levels of human beta defensins 2, 3 and 4 -- which are strongly upregulated in those with the disease -- were significantly reduced. This was also true of the inflammatory cytokines tumor necrosis factor alpha and interleukin 1 alpha.

Biopsies also showed that the synbiotic group had reduced inflammation as well as regeneration of epithelial tissue.

Following these encouraging results, the researchers call for a large-scale trial to "investigate the long term effect of synbiotic use in inducing and maintaining remission in patients with active disease."

Gut 2005;54:242-249.

http://www.merckmedicus.com/pp/us/hcp/hcp_newsarticle.jsp?newsid=345863&newsgroup=2

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Fish oil, soluble fiber, and antioxidants for corticosteroid sparing in ulcerative colitis new
      #173164 - 04/24/05 03:33 PM
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Clinical Gastroenterology and Hepatology
April 2005 • Volume 3 • Number 4

Original Articles

An oral supplement enriched with fish oil, soluble fiber, and antioxidants for corticosteroid sparing in ulcerative colitis: A randomized, controlled trial

Douglas L. Seidner &#8270; &#8270; [MEDLINE LOOKUP]
Bret A. Lashner &#8270; [MEDLINE LOOKUP]
Aaron Brzezinski &#8270; [MEDLINE LOOKUP]
Phillip L.C. Banks ‡ [MEDLINE LOOKUP]
John Goldblum § [MEDLINE LOOKUP]
Claudio Fiocchi ¶ [MEDLINE LOOKUP]
Jeffry Katz ¶ [MEDLINE LOOKUP]
Gary R. Lichtenstein &#8741; [MEDLINE LOOKUP]
Peter A. Anton # [MEDLINE LOOKUP]
Lori Y. Kam &#8270;&#8270; [MEDLINE LOOKUP]
Keith A. Garleb ‡‡ 1 [MEDLINE LOOKUP]
Stephen J. Demichele ‡‡ 1 [MEDLINE LOOKUP]

The Enteral Nutrition in Ulcerative Colitis Study Group

Background & Aims: N-3 fatty acids from fish oil, antioxidants, and short-chain fatty acids (SCFAs) produced during the fermentation of soluble fiber may attenuate inflammation associated with ulcerative colitis (UC). We assessed the efficacy of a nutritionally balanced oral supplement enriched with fish oil, fructooligosaccharides, gum arabic, vitamin E, vitamin C, and selenium on disease activity and medication use in adults with mild to moderate UC.

Methods: A total of 121 patients with UC and a disease activity index (DAI) from 3–9 on a 12-point scale were block randomized for extent of disease and smoking status. In addition to their usual diet, patients consumed 18 oz of the oral supplement or a carbohydrate-based placebo formula each day for 6 months. Clinical and histologic responses were assessed at 3 and 6 months or at the final visit. A change in average prednisone use between groups was tested by using a linear mixed-effects model. Results: Eighty-six patients completed the study. Baseline characteristics were not different between groups except for a higher total DAI score in the oral supplement group (7.3 ± 1.3; n = 36) compared with the placebo group (6.2 ± 2.0; n = 50) (P < .05). Both groups showed significant and similar degree of improvement at 6 months in DAI (&#8722;2.5 for oral supplement and &#8722;2.8 for placebo) and histologic index (&#8722;1.9 for oral supplement vs. &#8722;2.0 for placebo). Both intent-to-treat and completed patients given oral supplement had a significantly greater rate of decrease in the dose of prednisone required to control clinical symptoms over 6 months as compared with the placebo group (P < .001).

Conclusions: The improvement in clinical response combined with a decreased requirement for corticosteroids suggest that this enriched oral supplement can be a useful adjuvant therapy in patients with UC.

Department of Gastroenterology, Cleveland Clinic Foundation, Cleveland, Ohio, USA
§Department of Anatomic Pathology, Cleveland Clinic Foundation, Cleveland, Ohio, USA
‡STATPROBE, Dublin, Ohio, USA
¶Department of Gastroenterology, Case Western Reserve University, Cleveland, Ohio, USA
&#8741;Department of Gastroenterology, University of Pennsylvania, Philadelphia, Pennsylvania
#Department of Gastroenterology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California
&#8270;&#8270;Department of Gastroenterology, University of Southern California Medical Center, Los Angeles, California
‡‡Strategic Discovery R&D, Ross Products Division, Abbott Laboratories, Columbus, Ohio, USA
Supported in part by a grant from Ross Products Division, Abbott Laboratories.
1Drs Garleb and Demichele are employees of Ross Products Division, Abbott Laboratories.
&#8270;Address requests for reprints to: Douglas L. Seidner, MD, Department of Gastroenterology\A30, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195fax: (216) 444-6305.
Email address: seidned@ccf.org (Douglas L. Seidner)
Copyright © 2005 by American Gastroenterological Association

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IBD Patients May Benefit From Folic Acid Supplementation new
      #180700 - 05/22/05 07:02 PM
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IBD Patients May Benefit From Folic Acid Supplementation

NEW YORK (Reuters Health) Apr 29 - Homocysteine levels are increased in both the mucosa and blood of patients with Crohn's disease and ulcerative colitis, according to a new study, suggesting that this molecule may play a pathogenic role in intestinal inflammation. Further, the effect could be abolished by folate supplementation.

Elevated homocysteine "contributes to the pathophysiology" of several chronic inflammatory diseases, investigators note in the April issue of the American Journal of Gastroenterology. But whether homocysteine is involved in mucosal inflammation in patients with inflammatory bowel disease (IBD) has not been explored, until now.

In their study of 83 patients with Crohn's, 83 with ulcerative colitis, and 70 healthy controls, plasma and mucosal homocysteine levels were significantly higher in IBD patients relative to control subjects.

Specifically, they observed that IBD-derived intestinal lamina propria mononuclear cells (LPMC) released higher homocysteine than control-derived LPMC.

Culturing intestinal microvascular endothelial cells in homocysteine alone, or in combination with TNF-alpha to mimic the in vivo IBD intestinal conditions, effectively triggered an inflammatory reaction in these cells, leading to upregulation of various endothelial cell adhesion molecules.

The team also observed low folate levels in the IBD patients. Folate levels were inversely correlated with homocysteine levels and, in in vitro studies, the addition of folic acid, a homocysteine scavenger, blocked the homocysteine-triggered inflammatory effects.

Therefore, Dr. Silvio Danese, from Catholic University in Rome, Italy and colleagues think it would be "reasonable to hypothesize a beneficial effect of folic acid supplementation in IBD patents to eliminate the homocysteine-mediated inflammatory events, especially mononuclear cell adhesion."

Am J Gastroenterol 2005;100:896-895.:


http://www.medscape.com/viewarticle/504063?src=mp

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The Clinical Epidemiology of Inflammatory Bowel Disease new
      #207552 - 08/22/05 04:45 PM
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The Clinical Epidemiology of Inflammatory Bowel Disease

Bret A. Lashner, MD


Introduction
Several important advances regarding the clinical epidemiology of inflammatory bowel disease (IBD) were presented during this year's Digestive Disease Week (DDW) meeting. Among the advanced imaging techniques examined, computed tomography (CT) enterography, chromoendoscopy, and magnetic resonance (MR) colography appear to be the leading technologies, whereas wireless capsule endoscopy appears to be less useful than previously believed. Additionally, genetic linkages in IBD are being discovered or confirmed at a very rapid rate, as highlighted in key discussions during these meeting proceedings. Investigators are also elucidating the natural history of IBD from large, meticulously maintained databases to confirm incidence and surgery rates, associations with other diseases, and risk of complications, such as pouchitis or cancer. As further evident from the focus of key sessions at this year's meeting, cancer surveillance in IBD remains a hotly debated topic with somewhat conflicting studies to sort through.

This clinical overview discusses some of the more key DDW sessions documenting these advances.

Advanced Imaging in IBD
There is mounting evidence that chromoendoscopy is a preferred imaging technique for cancer surveillance in ulcerative colitis. This technique could be improved even further with the addition of confocal laser microscopy. In a randomized clinical trial involving 153 patients with long-standing ulcerative colitis, 80 patients underwent conventional colonoscopic surveillance and 73 underwent chromoendoscopy with confocal endomicroscopy for detection of lesions suspicious for neoplasia.[1] Significantly more neoplastic lesions were found in the chromoendoscopy group (19 vs 4; P = .0007). Compared with conventional histology, confocal endomicroscopy had a sensitivity of 95% and a specificity of 98% for identifying neoplastic lesions Therefore, the study authors concluded that chromoendoscopy, as compared with conventional endoscopy, was able to identify lesions likely to be neoplastic, and that confocal laser microscopy could confirm neoplasia in these lesions in vivo.

Wireless capsule endoscopy is used in clinical practice to diagnose Crohn's disease or as a tool to assess extent and severity of disease. In a study by Esrailian and colleagues[2] presented during these meeting proceedings, 41 experts in IBD were asked to judge the appropriateness of wireless capsule endoscopy in 5 case scenarios. The overwhelming majority of experts (> 83% for each case) deemed wireless capsule technology to be "inappropriate" in cases of (1) suspected Crohn's disease; (2) newly diagnosed Crohn's disease; (3) new perianal fistulas; (4) steroid-refractory stricture in Crohn's disease; and (5) postoperative fibrostenotic Crohn's disease. At the present time, experts seem to agree that wireless capsule endoscopy is not helpful in the diagnosis or management of patients with Crohn's disease. Children may be at higher risk than adults for complications from wireless capsule endoscopy. Indeed, a retrospective review by Moy and colleagues[3] found a 22.5% risk for complications among 32 studies in 31 children. Three patients had capsules that did not pass the pylorus by 8 hours (2 patients needed endoscopic removal) and 4 had capsules that did not pass through the small bowel (3 required surgical removal or bowel resection and 1 required steroid treatment). Thus, it is doubtful that the potential benefits of wireless capsule endoscopy justify the risk in pediatric patients.

The utility of CT enterography was evaluated in 51 patients with Crohn's disease of the small bowel to determine whether the additional information provided by this modality changed clinical management (eg, steroid use choices).[4] Although CT enterography correlated poorly with other radiologic and clinical findings, it did change management in 34 (67%) of the patients. On the basis of the additional findings on CT enterography, steroids were added in the management of 14 patients, and 20 patients had steroid therapy reduced or eliminated. Therefore, such application of technology appears to be promising.

Solem and colleagues[5] compared the sensitivity, specificity, and accuracy of CT enterography, wireless capsule endoscopy, small bowel x-ray, and ileoscopy during colonoscopy in the diagnosis of small bowel Crohn's disease. Forty-two patients with suspected or known Crohn's disease were offered all 4 tests sequentially. CT enterography and ileocolonoscopy had the highest accuracy (86% and 85%, respectively). Small bowel x-ray had an accuracy of 79% due to a relatively low sensitivity (65%), and wireless capsule endoscopy had a low accuracy (67%) due to a poor specificity (53%). On the basis of these results, CT enterography appears likely to improve our current approach to diagnosing Crohn's disease.

MR colonography, without colonic cleansing, has been proposed for use in the pediatric IBD patient. In a study by Falconieri and colleagues,[6] 22 pediatric patients (14 with ulcerative colitis, 2 with Crohn's disease, and 6 normal [controls]) underwent unprepped MR colonography to compare the findings with colonoscopy. Twelve of the 14 patients with ulcerative colitis had thickened bowel wall (abnormal MR colonography) that correlated with the extent of disease. The sensitivity and specificity of this test was 81% and 85%, respectively. Thus, on the basis of these findings, MR colonography, with no radiation exposure and no preparation, has certain advantages over other forms of testing for investigation of colonic involvement in pediatric IBD.

Genetic Susceptibility in IBD
Some patients with chronic pouchitis may have undiagnosed Crohn's disease. Pouchitis is a common complication after ileal pouch-anal anastomosis for ulcerative colitis, and innate immune responses targeted against enteric bacteria have a role in its pathogenesis. Meier and colleagues[7] conducted a retrospective study of 97 patients with ileal pouch-anal anastomoses to determine whether genetic polymorphisms in the innate immune receptor toll-like receptor 4 and the IBD susceptibility gene NOD2/CARD15 were associated with pouchitis. The L1007fsinsC mutation in CARD15 was found to be associated with chronic pouchitis -- all patients who harbored this mutation developed pouchitis. No patient with intermittent pouchitis or no pouchitis was found to harbor this mutation. Additionally, the toll-like receptor 4 polymorphisms, a common defect in innate immunity dysfunction, were not associated with pouchitis. The study authors concluded that patients with chronic pouchitis had genetic polymorphisms similar to those found in patients with Crohn's disease, whereas in those without pouchitis, the frequency of these polymorphisms was similar to that reported in ulcerative colitis patients and the general population. Thus, CARD15 mutations, particularly the L1007fsinsC polymorphism, may predispose to the development of chronic pouchitis following ileal pouch-anal anastomosis for ulcerative colitis.

There is a purported linkage with IBD on chromosome 10 near the DLG5 gene (codes for an important scaffolding protein). Cummings and colleagues[8] conducted a case-control study to examine the contribution of variants in this gene to disease heterogeneity in IBD. The study authors compared 699 IBD patients with 360 controls; no associations with DLG5 polymorphisms were found, even when patients were stratified according to CARD15 polymorphisms. In another cohort involving 981 IBD patients and 305 controls, the OCTN (carnitine/organic cation transporter) gene cluster on chromosome 5 (the IBD5 locus) was found to be associated with fistulizing Crohn's disease (odds ratio [OR]: 1.47, 95% confidence interval [CI] 1.03-2.11).[9] No associations with IBD (ie, a particular phenotype) were found for the DLG5 gene.

Studying phenotypic homogeneous subgroups of IBD patients may increase the likelihood of finding genotype-phenotype correlations. In a study involving 867 IBD-affected relative pairs, linkage was found for CARD15 (IBD1 locus) and ileal Crohn's disease (lod score [measure of degree of linkage] = 2.56; P = .035), the IBD2 locus and extensive ulcerative colitis (lod = 3.27; P < .001), Crohn's disease in non-Jewish patients and IBD3 (lod = 2.93 for colonic disease, lod = 2.97 for perianal disease), and evidence for linkage on IBD5 was seen in non-Jewish patients with colonic disease (lod =2.85).[10] Very few of these associations could have been identified without examining homogeneous subgroups.

Blood samples were collected from 595 patients with IBD and 627 controls followed for more than 10 years in the European Cooperative IBD study. Data from this cohort are unique in that they can facilitate the investigation of whether genetic or immune markers influence longitudinal changes in disease phenotypes. Riis and colleagues[11] studied mutations in CARD15 and ASCA (anti-Saccharomyces cerevisiae) with regard to longitudinal changes in disease phenotype among IBD patients The immune marker ASCA and CARD15 were found to be associated with a change in behavior over time from inflammatory to stricturing or fistulizing Crohn's disease (OR: 3.2; 95% CI: 1.2-8.8). Indeed, both genetic factors and abnormal immune responses to bacterial stimuli are believed to play a role in the pathogenesis underlying Crohn's disease. Recently, an association between Crohn's disease and CARD8 located in the IBD6 region (19p13) has been reported. In a study of 354 patients with Crohn's disease and 225 matched controls, the combination of CARD8 mutations in the IBD6 region on chromosome 19 and anti-OmpC (antibody to a protein expressed by Escherichia coli) was found to be synergistically associated with fistulizing Crohn's disease.[12] The study authors theorized that a mutation in the CARD8 protein could lead to a dysregulated immune response that when coupled with an aberrant immune response to commensal bacteria (anti-OmpC mutation) could lead to an aggressive, transmural inflammatory disease.

Natural History of IBD
Autoimmune manifestations are reported to be associated with both Crohn's disease and ulcerative colitis. In this context, Bernstein and colleagues[13] assessed the coincident occurrence of IBD and other autoimmune disorders using population-based data from Manitoba. Odds ratios significantly greater than 1 were found for asthma, bronchitis, and psoriasis with Crohn's disease, and for asthma, bronchitis, psoriasis, multiple sclerosis, and chronic renal disease with ulcerative colitis. Asthma was the most common autoimmune disorder found to be coincident with IBD. Thyroiditis and neuropathy were not more common in patients with IBD compared with controls. In a related investigation, Tang and colleagues[14] conducted a retrospective study using the University of Manitoba IBD database to examine fistula formation in patients with Crohn's disease. They found that 19.2% of the Crohn's disease population had fistulas. If perianal fistulas were present, the risk of having a concomitant luminal fistula was found to be significantly increased (OR: 4.45; 95% CI: 2.92-6.76). Therefore, the presence of perianal fistulas should prompt an examination for luminal fistulous disease. In another study reported during these meeting proceedings, Bernstein and colleagues[15] assessed the burden of IBD using population-based data from 5 provinces in Canada. Incidence rates for Crohn's disease per 100,000 ranged between 12.2 and 22.5, and for ulcerative colitis ranged between 8.6 and 21.2. Prevalence of disease per 100,000 persons ranged between 231 and 325 for Crohn's disease, and between 182 and 255 for ulcerative colitis. For all IBD, the female:male ratio ranged from 1.14 to 1.29. Thus, overall, the prevalence of IBD in Canada was found to be 491/100,000 persons; that is, 0.5% of the population has IBD.

Is there an association between early postoperative pouch histology and development of pouchitis after ileal pouch-anal anastomosis for ulcerative colitis? To predict the development of acute or chronic pouchitis, investigators from Toronto took biopsies from the pouch of patients soon after surgery and evaluated 109 patients for a mean of 11.5 years.[16] Early inflammation was found to be a predictor of chronic pouchitis (hazard ratio 7.4; 95% CI: 2.14-24.2). The investigators suggested that such patients should be considered for early prophylactic therapy to prevent development of chronic pouchitis. Early histology did not predict the occurrence of acute pouchitis.

What is the colectomy risk in ulcerative colitis after 10 years? The European Cohort IBD group studied 784 patients with ulcerative colitis for a minimum of 10 years to evaluate colectomy rates.[17] They found that only 7.6% of patients had colectomies. It is interesting to note that northern European countries had much higher colectomy rates than southern European countries. Despite the fact that no information on extent of disease was presented, the purported colectomy rate of 20% to 30% in patients with ulcerative colitis is likely to be a gross overestimate.

Cancer Surveillance in IBD
Are older patients with late-onset IBD at risk for colorectal cancer and do they require frequent colonoscopic surveillance? Investigators from the Hines VA Hospital in Hines, Illinois, followed 114 older ulcerative colitis patients with late-onset disease and compared outcomes with a comparable group of 6829 non-IBD controls.[18] The annual incidence of cancer in the ulcerative colitis group was 0.14% compared with 0.11% in controls (P = not significant). On the basis of these findings, the investigators suggested that older patients with late-onset ulcerative colitis should undergo surveillance at the same intervals suggested for those with sporadic disease.

The long-term safety of infliximab, an anti-tumor necrosis factor-alpha monoclonal antibody, is currently under investigation. In a case-control study, Biancone and colleagues[19] evaluated the development of neoplasia in 392 patients with Crohn's disease treated with infliximab compared with matched controls. Nine patients treated with infliximab and 6 controls developed neoplasia (OR: 1.51; P = .60). Among those patients in the infliximab-treated group who developed neoplasia, there was 1 cholangiocarcinoma, 3 breast cancers, 2 skin cancers, 1 laryngeal cancer, and 2 anal canal cancers. Among the controls who developed neoplasia, there was 1 ileal adenocarcinoma, 2 skin cancers, 1 lymphoma, 1 cecal adenocarcinoma, and 1 breast cancer. Thus, the results of this study suggest that infliximab did not significantly increase the risk of neoplasia.

Recent reports have suggested that dysplasia and colorectal cancer may be endoscopically visible in many patients with IBD. Rubin and colleagues[20] conducted a retrospective review of a large registry of patients with ulcerative colitis who underwent surveillance examinations over a 10-year period; 1339 examinations were performed in 622 patients. Sixty-four dysplastic lesions were found in 44 patients during this study interval; 35 of 56 (62.5%) dysplastic lesions were visible to the endoscopist, and 7 of 8 (87.5%) cancers were visible. Visible lesions included polyps or masses, strictures, or irregular mucosa. The sensitivity of visibly (ie, by endoscopy) identifying neoplastic lesions was 79.5%. Chromoendoscopy is likely to increase this sensitivity rate much further by making even more lesions visible.

At present, it remains unclear why some patients with IBD have an increased risk of colorectal neoplasia. Jess and colleagues[21] conducted a nested case-control study to investigate risk factors for colorectal neoplasia in 2 large population-based IBD cohorts; 52 patients with ulcerative colitis and neoplasia were compared with a matched set of controls. Significant risk factors for neoplasia included primary sclerosing cholangitis (OR: 8.7), active disease (OR: 3.1), continuously active disease for more than 1 year (OR: 4.0), sulfasalazine use (OR: 1.13), mesalamine use (OR: 1.22), and a higher cumulative dose of steroids (OR: 1.05). These study findings did not support the accumulating evidence that mesalamine may have chemopreventive effects for neoplasia.

Results of population-based studies have demonstrated a slightly increased mortality rate for patients with Crohn's disease over the last 40 years. Wolters and colleagues[22] presented the results of a study assessing mortality risk in a European cohort of Crohn's disease patients 10 years post diagnosis. In this European cooperative study of 371 incident cases of Crohn's disease followed for at least a decade, there were 37 deaths (SMR [standardized mortality ratio] 1.72; 95% CI: 1.21-2.38). There were 8 deaths from gastrointestinal malignancies vs only 0.86 expected (SMR 8.14; 95% CI: 3.26-16.78). In this cohort, patients with Crohn's disease had an increased mortality risk, especially from gastrointestinal malignancies.

Recent reports have suggested a high risk for progression to high-grade dysplasia or cancer among IBD patients with flat low-grade dysplasia; this has led to more aggressive surgical intervention. Jess and colleagues[23] reported the results of a study to assess the true long-term outcome of colorectal dysplasia in a population-based IBD cohort. Among 691 incident ulcerative colitis cases followed in a cancer surveillance program, there were 9 with dysplasia in flat mucosa, 1 with a dysplasia-associated lesion or mass (DALM), and 23 with adenoma-like masses (ALMs). In patients with ALMs, 3 had recurrent adenomas, 3 developed flat low-grade dysplasia, 2 developed DALMs, and 1 developed multifocal Dukes' C adenocarcinoma. Although these findings did not confirm the previously reported risk for progression in flat dysplastic lesions, they did document ALMs as worrisome lesions in patients with ulcerative colitis.

Conclusion
On the basis of data presented during this year's DDW meeting, and as discussed above, the clinical care of IBD patients may evolve and change. Although findings suggest that CT enterography and MR colography will be used more often to diagnose IBD and its complications; wireless capsule endoscopy has not yet found its place in the care of these patients. Chromoendoscopy is sure to improve outcomes from cancer in IBD, but much additional study is needed regarding treatment recommendations for lesions found with such testing. Last, as investigators continue to identify and confirm genes associated with IBD, the closer clinicians are to finding the cause and cure of IBD.

References
Kiesslich R, Goetz M, Schneider C, et al. Confocal endomicroscopy as a novel method to diagnose colitis-associated neoplasm in ulcerative colitis: A prospective randomized trial. Gastroenterology. 2005;128(suppl 2):A-73. [Abstract 483]
Esrailian E, Targownik EL, Spiegel BM, et al. Is wireless capsule endoscopy appropriate for the diagnosis and management of Crohn's disease? A survey of North American Inflammatory Bowel Disease experts. Gastroenterology. 2005;128(suppl 2):A-73. [Abstract 484]
Moy L, Levine J. Wireless capsule endoscopy in the pediatric age group: Experience and complications. Gastroenterology. 2005;128(suppl 2):A-73. [Abstract 485]
Higgins PD, Caoili E, Zimmermann M, et al. CT enterography adds information to clinical management in small bowel Crohn's disease. Gastroenterology. 2005;128(suppl 2):A73-A74. [Abstract 487]
Solem CA, Loftus EV, Fletcher JG, et al. Small bowel imaging in Crohn's disease: A prospective, blinded, 4-way comparison trial. Gastroenterology. 2005;128(suppl 2):A74 [Abstract 488]
Falconieri P, Laghi A, Paolantonio P, et al. Un-prepped MR colonography in pediatric patients with inflammatory bowel disease. Gastroenterology. 2005;128(suppl 2):A-49. [Abstract 342]
Meier C, Aisenberg J, Legnant P, et al. Innate immune receptor polymorphisms in pouchitis: Is NOD2/CARD15 a susceptibility factor? Gastroenterology. 2005;128(suppl 2):A-112. [Abstract 726]
Cummings JRF, Kerrlinger KR, Ahmad T, Jewell DP. Genotype-phenotype analyses of the IBD susceptibility gene DLG5. Gastroenterology. 2005;128(suppl 2):A-112. [Abstract 727]
Vermeire S, Pierik M. Henckaerts L, et al. Study on DLG5 and OCTN polymorphisms shows association of the OCTN TC risk haplotype with perianal and fistulizing Crohn's disease but not with susceptibility to IBD. Gastroenterology. 2005;128(suppl 2):A-113. [Abstract 731]
Achkar JP, Dassopoulous T, Silverberg M, et al. Disease location refines genomic localization in inflammatory bowel disease: IBD is an extensive ulcerative colitis locus. Gastroenterology. 2005;128(suppl 2):A-112-A113. [Abstract 728]
Riis L, Wolters F, Solberg C, et al. ASCA is associated with CARD15 mutations and longitudinal changes in behavior of Crohn's disease: A population based ED-IBD study. Gastroenterology. 2005;128(suppl 2):A-113. [Abstract 729]
Picornell Y, Abreu MT, Ippoliti A, et al. CARD8 variant and the expression of anti-OmpC are synergistically associated with internal penetrating Crohn's disease. Gastroenterology. 2005;128(suppl 2):A-113.[Abstract 730]
Bernstein CN, Blanchard JF, Wajda A. A population-based study of comorbidity and other autoimmune diseases in IBD. Gastroenterology. 2005;128(suppl 2):A-113. [Abstract 732]
Tang LY, Rawsthorne P, Bernstein CN. In Crohn's disease is there an association between perianal fistulzing disease and luminal fistulizing disease? A population-based study. Gastroenterology. 2005;128(suppl 2):A-113-A114. [Abstract 733]
Bernstein CN, Wajda A, Blanchard JF, et al. The burden of IBD in Canada: A population-based study. Gastroenterology. 2005;128(suppl 2):A-114. [Abstract 735]
Johnson P, MacNeill N, Baladjay L, et al. Early post-operative pouch histology predicts future chronic pouchitis after ileal pouch-anal anastomosis for ulcerative colitis. Gastroenterology. 2005;128(suppl 2):A-114. [Abstract 734]
Hoie C, Wolters F, Riis L, et al. Colectomy rates in ulcerative colitis in a European inception cohort followed for ten years by the EC-IBD study group. Gastroenterology. 2005;128(suppl 2):A-114. [Abstract 736]
Hoffman SD, Sontag SJ, Levis W, et al. Late onset inflammatory bowel disease in older patients does not require frequent surveillance. Gastroenterology. 2005;128(suppl 2):A-121-A122. [Abstract 777]
Biancone L, Kohn A, Colombo E, et al. Development of neoplasia in Crohn's disease patients treated with infliximab: A case-control study in an Italian population. Gastroenterology. 2005;128(suppl 2):A-122. [Abstract 778]
Rubin DT, Rothe JA, Cohen RD, Hanauer SB. Is dysplasia and colorectal cancer endoscopically visible in patients with ulcerative colitis? Gastroenterology. 2005;128(suppl 2):A-122. [Abstract 779]
Jess T, Loftus EV, Velayos FS, et al. Risk factors for cancer and dysplasia in inflammatory bowel disease: A nested case-control study of population-based cohorts from Copenhagen County and Olmsted County. Gastroenterology. 2005;128(suppl 2):A-122. [Abstract 780]
Wolters F, Schouten L, Sijbrandij J, et al. Increased mortality ten years after diagnosis in a Europe-wide population based cohort of Crohn's disease patients (EC-IBD Study Group). Gastroenterology. 2005;128(suppl 2):A-122. [Abstract 781]
Jess T, Loftus EV, Velayos FS, et al. Are adenomas more harmful than flat low-grade dysplasia in patients with inflammatory bowel disease? A population-based cohort study from Olmsted County, Minnesota, 1940-2002. Gastroenterology. 2005;128(suppl 2):A-123. [Abstract 782]

http://www.medscape.com/viewarticle/506628

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Differentiation of Inflammatory Bowel Disease and Irritable Bowel Syndrome new
      #210440 - 09/01/05 11:13 AM
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Rectal Mucosal Nitric Oxide in Differentiation of Inflammatory Bowel Disease and Irritable Bowel Syndrome

Clinical Gastroenterology and Hepatology
Volume 3, Issue 8 , August 2005, Pages 777-783

Claudia I. Reinders, Max Herulf;, Tryggve Ljung, Jakob Hollenberg, Eddie Weitzberg§, Jon O. Lundberg, and Per M. Hellström

Division of Pharmacology, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
‡Department of Gastroenterology and Hepatology, Karolinska University Hospital Solna, Stockholm, Sweden
§Department of Anaesthesiology and Intensive Care, Karolinska University Hospital Solna, Stockholm, Sweden


Background & Aims: Differentiating patients with functional bowel disorders from those with inflammatory bowel disease (IBD) can be difficult. Rectal luminal levels of nitric oxide (NO) are greatly increased in IBD. To further evaluate this disease marker, we compared NO in patients with irritable bowel syndrome (IBS) with those found in patients with active IBD and in healthy control subjects. Methods: Rectal NO was measured with chemiluminescence technique by using a tonometric balloon method in 28 healthy volunteers, 39 patients with IBS, 86 with IBD (Crohn's disease and ulcerative colitis), and 12 patients with collagenous colitis. In addition, NO was measured before and after a 4-week treatment period in patients with active ulcerative colitis and repeatedly during 2 weeks in healthy volunteers. Results: NO was low in healthy control subjects (median, 45; 25th–75th percentile, 34–64 parts per billion [ppb]), and variations over time were small. In IBS patients NO was slightly increased (150, 53–200 ppb; P < .001), whereas patients with active IBD or collagenous colitis had greatly increased NO levels (3475, 575–8850 ppb, and 9950, 4475–19,750 ppb, respectively; P < .001). With a cutoff level of 250 ppb, NO had a sensitivity of 95% and a specificity of 91% in discriminating between active bowel inflammation and IBS. Rectal NO correlated with disease activity in IBD and collagenous colitis and decreased markedly in IBD patients responding to anti-inflammatory treatment. Conclusions: Rectal NO is a minimally invasive and rapid tool for discriminating between active bowel inflammation and IBS and a possibly useful add-on for monitoring patients with IBD.

Abbreviations used in this paper: CI, confidence interval; GI, gastrointestinal; HBI, Harvey Bradshaw index; IBD, inflammatory bowel disease; IBS, irritable bowel syndrome; NO, nitric oxide; ppb, parts per billion


Supported by grants from the Knowledge Foundation, the Swedish Research Council, and Karolinska Institutet. Eddie Weitzberg and Jon O. Lundberg own shares in Aerocrine AB, a company that manufactures equipment for measurements of nitric oxide.
Address requests for reprints to: Claudia Reinders, MSc, Department of Physiology and Pharmacology, Division of Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden. fax: +46 8 33 22 78.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7GGW-4GV2755-K&_user=10&_handle=V-WA-A-W-WC-MsSAYVA-UUW-U-AAWDWECCVA-AAWVYDZBVA-WECDUEZWB-WC-U&_fmt=summary&_coverDate=08%2F31%2F2005&_rdoc=17&_orig=browse&_srch=%23toc%2320161%232005%23999969991%23603702!&_cdi=20161&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=f0dd70723cf0e5dc95f617a69215484f

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Cannabinoids Show Promise for Inflammatory Bowel Disease new
      #210445 - 09/01/05 11:23 AM
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Cannabinoids Show Promise for Inflammatory Bowel Disease

NEW YORK (Reuters Health) Aug 12 - Cannabis-based drugs may have therapeutic potential in inflammatory bowel disease, UK researchers report in the August issue of Gastroenterology.

"The system that responds to cannabis in the brain is present and functioning in the lining of the gut," lead researcher Dr. Karen Wright, of the University of Bath, explained to Reuters Health. "There is an increased presence of one component of this system during inflammatory bowel diseases -- Crohn's and ulcerative colitis."

Dr. Wright and her colleagues established the location of cannabinoid receptors CB1 and CB2 in human colonic tissue and used human colonic epithelial cells lines in cannabinoid-binding and in wound-healing experiments.

Expression of both receptors was detected on plasma cells in the lamina propria, but only CB2 was present on macrophages.

CB2 was increased and immunoreactivity was seen in the epithelium of colonic tissue characteristic of inflammatory bowel disease. Cannabinoids enhanced epithelial wound closure via CB1-related mechanisms.

Thus continued Dr. Wright, "cannabinoids, which we make ourselves, as well as synthetic cannabinoids, can promote wound healing in the gut, which is extremely interesting given that inflammatory bowel disease involves damaged gut linings."

Although no data are available yet, she added, relevant case studies of the use of cannabinoids are taking place in the UK and a clinical trial is being conducted in Germany.

Gastroenterology 2005.


http://www.medscape.com/viewarticle/510626?src=mp

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Oral Contraceptives and HRT a Risk Factor for Inflammatory Bowel Disease new
      #213003 - 09/13/05 01:22 PM
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Risk Factors for Inflammatory Bowel Disease in the General Population

L. A. García Rodríguez; A. González-Pérez; S. Johansson; M.-A. Wallander


Background: The aetiology of inflammatory bowel disease remains largely unknown.

Aim: We performed a comprehensive assessment of potential risk factors associated with the occurrence of inflammatory bowel disease.

Methods: We identified a cohort of patients 20–84 years old between 1995 and 1997 registered in the General Practitioner Research Database in the UK. A total of 444 incident cases of IBD were ascertained and validated with the general practitioner. We performed a nested case–control analysis using all cases and a random sample of 10 000 frequency-matched controls.

Results: Incidence rates for ulcerative colitis, Crohn's disease, and indeterminate colitis were 11, 8, and 2 cases per 100 000 person-years, respectively. Among women, we found that long-term users of oral contraceptives were at increased risk of developing UC (OR: 2.35; 95% CI: 0.89–6.22) and CD (OR: 3.15; 95% CI: 1.24–7.99). Similarly, long-term users of HRT had an increased risk of CD (OR: 2.60; 95% CI: 1.04–6.49) but not UC. Current smokers experienced a reduced risk of UC along with an increased risk of CD. Prior appendectomy was associated with a decreased the risk of UC (OR: 0.37; 95% CI: 0.14–1.00).

Conclusions: Our results support the hypothesis of an increased risk of inflammatory bowel disease associated with oral contraceptives use and suggest a similar effect of hormone replacement therapy on CD. We also confirmed the effects of smoking and appendectomy on inflammatory bowel disease.


L. A. García Rodríguez*, A. González-Pérez*, S. Johansson, M.-A. Wallander

*Centro Español de Investigación Farmacoepidemiológica (CEIFE), Madrid, Spain;

AstraZeneca R&D Mölndal, Sweden;
Section of Preventive Cardiology, Göteborg University, Sweden;
Department of Public Health and Caring Science, Uppsala University, Sweden


Aliment Pharmacol Ther. 2005;22(4):309-315.

©2005 Blackwell Publishing

To read this article in full, please click here:

http://www.medscape.com/viewarticle/510581?src=mp

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Colonoscopic Surveillance in Inflammatory Bowel Disease new
      #218946 - 10/11/05 01:33 PM
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From Current Opinion in Gastroenterology

Colonoscopic Surveillance in Inflammatory Bowel Disease

Thomas A Ullman, Mount Sinai School of Medicine, New York, New York


Curr Opin Gastroenterol. 2005;21(5):585-588. ©2005 Lippincott Williams & Wilkins

Posted 09/28/2005

Thomas A Ullman

Abstract and Introduction
Abstract
Purpose of Review: To describe recent findings in the literature aimed at decreasing systematic error in dysplasia surveillance in inflammatory bowel disease.
Recent Findings: Despite great promise, colonoscopic surveillance in inflammatory bowel disease has yet to be demonstrated to reduce colorectal cancer mortality. In part, this stems from a number of inherent systematic troubles, including low rates of observer agreement among pathologists; lack of consensus on the natural history of dysplasia, particularly low-grade dysplasia; the patchy nature of dysplasia, which leads to sampling error caused by insufficient biopsy by endoscopists; and incomplete patient follow-up. Recent publications that have focused on defining better the natural history of different levels of dysplasia and improving dysplasia identification at the time of colonoscopy may aid in overcoming the flaws of surveillance. The key recent findings include conflicting evidence on the relative danger of flat low-grade dysplasia, the safety of treating polypoid low-grade dysplasia as a benign adenoma in the absence of flat dysplasia in the rest of the colon or the surrounding mucosa, and preliminary support of chromoendoscopy to target dysplasia better during colonoscopy and to limit unnecessary nontargeted biopsies.
Summary: These and other advances stand a reasonable chance of making surveillance a more accurate tool to discriminate between patients with chronic colitis likely to progress to advanced pathology and those less likely to do so. Such advances may result in effective surveillance in which both colorectal cancer mortality and unnecessary colectomy may be limited.

http://www.medscape.com/viewarticle/510593?src=mp

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Carbon Monoxide Eases Ulcerative Colitis new
      #239575 - 01/18/06 04:12 PM
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Carbon Monoxide Eases Bowel Condition


MONDAY, Dec. 12 (HealthDay News) -- Carbon monoxide helps soothe a common form of inflammatory bowel disease called ulcerative colitis by shutting down the inflammation that causes the condition, a new study found.

University of Pittsburgh researchers used low concentrations of inhaled carbon monoxide to ease inflammatory bowel disease symptoms in mice. The carbon monoxide inhibited production of a protein called interleukin-12 (IL-12), which is normally produced during infection and helps activate immune cells that attack invading pathogens.

However, chronic production of IL-12 in the gut results in inflammation that causes ulcerative colitis. Inhibiting production of IL-12 prevents such inflammation, the researchers said.

The researchers are now trying to learn exactly how carbon monoxide inhibits IL-12.

Carbon monoxide is most widely known as a toxic air pollutant, but the body does produce small amounts of it as a normal byproduct of metabolism. High does of carbon monoxide are deadly because it robs the body of oxygen. However, recent studies have shown that low concentrations of carbon monoxide act as an anti-inflammatory, the researchers said.

The study findings appear in the Dec. 19 issue of the Journal of Experimental Medicine.


SOURCE: Dec. 19, 2005, Journal of Experimental Medicine news release
Copyright © 2005 ScoutNews LLC. All rights reserved.


http://generic.e-healthsource.com/index.php?p=news1&id=529540

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Viagra May Help Crohn's Disease new
      #249989 - 03/04/06 12:50 PM
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Crohn's Disease Etiology Questioned

By Jeff Minerd, MedPage Today Staff Writer
Reviewed by Rubeen K. Israni, M.D., Fellow, Renal-Electrolyte and Hypertension Division, University of Pennsylvania School of Medicine
February 23, 2006
Also covered by: BBC, Forbes

LONDON, Feb. 23 - The exaggerated immune response that is considered part and parcel of Crohn's disease may have been exaggerated, reported investigators here.


In fact, Crohn's therapies aimed at reducing chronic inflammation may be doing more harm than good, reported Anthony W. Segal, F.R.S., and colleagues of University College London here in the February 25 issue of The Lancet.


Not only that, they suggested that one aspect of this weak response-sluggish blood flow in reaction to bacterial invaders-may be improved by Viagra (sildenafil).


Crohn's disease and colitis, known collectively as inflammatory bowel diseases, affect approximately 1.4 million Americans, including some 140,000 children under the age of 18, according to the Crohn's and Colitis Foundation of America.


Compared with 13 healthy controls, 13 patients with Crohn's disease produced abnormally low levels of neutrophils and the inflammatory cytokine interleukin 8 in response to experimental wounds and abrasions (with sandpaper) the researchers made at various sites on the body.


Neutrophil production was 79% lower than normal in the rectum (P=.0003) and 50% of normal in the skin (P<.0001). IL-8 levels were 63% lower in the rectum (P=.003) and 45% lower in the skin (P<.0001), the investigators reported.


To assess response to the presence of bacteria, the researchers injected heat-killed Escherichia coli under the skin of study participants. Healthy controls showed a vigorous inflammatory response, characterized by redness, swelling, and increased blood flow.


While superficially similar, the responses of Crohn's patients were characterized by sluggish increases in blood flow. Blood flow was reduced by 77% compared with controls in patients with colonic disease (P=.0003) and by 50% compared with controls in patients with ileal disease (P=.01).


Oral administration of 50 mg of Viagra to Crohn's patients after the bacterial injection markedly increased blood flow, bringing it up to normal or near-normal in half of the individuals within 30 minutes, the investigators said.


The researchers also tested three patients with ulcerative colitis, but the responses of these patients were more similar to the control participants than to the patients with Crohn's disease, suggesting that ulcerative colitis has a different etiology than Crohn's, the authors said.


The authors believe that in Crohn's disease, reduced or delayed recruitment of neutrophils to sites at which bacteria penetrate the intestinal wall might lead to the persistence of bacteria and other organic debris in the tissue. The body may respond to this buildup of bacteria by secreting inflammatory molecules, which accumulate and lead to the chronic inflammation typical of Crohn's.


"Causation of Crohn's disease by failure of the acute inflammatory response would fit very well with the so-called hygiene hypothesis, in which the increased incidence of the disease has been attributed to improved standards of sanitation," the authors wrote, noting that incidence of the disease rose greatly in the latter part of the 20th century.


"These findings provide hope for the development of more effective therapies for Crohn's disease," the authors said. Current treatments are immunosuppressive, but although they reduce symptoms by dampening the proposed secondary inflammation, they might actually accentuate the underlying immunodeficiency.


A more successful treatment approach might be to introduce IL-8 or other proinflammatory stimuli directly into acute lesions, either by direct enteral administration or through synthesis by genetically modified gut organisms, they proposed.


"Agents that increase blood flow, such as long-acting phosphodiesterase-5 inhibitors or other vasodilatatory or proinflammatory drugs, might be useful in healing or preventing lesions in Crohn's disease," they concluded.



Primary source: The Lancet
Source reference:
Marks DJB et al. Defective acute inflammation in Crohn's disease: a clinical investigation. The Lancet. 2006; 367:668-678.

http://www.medpagetoday.com/Gastroenterology/InflammatoryBowelDisease/dh/2737

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Novel Compound Targets Mucosal Healing in Crohn's new
      #266198 - 05/29/06 02:19 PM
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LOS ANGELES, May 23 — A novel treatment that targets mucosal protection and healing rather than inflammation led to fast and significant efficacy in patients with moderate to severe Crohn's disease, researchers said here.


At the highest tested dose, teduglutide, an analog of the naturally occurring human peptide glucagon like peptide-2 (GLP-2), elicited a response at two weeks in more than 50% of patients, reported Alan L. Buchman, M.D., of Northwestern University in Chicago at Digestive Disease Week sessions here. The agent was self injected subcutaneously daily.


At eight weeks more than 60% of patients randomized to 0.20 mg/kg daily had more than a 100-point drop in the Crohn's Disease Activity Index (CDAI). The response rate was similar in the placebo group (57%). Moreover, the clinical remission rate, defined as a CDAI of less than 150 points, was more than 50% for patients in the 0.20 mg/kg group.


The dose-ranging, proof of concept trial tested three dose regimens: 0.05 mg/kg/day; 0.10 mg/kg/day; and the 0.20 mg/kg/day dose.


"We still don't know maximum dose or maximum efficacy," said Dr. Buchman.


"We sent the bar very high in this trial," he said. "Our endpoint was complete remission by primary healing of the mucosa. Our secondary endpoint was reduction of inflammation." Inflammation was measured by surrogate markers, but Dr. Buchman did not report those data.


"Inflammatory bowel disease starts in the gut, so if you can heal the gut, you can probably heal the rest of the body," Dr. Buchman said, suggesting why teduglutide demonstrated such surprising efficacy.


Maria Abreu, M.D., of Mount Sinai in New York, said she, too was impressed with the results. The typical response with biologics is about 30%, said Dr. Abreu, so the teduglutide response was significantly better.


Dr. Buchman said it was not clear just how teduglutide works. For example, the compound has a short half life, just 2 hours, a very high absolute bioavailability (87%), and it reaches its median peak concentration in 20 minutes to an hour, he said.


He proposed a number of potential mechanisms of action including, stimulation of crypt cell proliferation, inhibition of enterocyte apoptosis and stimulation of mesenteric blood flow.


But, these effects are observed even when "we can no longer detect teduglutide," he said. "So, we can't detect it, yet we see the results."


In an interview, he predicted on the basis of some open-label data, that teduglutide would be durable. "In the open label study, we don't see any dose erosion, which is a problem with the biologics because after a time you need to increase dose amount or frequency in order to maintain response. We are not seeing that effect."


The study was funded by NPS Pharmaceuticals. Dr. Buchman said NPS plans to use these data will be used to design a phase III study.



Primary source: Digestive Disease Week
Source reference:
Buchman, AL et al. "Effect of Teduglutide on Patients with Moderate-Severe Crohn's Disease after 8 Weeks of Therapy: A Prospective, Double-Blind, Placebo Controlled Trial" Abstract 686c.

http://www.medpagetoday.com/2005MeetingCoverage/2005DDWMeeting/dh/3368

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Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified? new
      #354009 - 01/05/10 12:03 PM
HeatherAdministrator

Reged: 12/09/02
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Current Opinion in Gastroenterology

Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified?
Sylvie Bradesi, PhD, James A. McRoberts, Ph.D, Peter A. Anton, MD, Emeran A. Mayer, MD

Posted: 07/15/2003; Curr Opin Gastroenterol. 2003;19(4) © 2003 Lippincott Williams & Wilkins

Abstract and Introduction
Abstract
Both irritable bowel syndrome and inflammatory bowel diseases share symptoms of altered bowel habits associated with abdominal pain or discomfort. Irritable bowel syndrome has been referred to as a functional bowel disorder, which is diagnosed by a characteristic cluster of symptoms in the absence of detectable structural abnormalities. Inflammatory bowel disease is a heterogeneous group of disorders characterized by various forms of chronic mucosal and/or transmural inflammation of the intestine. In this review, the authors discuss recent evidence suggesting several potential mechanisms that might play a pathophysiologic role in both syndromes. Possible shared pathophysiologic mechanisms include altered mucosal permeability, an altered interaction of luminal flora with the mucosal immune system, persistent mucosal immune activation, alterations in gut motility, and a role of severe, sustained life stressors in symptom modulation. It is proposed that similarities and differences between the two syndromes can best be addressed within the framework of interactions between the central nervous system and the gut immune system. Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeting current diagnostic criteria for irritable bowel syndrome, therapeutic approaches shown to be effective in inflammatory bowel disease, such as probiotics, antibiotics, and antiinflammatory agents, have been suggested as possible therapies for certain patients with irritable bowel syndrome.

Introduction
Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) represent two conditions characterized by chronically recurring symptoms of abdominal pain, discomfort (urgency and bloating) and alterations in bowel habits. However, whereas IBD is characterized by inflammation or ulcerations in the small and/or large intestine, such "organic" changes have traditionally not been associated with IBS. IBD is usually classified as ulcerative colitis or Crohn disease, but it also includes forms of microscopic colitis, eg, histologic evidence of mucosal inflammation without macroscopic abnormalities. IBD is characterized by a constellation of patient-reported history and endoscopic, histopathologic, and radiologic findings, often with serologic correlates. Classic signs that reflect the inflammatory process within the gastrointestinal tract are rectal bleeding, diarrhea, fever, and weight loss, occasionally associated with extraintestinal manifestations. Interestingly, in the absence of complications, abdominal pain is not necessarily the most prominent symptom in IBD, despite extensive mucosal inflammation and presumably sensitization of peripheral visceral pain pathways. Genetic predisposition, environmental factors, infectious agents, altered gut epithelial permeability, and impaired immune responses have been incriminated in the still unclear cause of IBD.

By contrast, IBS, classified as functional (as opposed to organic) bowel disorder, is currently diagnosed on the basis of a characteristic cluster of symptoms in the absence of detectable structural abnormalities. As a matter of fact, according to the currently used symptom criteria (Rome criteria), once organic changes are detected, a diagnosis of a functional syndrome can no longer be made.[1] Because of the nonspecificity of the cardinal symptoms of abdominal pain or abdominal discomfort (the latter including bloating-type symptoms, a sensation of rectal urgency, or incomplete evacuation), the current diagnosis of IBS applies to a heterogeneous group of patients, even after attempts to define subgroups based on predominant bowel habit. Current theories to explain the pathophysiology of IBS include alteration in visceral perception, gastrointestinal motility and gut epithelial and immune function. Considerable evidence supports a role of psychosocial and physical (ie, gastroenteric infections) stressors as central and peripheral triggers, respectively, of first symptom onset or exacerbation.[2*] As reflected by an increasing number of publications on the subject, considerable interest in the putative role of low-grade chronic inflammation in the pathogenesis of IBS has recently emerged.[3] Enhanced responsiveness to psychosocial and physical stressors has been suggested as a plausible mechanism that could explain most clinical and experimental findings in IBS, and that is consistent with the majority of the reported physiologic alterations.[4]

Evidence of Mucosal Immune Activation in Patients Meeting Symptom Criteria for Inflammatory Bowel Diseases
Several recent independent studies have demonstrated alterations in the gut-associated immune system. Quantitative assessment in unselected patients with IBS have shown increased mast cell numbers in the ileum[5] and colonic mucosa.[6] Preliminary evidence suggests an increase of overall cellularity in the colonic mucosa[7] and a higher number of mast cells containing tryptase (known to have proinflammatory effects) in the colonic lamina propria of patients with IBS.[8] Additional preliminary results indicate a significant increase of inducible nitric oxide synthase (iNOS) expression in the colonic mucosa from unselected patients with IBS compared with control patients.[9] In the human colon, upregulation of iNOS has been implicated in inflammatory processes, and increased expression has been documented in IBD.[10] More recently, a study by Chadwick et al. [11*] demonstrated intestinal mucosal immune activation in 77 symptomatic patients meeting the Rome criteria (the authors did not specify Rome I vs II criteria). The study included patients with diarrhea, constipation, or both. In 38 of the patients (50%), a normal conventional histologic appearance was seen, but the immunohistologic results were abnormal (intraepithelial lymphocytes-IEL, lamina propria CD25+ and CD3+ lymphocytes). In 40% of patients, nonspecific microscopic inflammation was seen, whereas immunohistologic results showed similar increases in lymphocyte populations as in the first group. However, in contrast to the first group, they also showed increased numbers of neutrophils and mast cells. Ten percent of patients fulfilled the histologic and immunohistologic criteria for lymphocytic colitis. Even though the magnitude of changes in cell numbers was far less than observed in patients with IBD, the increased numbers of IEL, T cells, IL-2 receptor expressing cells, suppressor/cytotoxic T cells, and NK cells were consistent with an increased inflammatory cell presence in a subset of patients with altered bowel habits who met the symptom-based Rome criteria. Because a significant number of patients meeting the Rome criteria also met the histologic criteria for a diagnosis of lymphocytic colitis, the findings highlight a major problem with the way we currently diagnose IBS. By definition, the diagnosis of an organic disease such as lymphocytic colitis is inconsistent with a diagnosis of IBS. Furthermore, it is unclear whether the patients met the Rome criteria because of the presence of discomfort (urgency, bloating) relieved by bowel movements, or whether they reported abdominal pain. Using the current Rome criteria, a diagnosis of IBS can be made in any patient experiencing abdominal discomfort (for example, in the form of urgency or bloating-type symptoms), that is relieved by a bowel movement. In the absence of mucosal histology to rule out macroscopic or microscopic forms of colitis, such a symptom cluster is likely to include a wide range of syndromes with different causes and pathologic mechanisms.

Another study reported neuromuscular and inflammatory abnormalities in the small bowel of 10 patients (8 women; age range 24-55 years) with severe IBS symptoms.[12] Surprising for an IBS population, the symptoms apparently were severe and refractory enough to justify a laparoscopic full-thickness biopsy. The durations of IBS symptoms ranged from 2 to 30 years, and the predominant bowel habits included constipation, diarrhea, and alternating bowel habits. In this study, analysis of full-thickness biopsy specimens of the jejunum from IBS patients (diagnosis having been made on the basis of absence of detectable structural lesions and fulfillment of the Rome I criteria for IBS) showed several histopathologic abnormalities. The authors reported in most patients some neural degeneration in the ganglia of the myenteric plexus associated with infiltration of CD3+ T lymphocytes and longitudinal muscle hypertrophy. In some cases, IEL numbers were increased, and the numbers of interstitial cells of Cajal were also increased. There are two major problems with the reported findings. First is the absence of an appropriate control group. For example, the observed mucosal alterations in the proximal jejunum were compared with biopsy specimens obtained from the distal ileum during colonoscopy, and alterations in the jejunal wall were compared with findings obtained in tissues from deceased patients (of unspecified sex and age). Second, as admitted by the authors, the patients in this study represented a highly selected group with severe symptoms that were apparently refractory to current management. Even though it was stated that patients had normal or nonspecific changes on small intestinal manometry, it is conceivable that the patients had a mild or early form of chronic intestinal pseudoobstruction. Analogous to the comments made above about the nonspecificity of the Rome criteria to differentiate microscopic colitis from IBS, the same argument could be made for chronic intestinal pseudoobstruction.

Patients in another group, frequently discussed as evidence for a possible role of altered gut immune function in IBS, are those in whom IBS-like symptoms develop after a documented gastroenteric infection (so-called postinfectious IBS [PI-IBS] patients). A history of acute gastroenteritis caused by a variety of bacterial infections as well as parasitic infections was found to increase the risk of the development of persistent IBS symptoms. The risk factors associated with PI-IBS include female gender, duration of the acute illness episode, and a major stressful life event at the time of the infection. Patients with PI-IBS have been reported to show changes in gut motility (eg, reduced rectal compliance) and epithelial function and an increase in enterochromaffin cells.[13, 14] In addition, mucosal immune parameters in these patients exhibit changes that include altered macrophage (CD68) and T lymphocyte (CD3, CD4, CD8) populations and increased expression of IL-1 mRNA.[15] Some of these changes, as well as symptoms of diarrhea, were shown to persist for more than a year in some cases, suggesting chronic immune system activation.[15] Although the mechanisms involved in the ongoing inflammation after clearance of the infectious agent remain unclear, it has been suggested that a subset of IBS patients may have a genetic predisposition to inflammatory dysregulation. Preliminary evidence suggests a reduced frequency of the high producer allele for the antiinflammatory cytokines IL-10 and TGF-, suggesting a reduced production of these cytokines in patients with IBS compared with healthy control subjects.[16] Several important questions have to be addressed before the existence of a distinct pathophysiologic entity of PI-IBS can be confirmed. (1) Even though persistence of low-grade inflammation has been described in individuals who continued to be symptomatic, a causal role of these mucosal changes with IBS symptoms has not been demonstrated.[14, 15] Preliminary reports from a therapeutic trial with an antiinflammatory agent in PI-IBS did not demonstrate any effect on symptoms.[17] (2) There is currently no evidence of visceral hypersensitivity in this patient group, and the reported lower volume thresholds for discomfort simply reflect a reduced rectal compliance. (3) It is unclear whether patients who report their first onset of IBS symptoms after an enteric infection have a history of other intestinal or extraintestinal functional syndromes (such as dyspepsia or chronic constipation) or anxiety disorders. In this case, the persistence of bowel symptoms may simply be a reactivation of a preexisting functional syndrome.

Tibble et al. [18**] compared a large population of patients with altered bowel habits meeting the Rome I criteria for IBS and patients with different organic diseases of the intestine, including IBD, cancer, infectious diarrhea, and celiac disease. They observed that markers for intestinal inflammation, such as fecal calprotectin levels, were elevated in the majority of patients with organic gastrointestinal conditions and decreased in the majority of patients with IBS. The sensitivity and specificity of fecal calprotectin levels for organic intestinal disease were 89% and 79%, respectively. However, the authors observed a significant number of IBS patients whose fecal calprotectin levels were above a normal cutoff value, suggesting some degree of inflammation.

Taken together, the above findings are most consistent with the concept that in a subset of patients meeting the current diagnostic criteria for IBS, chronic low-grade immune activation may be associated with chronic changes in gut motor and secretory function resulting in chronic abdominal discomfort associated with altered bowel habits. However, a causal relationship between visceral hypersensitivity and chronic immune activation has not been demonstrated.

Altered Immune System and Inflammation in Inflammatory Bowel Diseases
Classic histopathologic inspection of tissue from patients with IBD reveals vasodilatation, venocongestion, edema, infiltration of large numbers of inflammatory cells (lymphocytes as well as macrophages and monocytes), and architectural disarray, often with mucosal erosions and/or frank ulcerations. Although the causative triggers remain unclear, the role of a persistent and likely dysregulated mucosal immune response is central to the pathogenesis of IBD. However, it remains unclear whether the persistent inflammation, an intrinsic feature of IBD, reflects a primary aberration in mucosal response or results from an inappropriate persistent stimulation. Accumulating evidence indicates that excessive activation of immunoinflammatory responses in IBD may be initiated by luminal flora. In this regard, recent data showed no difference in the overall composition of mucosal flora in patients with IBD and control subjects but demonstrated a higher concentration of mucosa-associated bacteria in patients with IBD.[19] The authors suggest that the changes in the concentrations of mucosal flora in IBD are not secondary to inflammation but result from a host-specific altered immunoinflammatory mucosal response to "self-flora" in susceptible individuals. The role of genetic factors continues to be explored, with disease susceptibility associated with genetic markers for particular subsets of IBD patients. Recent studies using genome-wide screening provided the first link between NOD2 mutations and the clinical characterization of Crohn disease.[20, 21] NOD proteins are thought to be cytosolic receptors for bacterial signals, and NOD2 is expressed in monocytes and activates nuclear factor kB (NF-kB). However, the mechanisms by which NOD2 mutations contribute to Crohn disease need further investigation. It has been hypothesized that different concentrations of bacteria in the ileum relative to the colon may contribute to the association between NOD2 mutations and ileal disease. A genetic background was also identified in ulcerative colitis associated with HLA genes and regions of the chromosomes 3, 7, and 12.[22] In a recent review, Ardizzone et al. [23**] compiled the genetic factors recently involved in the pathogenesis of IBD. Considering the central role of cytokines in modulating intestinal inflammation, several studies have focused on cytokine genes, looking for mutations or polymorphisms and expression dysregulation.[24] In Crohn disease, an increased expression of T-helper-1 (Th1) cytokines was initially described, whereas an atypical Th2 response was associated with ulcerative colitis, but this assessment is now thought to be too simplistic. Cytokine gene-regulated differences between and within the diseases are clearly more complex. Advances in the understanding of the immune response in IBD have stimulated the development of new therapeutic agents directed against key players in the inflammatory process. A range of therapeutic strategies to block the biosynthesis or action of proinflammatory cytokines, acting directly or though targeting immunoregulatory cytokines, has been developed.[25]

Among specific targets, tumor necrosis factor- (TNF-) was among the first mucosal cytokines identified as critical in the development and amplification of mucosal inflammation in IBD.[26] Recent clinical trials showed that anti-TNF- antibodies provide marked clinical benefits in some patients with Crohn disease: a translational insight that has now become commonplace in IBD clinical therapy.[27, 28] An inhibitor of mitogen-activated protein kinase (MAPK) appears to be another candidate in novel therapeutic strategies. A beneficial effect of CNI-1493 (MAPK inhibitor) in patients with severe Crohn disease was recently described.[29] A better characterization of the molecular signaling pathways involved in the activation of key immune and inflammatory cells will indubitably provide new targets for the development of therapeutic agents for IBD.

What Unifies and Separates Irritable Bowel Syndrome and Inflammatory Bowel Diseases
Possible Role of Failure to Downregulate Immune Response
A comparison of published data on the activation of the gut-associated mucosal immune system in IBS and IBD reflects both the similarities and the differences in the altered immune response observed in these disorders. However, the triggering factor initiating the inflammatory response remains unclear. In IBS, an immune response to infection,[30] a disinhibition of the immune system during chronic sustained stress (Fig. 1), or a combination of both are plausible mechanisms that could result in the initial immune activation. The persistence of low-grade inflammation after pathogen clearance or after resolution of the psychosocial stressor, in a subset of individuals, may be related to an inability to efficiently downregulate the inflammatory response. This inability may be related to genetic factors or to early programming of antiinflammatory systems, such as the hypothalamic-pituitary-adrenal (HPA).[31*] For example, a hyporesponsive HPA axis in the Lewis rat has been shown to be associated with exaggerated immune responses to various stimuli, including chemically induced colitis.[32] The most recent available data on IBD increasingly emphasize the role of immunogenetics in the predisposition, modulation, and perpetuation of the disease.[33] The abnormal amplification and persistence of inflammation leading to tissue injuries likely reflects the continuing presence of the driving stimulus and self-reinforcing activation of mucosal inflammatory cells mediated by increased expression of cytokines.




Figure 1. Brain-gut immune interactions in irritable bowel syndrome and inflammatory bowel disease: effect of chronic stress on the mucosal immune system. Acute stress causes increases in the activity of the hypothalamic-pituitary-adrenal (HPA) axis and of the two branches of the autonomic nervous system (ANS), the sympathetic nervous system (SNS), and the parasympathetic (vagal) system. In patients with irritable bowel syndrome, the peripherally acting products of each of these pathways (cortisol, CORT; norepinephrine, NE; acetylcholine, Ach) can inhibit the mucosal immune system, especially Th1-type responses. This results in a temporary shift toward Th2 cytokine responses (IL-4 and others) that are not as strongly inhibited and that can further inhibit Th1 responses. In patients with inflammatory bowel diseases, the corticotropin-releasing factor (CRF) response may be blunted, leading to diminished CORT and NE release. These changes favor the production of Th1 cytokines and the proliferation of macrophages, natural killer (NK) cells, and cytotoxic T cells (Tc). TNF, which is produced by activated macrophages but can also be released by activated mast cells, stimulates the production of IL-1 (in the Th1 pathway) and IL-6 (by lymphoid and nonlymphoid tissues). With chronic stress in both types of patients, the shift to a Th1 response becomes predominant, with positive feedback loops developing between the gut and the brain. The restraints on immune cell proliferation and activation are compromised by blunting of the HPA axis response due to downregulation of pituitary CRF1 receptors, decreased vagal tone, and downregulation of 2-adrenergic receptors (2-AR) on Th1 immune cells by chronically elevated catecholamines. Circulating levels of TNF-, IL-1, and IL-6 increase to concentrations that synergistically stimulate CRF production in the PVN of the hypothalamus. In irritable bowel syndrome, TNF and IL-1 sensitize primary afferent terminals through long-lasting effects on gene expression, including the expression of neurokinin receptors. Locally acting mast cell products (tryptase and histamine) and proinflammatory compounds (PGE2) can also sensitize primary afferents. Both IFN (Th1 cytokine), which is produced by NK cells in response to TNF, and IL-4 (a Th2 cytokine) have been shown to decrease mucosal barrier function by increasing epithelial permeability,[54,55] thus perpetuating a local inflammatory response by allowing entry of bacteria and bacterial products. Subjective pain responses to peripheral sensitization of visceral afferents in irritable bowel syndrome and inflammatory bowel diseases are likely to be modulated differentially by endogenous pain modulation pathways. DMN, dorsal motor nucleus of the vagus; ACTH, adrenocorticotropin hormone.
Increased Permeability
For both syndromes, histologic and functional alterations of the mucosal barrier have been recently reported.[11*, 12, 24, 25] Small intestinal permeability is abnormal in a wide variety of conditions affecting the small intestine, including celiac disease, Crohn disease, and intestinal infections.[18**] Interestingly, gut permeability assessed by the lactulose/mannitol ratio is significantly elevated in PI-IBS patients.[15] This functional alteration of the intestinal barrier function may be a cause or consequence of inflammation, and a direct link between increased intestinal permeability and the exaggerated immune activation in IBD still needs to be confirmed. In addition to a causative role of peripheral factors, gut permeability changes in animal models have also been reported in response to various stressors. For example, in a rat model of chronic stress, an increase in intestinal epithelial permeability, associated with an increase in mucosal neutrophils and mast cells, has been demonstrated.[34**] In this model, the combination of stress-induced increases in intestinal permeability, allowing easier access of antigens to gut-associated macrophages and dendritic cells, together with stress-induced changes in HPA axis responsiveness and cytokine profiles, resulted in the development of colitis, without any additional chemical or immunologic manipulations. Rats with a history of aversive early life events were more susceptible to these stress-induced changes in gut permeability,[35*] possibly related to early programming of the HPA axis.[31*]

Changes in Luminal Flora
A change in intestinal microflora has been implicated, in association with genetic factors, as a putative mechanism responsible for the initiation and persistence of inflammation in IBD. Indeed, it has been suggested that the failure to maintain immunologic tolerance toward the indigenous microflora leads to a disease-associated dysregulation of the gut-associated immune system. Direct and indirect evidence of altered flora of the large and small intestine has been reported in IBS patients. For example, Balsari et al. [36] observed a decrease in coliforms, lactobacilli, and, to some extent, bifidobacteria in a small group of IBS patients. More recently, preliminary evidence of an alteration of bacterial concentration in colonic biopsy specimens from IBS patients has been reported.[37] Indirect evidence for bacterial overgrowth of the small intestine (in the form of altered hydrogen breath test results) has been reported in patients with IBS, and a recent randomized controlled trial found evidence that antibiotic treatment was beneficial for IBS symptoms of bloating and discomfort.[38] Based on the concept of altered interactions between the colonic flora and the gut-associated immune system, probiotics have been proposed as an alternative strategy for the treatment of several gastrointestinal diseases, including IBD[39] and more recently IBS.[40, 41] However, the reported results are conflicting, and only a small number of double-blind controlled clinical trials support a beneficial health effect in IBD or IBS.[42] The epithelium has recently been recognized as playing an important role in innate immune responses in response to intestinal microorganisms.[43, 44] It expresses a variety of receptors (Toll-like receptor) involved in the recognition of a spectrum of microbial products. This recognition capability may enable an appropriate cytokine and chemokine secretion in response to changes in luminal flora.

Influence of Sustained Psychosocial Stressors on Mucosal Immune System Activation
Even though stress has been less recognized as a factor in the natural history of IBD, considerable evidence supports a prominent role for it in the pathophysiology and clinical presentation of both IBD and IBS symptoms.[45] Patients with IBS seem to have a greater reactivity to stress than do control subjects or IBD patients. Yet, sustained psychologic stressors have been associated with the onset and exacerbation of symptoms in both IBS and IBD.[46-48] The development of persistent IBS symptoms after acute gastroenteritis has been associated with major life events around the time of infection.[14] Similarly, for IBD, a wide range of clinical studies indicates a strong link between sustained psychosocial stressors and IBD activity.[49] Levels of long-term perceived stress have been shown to correlate with changes in mucosal appearance and relapse in ulcerative colitis.[50*] Further evidence of an influence of stress on inflammatory processes comes from animal studies showing a modulation of the immune function at different levels, including immune cell distribution, cytokine profiles, or susceptibility to infection in naïve or colitic animals.[51] In view of the established concept of an altered immune response in IBD patients, and the suspected low-grade inflammation in some patients meeting the symptom criteria for IBS, it is reasonable to consider a bidirectional model of brain-gut interactions as an important determinant of gut-associated immune activation in both disorders.

Chronic Inflammation and Alteration of Sensory-Motor Functions of the Gastrointestinal Tract
Despite the common assumption that chronic gut mucosal inflammation is associated with sensory-motor dysfunction of the gastrointestinal tract in inflammatory as well as functional intestinal disorders, the relationship between chronic inflammation and the generation of gastrointestinal symptoms remains unclear. The development of IBS-like symptoms in some patients with quiescent ulcerative colitis was suggested as an indication of the role of inflammation on altered sensory and motor function.[8] The concept of long-lasting postinflammatory changes in gut motility is supported by the observation of altered anorectal and colonic motility in patients in remission from ulcerative colitis and Crohn disease.[52] However, chronic abdominal pain and visceral hypersensitivity-classic features in patients with IBS-do not appear to be a hallmark of ulcerative colitis or Crohn disease.[53] One may speculate that various patient populations with different degrees of intestinal inflammation (patients with IBD and PI-IBS, and possibly small subsets of those with IBS) do not necessarily experience pain and discomfort from these mucosal changes. Whereas the effects of the immune activation are likely to affect enteric nervous system circuits and smooth muscle function, altering intestinal compliance and reflex activity and producing such symptoms as diarrhea and urgency, the effects on visceral perception are less predictable. An important variable in symptom generation is the differences in the ability of the brain and its endogenous pain inhibitory pathways to counteract the changes in peripheral viscerosensory pathways.

Conclusion
The recent observation of an activated immune system in some IBS patients associated with persistent low-grade mucosal inflammation provides evidence for the reconsideration of the symptom-criteria-based diagnosis of functional bowel disorders. The development and use of biologic markers identifying low-grade inflammation would improve the characterization of subsets of IBS patients in whom peripheral mechanisms may participate in specific symptom genesis and could be considered in the choice of the therapy.

[ CLOSE WINDOW ]
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Pimentel M, Chow EJ, Lin HC: Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. Am J Gastroenterol 2003, 98:412-419.
Gionchetti P, Rizzello F, Venturi A, et al.: Probiotics in infective diarrhoea and inflammatory bowel diseases. J Gastroenterol Hepatol 2000, 15:489-493.
Sen S, Mullan MM, Parker TJ, et al.: Effect of Lactobacillus plantarum 299v on colonic fermentation and symptoms of irritable bowel syndrome. Dig Dis Sci 2002, 47:2615-2620.
Madden JA, Hunter JO: A review of the role of the gut microflora in irritable bowel syndrome and the effects of probiotics. Br J Nutr 2002, 88 (Suppl 1): S67-S72.
Marteau PR, de Vrese M, Cellier CJ, et al.: Protection from gastrointestinal diseases with the use of probiotics. Am J Clin Nutr 2001, 73 (Suppl 2): S430-S436.
Cario E, Podolsky DK: Differential alteration in intestinal epithelial cell expression of toll-like receptor 3 (TLR3) and TLR4 in inflammatory bowel disease. Infect Immun 2000, 68:7010-7017.
Cario E, Rosenberg IM, Brandwein SL, et al.: Lipopolysaccharide activates distinct signaling pathways in intestinal epithelial cell lines expressing Toll-like receptors. J Immunol 2000, 164:966-972.
Mayer EA: The neurobiology of stress and gastrointestinal disease. Gut 2000, 47:861-869.
Monnikes H, Tebbe JJ, Hildebrandt M, et al.: Role of stress in functional gastrointestinal disorders: evidence for stress-induced alterations in gastrointestinal motility and sensitivity. Dig Dis 2001, 19:201-211.
Levy RL, Cain KC, Jarrett M, et al.: The relationship between daily life stress and gastrointestinal symptoms in women with irritable bowel syndrome. J Behav Med 1997, 20:177-193.
LeResche L, Dworkin SF: The role of stress in inflammatory disease, including periodontal disease: review of concepts and current findings. Periodontol 2000 2002, 30:91-103.
Levenstein S, Prantera C, Varvo V, et al.: Stress and exacerbation in ulcerative colitis: a prospective study of patients enrolled in remission. Am J Gastroenterol 2000, 95:1213-1220.
Hart A, Kamm MA: Mechanisms of initiation and perpetuation of gut inflammation by stress. Aliment Pharmacol Ther 2002, 16:2017-2028.
* Comprehensive review of the mechanisms by which stress can alter intestinal physiologic functions. Identification of the different mediators involved in the brain-gut-immune axis contributing to the initiation, perpetuation, and reactivation of gut inflammation.
Collins SM, McHugh K, Jacobson K, et al.: Previous inflammation alters the response of the rat colon to stress. Gastroenterology 1996, 111:1509-1515.
Annese V, Bassotti G, Napolitano G, et al.: Gastrointestinal motility disorders in patients with inactive Crohn's disease. Scand J Gastroenterol 1997, 32:1107-1117.
Chang L, Munakata J, Mayer EA, et al.: Perceptual responses in patients with inflammatory and functional bowel disease. Gut 2000, 47:497-505.
Madara JL, Stafford J: Interferon-gamma directly affects barrier function of cultured intestinal epithelial monolayers. J Clin Invest 1989, 83:724-727.
Colgan SP, Resnick MB, Parkos CA, et al.: IL-4 directly modulates function of a model human intestinal epithelium. J Immunol 1994, 153:2122-2129.
[CLOSE WINDOW]
Authors and Disclosures
Sylvie Bradesi, PhD*; James A. McRoberts, Ph.D*; Peter A. Anton, MD*; Emeran A. Mayer, MD*

CNS: Center of Neurovisceral Sciences & Women's Health, Division of Digestive Diseases and Brain Research Institute, Departments of Medicine*, Physiology, and Psychiatry & Biobehavioral Sciences, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California, USA



Reprint Address
Emeran A. Mayer, MD, CNS: Center of Neurovisceral Sciences and Women's Health, VAGLAHS, Bldg.115/CURE, Room 223, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA;

Abbreviation Notes
HPA: hypothalamic-pituitary-adrenal; IBD: inflammatory bowel diseases; IBS: irritable bowel syndrome; IELs: intraepithelial lymphocytes; iNOS: inducible nitric oxide synthase; MAPK: mitogen-activated protein kinase; PI-IBS: postinfectious irritable bowel syndrome; Th1: T helper 1; TNF-

http://www.medscape.com/index/list_4761_0

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Red meat may raise odds for ulcerative colitis, but oily fish could be protective new
      #356594 - 03/11/10 01:22 PM
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Fatty Acids in Diet Linked to Bowel Disease Risk

Red meat may raise odds for ulcerative colitis, but oily fish could be protective, study shows

THURSDAY, July 23 (HealthDay News) -- Consuming too much of a common polyunsaturated fatty acid could be a contributing factor in an estimated 30 percent of all cases of ulcerative colitis, researchers say.

In a new study, participants who had the highest intake of linoleic acid had more than double the chance of developing the painful inflammation and blistering of the bowels as did those whose diet contained the least of the acid. The report is published online in Gut.

Red meat and some cooking oils and margarines are among the many dietary sources of linoleic acid.

However, the research also found that consuming lots of omega 3 fatty acids can cut the chance of developing ulcerative colitis by more than three quarters. Oily fish such as salmon and mackerel, flaxseed and certain dairy products are rich in omega 3, also known as docosahexanoic acid.

The European study, which looked at the dietary habits of more than 200,000 people in five countries, found that ulcerative colitis occurred about equally in men and women and at an average age of 60. The data analysis took into account other possible causes of the condition, including smoking, age, caloric intake and aspirin use.

The body converts linoleic acid to arachidonic acid, a component of the cell membranes in the bowel, and it then can turn into various chemicals that inflame tissue, according to information in a news release from the journal's publisher. People with ulcerative colitis have been found to have high levels of these chemicals in their bowel tissue.

Having ulcerative colitis, which is a chronic condition, puts a person at a higher risk of developing bowel cancer.

SOURCE: BMJ Specialist Journals, news release, July 22, 2009

http://healthday.com/Article.asp?AID=629293


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Accutane may cause ulcerative colitis new
      #357631 - 04/09/10 01:38 PM
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NEW YORK (Reuters Health) - Adding to evidence that the acne drug isotretinoin may lead to bowel disease in some users, a new study finds that patients on the medication were four times more likely than non-users to develop ulcerative colitis within a year.

Reporting in the American Journal of Gastroenterology, researchers say that the risk of any one isotretinoin user developing ulcerative colitis is "likely quite small."

However, the findings do strengthen the evidence of a cause-and-effect relationship between the acne drug and inflammatory bowel disease (IBD) -- a group of digestive disorders that includes ulcerative colitis and Crohn's disease.

Isotretinoin, which is used to treat severe acne, is probably best known by the brand-name Accutane. That drug was taken off the market last year in the face of competition from generic alternatives -- though in pulling the medication, maker Roche Pharmaceuticals also cited costs from defending personal-injury lawsuits.

Earlier this year, the company was ordered to pay $25 million in damages to a former Accutane user who claimed that the drug caused his IBD.

The company has maintained that there is no strong evidence that the acne drug triggers IBD. Between 1997 and 2002, 83 cases of IBD among isotretinoin users were reported to the U.S. Food and Drug Administration, but that does not prove that the drug itself is to blame.

For the new study, Dr. Seth D. Crockett and colleagues at the University of North Carolina Chapel Hill tried to test the cause-and-effect relationship.

Using a database of information from 87 U.S. health insurance plans, the researchers identified 8,189 people -- mostly adults -- who'd been diagnosed with IBD. They then compared each of those individuals with up to three other health plan members the same age and sex with no history of IBD.

Of the nearly 8,200 IBD patients, Crockett's team found, 24 had used isotretinoin in the year before diagnosis; and of the nearly 22,000 controls, 36 had used the acne drug over a one-year period.

Overall, the researchers found, isotretinoin users were roughly four times more likely than non-users to have ulcerative colitis. There was no association, however, between isotretinoin use and Crohn's disease.

The researchers also found that the risk of ulcerative colitis tended to climb in tandem with patients' daily dose of the drug -- which strengthens the case for a cause-and-effect relationship. There was no evidence that severe acne itself was linked to IBD risk.

Still, the findings do not definitively prove that isotretinoin was the cause of some patients' ulcerative colitis, and the researchers say that further studies are needed to confirm their results.

If the acne drug does lead to ulcerative colitis in some cases, the absolute risk of that happening to any one patient are probably quite small, Crockett and his colleagues point out. But, they add, patients with severe acne should be aware of the possible link between isotretinoin and IBD before they are prescribed the drug.

The biological mechanism by which isotretinoin might contribute to IBD is not clear, but some researchers have speculated that the drug may affect immune function in the intestines. Both Crohn's disease and ulcerative colitis are thought to involve abnormal immune system activity.

As for why isotretinoin was linked to ulcerative colitis, but not Crohn's, in this study, Crockett and his colleagues point out that while the two disorders are related, they are distinct and have different immune-system-related features.

SOURCE: here 4a.html American Journal of Gastroenterology, online March 30, 2010.

© Thomson Reuters 2010 All rights reserved.

http://uk.reuters.com/article/idUKTRE6354OK20100406?sp=true

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Olive Oil May Protect Against Ulcerative Colitis new
      #358398 - 05/05/10 10:32 AM
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Study finds diet rich in oleic acid may prevent development of ulcerative colitis

SATURDAY, May 1 (HealthDay News) -- Increasing your intake of olive oil may help protect against ulcerative colitis, a new study finds.

Ulcerative colitis is an inflammatory bowel disease that causes ulcers in the lining of the rectum and colon, resulting in abdominal pain, diarrhea and weight loss. This study found that people whose diet was rich in oleic acid were far less likely to develop ulcerative colitis.

Oleic acid is a monosaturated fatty acid found in foods such as olive oil, peanut oil, grapeseed oil, butter and some margarines.

This study included more than 25,000 people, aged 40-65, in Norfolk, U.K. who were recruited between 1993 and 1997. None of the participants had ulcerative colitis at the start of the study. By 2002, 22 participants had developed ulcerative colitis. The researchers compared the diets of these people to those who didn't develop the disease and found that those with the highest intake of oleic acid were 90 percent less likely to develop ulcerative colitis.

"Oleic acid seems to help prevent the development of ulcerative colitis by blocking chemicals in the bowel that aggravate the inflammation found in the illness," study leader Dr. Andrew Hart, of the University of East Anglia's School of Medicine, said in a news release.

"We estimate that around half the cases of ulcerative colitis could be prevented if larger amounts of oleic acid were consumed. Two-to-three tablespoons of olive oil per day would have a protective effect," he said.

The study was presented Saturday at the Digestive Disease Week conference in New Orleans.

-- Robert Preidt

SOURCE: University of East Anglia, news release, May 1, 2010

Last Updated: May 03, 2010

Copyright © 2010 HealthDay. All rights reserved.

http://healthday.com/Article.asp?AID=638501

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Infants' antibiotic use tied to IBD risk new
      #361863 - 11/03/10 01:42 PM
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Infants' antibiotic use tied to bowel disease risk

By Amy Norton

NEW YORK ' Fri Oct 29, 2010 11:39am EDT

NEW YORK (Reuters Health) - Babies treated with antibiotics for middle-ear and other infections may have increased odds of developing inflammatory bowel disease later in childhood, a small study suggests.

Canadian researchers found that among 36 children with either ulcerative colitis or Crohn's disease -- the two main forms of inflammatory bowel disease (IBD) -- 58 percent had been prescribed at least one course of antibiotics in the first year of life.

In contrast, only 39 percent of 360 IBD-free children studied for comparison had taken antibiotics during their first year.

The findings, published in the American Journal of Gastroenterology, do not prove that early antibiotic use causes IBD in some children. But they support the theory that factors affecting the early-life balance of "good" and "bad" bacteria in the intestines may contribute to IBD.

Both colitis and Crohn's disease are marked by chronic inflammation in the intestines, leading to symptoms like abdominal pain and diarrhea. The conditions are thought to arise from an immune-system overreaction that injures the body's own intestinal tissue, but the underlying reasons for the aberrant immune response are unclear.

There is a genetic component to IBD, since the conditions can run in families. However, experts believe that environmental triggers -- such as diet, an infection, or exposure to tobacco smoke - likely combine with genetic susceptibility to cause IBD in some people.

The new study appears to be the first to draw a connection between confirmed early antibiotic use and childhood IBD, according to the researchers.

The design of the study does not, however, allow any conclusions about cause-and-effect, senior researcher Dr. Charles N. Bernstein, of the University of Manitoba in Winnipeg, told Reuters Health in an e-mail.

Larger studies, as well as lab research into the effects of common antibiotics on different types of intestinal bacteria, are still needed, he said.

In theory, early antibiotic use could create an imbalance in the potentially beneficial and potentially harmful bacteria that establish residence in the gut during the first year of life. If the composition of these intestinal "microflora" is altered, the immune system may begin to react abnormally to some of the bacteria.

For the current study, Bernstein and his colleagues analyzed medical records for 36 children diagnosed with either ulcerative colitis or Crohn's between 1996 and 2008, at an average age of 8. Each child was compared with 10 IBD-free children of the same age, sex and area of residence.

The researchers found that children with IBD were more likely to have been prescribed an antibiotic during the first year of life -- most commonly for middle-ear infections, but also for respiratory and other types of infection.

Overall, antibiotic use in infancy was linked to a tripling of the risk of IBD relative to children who had no antibiotic prescriptions in their first year of life.

While that relative increase in risk is large, any one child's absolute risk of developing IBD from antibiotic use -- if the medications are, in fact, to blame -- would be small, according to Bernstein.

In the U.S., it's estimated that just over 1 million people have IBD, with new cases diagnosed at a rate of 10 per 100,000 people each year.

It is still possible that factors other than the antibiotics themselves explain the link between early use of the medications and IBD risk. One alternative, according to Bernstein, is that certain conditions for which antibiotics are used -- like middle-ear infections -- are related to IBD risk.

However, he added, the biological mechanisms that would underlie such a connection are not clear.

For now, Bernstein said, the findings offer a reminder "to avoid indiscriminate use of antibiotics when we can." Parents should be aware that antibiotics are often unnecessary for respiratory infections; in fact, many are caused by viruses and do not even respond to antibiotics, which target bacteria, he said.

As for the middle-ear infections so common in infancy, about 80 percent of children get better without antibiotics, according to the American Academy of Pediatrics. In its treatment guidelines, the academy says that infants and children without severe symptoms can often wait 48 to 72 hours before starting antibiotics to see if the infection improves on its own.

SOURCE: link.reuters.com/fec92q American Journal of Gastroenterology, online October 12, 2010.

http://www.reuters.com/article/idUSTRE69S39E20101029?pageNumber=1

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Loneliness Triggers Inflammatory Illnesses new
      #363404 - 02/10/11 10:05 AM
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Loneliness Triggers Inflammatory Illnesses

LOS ANGELES—UCLA researchers reported today that chronically lonely people may be at a higher risk for certain types of inflammatory disease, because their feelings of social isolation trigger the activity of pro-inflammatory immune cells.

The research appears in the Feb. 7-11 issue of the journal Proceedings of the National Academy of Sciences.

In their analysis of 93 older adults, the researchers screened for gene function among different types of immune cells and found that genes originating from two particular cell types—plasmacytoid dendritic cells and monocytes—were overexpressed in chronically lonely individuals, compared with the remainder of the sample. These cell types produce an inflammatory response to tissue damage, and are part of the immune system's first line of defense, which produces an immediate inflammatory response to tissue damage.

It's this same inflammatory response that, over the long-term, can promote cardiovascular disease, cancer and neurodegeneration.

The report provides further evidence of how lifestyle and social environments can impact human health. In addition, the researchers suggest that evolutionarily ancient immune system cells may have developed a molecular sensitivity to our social environment in order to help defend us against socially transmitted pathogens.

The authors are Steven Cole, a member of the UCLA Cousins Center for Psychoneuroimmunology, an associate professor of medicine in the division of hematology–oncology at the David Geffen School of Medicine at UCLA, and a member of UCLA's Jonsson Comprehensive Cancer Center.

Other authors were Lewis C. Hawkley and Jesusa M. Arevalo of UCLA, and John T. Cacioppo of the University of Chicago.

The research was funded by the National Institutes of Health, the John D. and Catherine T. MacArthur Foundation, the Norman Cousins Center at UCLA, the John Templeton Foundation, and the James B. Pendleton Charitable Trust.

Source: University of California, Los Angeles (UCLA), Health Sciences

http://www.endonurse.com/news/2011/02/study-loneliness-triggers-inflammatory-illnesses.aspx

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As Nations Develop, So May Bowel Disease new
      #366646 - 01/09/12 12:01 PM
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As Nations Develop, So May Bowel Disease

Related Health News

FRIDAY, Jan. 6 (HealthDay News) -- Inflammatory bowel disease (IBD) is becoming more common around the world, according to a new study.

Researchers who analyzed data from all population-based studies about the incidence and/or prevalence of IBD found that the rate of new cases is increasing or stable in virtually every region of the world that has been studied. Canada and Europe had the highest number of cases, while Asia had a lower prevalence, the investigators found.

IBD has been rare in developing nations, but incidence of the disease has increased as these countries become more industrialized, according to study lead author Dr. Gilaad Kaplan, of the University of Calgary, and colleagues.

IBD includes Crohn's disease and ulcerative colitis. Crohn's involves inflammation and ulceration in the deep layers of the intestinal wall. Symptoms include abdominal pain, diarrhea, weight loss and occasional bleeding. Ulcerative colitis occurs in the inner lining of the colon or rectum. Symptoms include abdominal cramps, diarrhea and rectal bleeding.

The researchers found that incidence rates for both Crohn's and ulcerative colitis were highest among people aged 20 to 40. This means that these diseases affect people in what are typically the most healthy and productive years of life, resulting in long-term cost to the patients, health care systems and society, the study authors noted.

The study is published in the January issue of the journal Gastroenterology.

"Insight into the worldwide epidemiology of inflammatory bowel disease is important for the identification of geographic patterns and time trends," Kaplan said in a news release from the American Gastroenterological Association.

"Our findings will help researchers estimate the global public health burden of inflammatory bowel disease so that appropriate health care resources are allocated, and targeted research is conducted in specific geographic regions," he added.


SOURCE: American Gastroenterological Association, news release, Jan. 4, 2012
Copyright © 2012 HealthDay. All rights reserved.
This is a story from HealthDay, a service of ScoutNews, LLC.

http://generic.e-healthsource.com/index.php?p=news1&id=660456

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Kids With Crohn’s Disease, Colitis Often Struggle at School new
      #367290 - 04/23/12 01:22 PM
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Kids With Crohn's Disease, Colitis Often Struggle at School

Frequent absences, depression can affect how well students with bowel disease do academically.

FRIDAY, Feb. 17 (HealthDay News) -- Children with inflammatory bowel disease may have difficulty in school due to frequent absences that are largely the result of mental struggles such as depression rather than the disease itself, a new study finds.

Researchers from Nationwide Children's Hospital in Columbus, Ohio, had students aged 11 to 17 years with and without inflammatory bowel disease -- which generally takes the form of Crohn's disease or ulcerative colitis -- answer questionnaires about their mental health, school functioning and quality of life. Schools provided report cards and school absence information.

Children with the condition missed more days of school than healthy kids, and those who missed lots of school had lower grade point averages, according to the study.

Kids with inflammatory bowel disease were also at risk of "internalizing" problems, such as depression, according to the study. Kids who were struggling more mentally also tended to have more absences.

"Youth with [inflammatory bowel disease] are at increased risk for depression, so the finding that internalizing problems are associated with school absence is a particular concern with important implications," said lead study author Laura Mackner, an investigator in the hospital's Center for Biobehavioral Health, in a hospital news release.

The study recently appeared in the Journal of Developmental & Behavioral Pediatrics.

Symptoms of inflammatory bowel disease include abdominal pain, fatigue and diarrhea. Children may be prescribed corticosteroids, which may affect learning and memory, or have to take intravenous medication requiring hours in an infusion clinic, according to Dr. Wallace Crandall, director of the hospital's Center for Pediatric and Adolescent Inflammatory Bowel Disease.

"Both [inflammatory bowel disease] and its treatment have the potential to disrupt school functioning," Crandall said in the release.

The study authors noted that most of the children studied were in remission or had only a mild form of the disease, so it's unclear if their findings would apply to children with more severe cases.


SOURCE: Nationwide Children's Hospital, news release, Feb. 14, 2012

Copyright © 2012 HealthDay. All rights reserved.

http://www.doctorslounge.com/index.php/news/hd/26852

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Smoking makes Crohn's disease worse new
      #367424 - 05/09/12 01:33 PM
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Smoking makes Crohn's disease worse

BALTIMORE -

Crohn's disease is an uncomfortable autoimmune disease that can be made worse by smoking, according to doctors.

Crohn's causes the body to attack itself. It happens in the gastrointestinal tract and causes inflammation of the intestines, as well as pain and diarrhea.

Mercy Medical Center's Dr. Richard Desi said smokers are twice as likely as nonsmokers to develop Crohn's.

"It's also shown that with Crohn's, smoking can cause flares and a recurrence of the disease, especially after you've had surgery," he said.

He said the theory is that it's exacerbated by the nicotine effect or from smoke by-products. But there is good news for those who quit.

"If you quit smoking, about a year out, it puts you back in a category as if you had never smoked, in terms of flares, recurrence and severity of the disease," Desi said.

Tiffany Delaney was diagnosed with Crohn's disease when she was 17.

"For years, I had terrible stomach pains. I was always balled over in pain, I didn't want to eat. I was getting sick for no reason, and my parents said, 'We've got to figure out what's wrong,'" she explained.

Delaney had never heard of Crohn's disease, so she smoked while she had it.

"I smoked from when I went to college on, for about 10 years," she said.

Delaney's first major flare was when she was 25 and still smoking, and she had to be hospitalized for four days.

"Especially for Crohn's patients, there are always things to alleviate pain. But (quitting smoking) should be the first one," she said.

For smokers, quitting could be just as good as taking medicine for Crohn's, doctors said. Quitters have a 65 percent lower risk of a flare-up and are less likely to need steroids or other medications.

Copyright 2012 by WBALTV.com All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

http://www.wbaltv.com/news/health/Woman-s-Doc-Smoking-makes-Crohn-s-disease-worse/-/9379230/11643652/-/item/0/-/r1h4ewz/-/index.html

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Inflammatory bowel, ulcerative colitis linked to intestinal fungi new
      #367614 - 06/15/12 01:23 PM
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By Thomas H. Maugh II

June 8, 2012, 9:44 a.m.

Bacteria in the gut play a crucial role in human health, and imbalances in bacterial populations can contribute to many disorders. New research suggests that fungi, though not as common in the intestines as bacteria, may also play a role in causing and modulating disease.

The results could lead to new treatments for conditions such as inflammatory bowel disease, ulcerative colitis and Crohn's disease. An estimated 1.4 million Americans have some form of inflammatory bowel disease, which can cause inflammation, ulcers in the bowel, abdominal pain, diarrhea, bleeding, fatigue, weight loss and loss of appetite. An additional 30,000 cases are diagnosed annually.

An estimated 100 trillion individual bacteria reside in the intestines -- more than the number of cells in the human body. They play crucial roles, such as aiding digestion of food, producing necessary vitamins and suppressing the growth of harmful microbes.

But according to Dr. David M. Underhill of the Inflammatory Bowel and Immunobiology Research Institute at Cedars-Sinai Medical Center, there has been little corresponding study of fungi in the intestine.

Working with mice, Underhill and his colleagues looked for fungal DNA in the animals' bowels. The team reported this week in the journal Science that they identified more than 100 species. "We were truly stunned to see just how common fungi are," he said.

The body's immune response to fungi is mediated by a protein called Dectin-1, which is produced by white blood cells and kills fungi. The team found that mice with a defective form of Dectin-1 were far more susceptible to developing ulcerative colitis than those with the normal form. When the mice with defective Dectin-1 and ulcerative colitis were given fluconazole, a drug commonly used to kill fungus, their symptoms moderated.

Underhill's team then looked at the Dectin-1 gene in humans. They found that the mutated form of the gene for Dectin-1 was much more common in patients with what is known as medically refractory ulcerative colitis -- that is, ulcerative colitis that does not respond to medical therapy, such as systemic corticosteroids, cyclosporine and biological therapies.

Intriguingly, the defective form of the gene, known as CLEC7A, has not been linked to ulcerative colitis in any genome-wide association studies.

The researchers' conclusion is not that the defective gene allows fungi to produce inflammatory bowel disease such as ulcerative colitis. Rather, they suggest that the presence of the defective gene makes the disease much more severe when it is caused by other things, but that treating the fungi might be of some help in treating the disease.

"Overall, the idea that fungi are present in the gut and that they interact strongly with the immune system will fundamentally alter how we think about the gut microflora and inflammatory bowel diseases," they concluded.

[Updated June 15: An earlier version of this story incorrectly referred to inflammatory bowel disease as irritiable bowel disease. The two are separate conditions.]

LATimesScience@gmail.com

twitter.com/@LATMaugh

Copyright © 2012, Los Angeles Times


http://www.latimes.com/news/science/sciencenow/la-sci-sn-fungus-irritable-bowel-20120608,0,4122971.story

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Genetic Clues May Help Unravel Cause of Crohn's new
      #368399 - 11/02/12 12:59 PM
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Genetic Clues May Help Unravel Cause of Crohn's

Video Presentation:

http://www.sciencefriday.com/segment/11/02/2012/genetic-clues-may-help-unravel-cause-of-crohn-s.html


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Dietary changes may reduce effects of IBD new
      #369646 - 06/27/13 05:43 PM
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Dietary changes may reduce effects of IBD, study finds
Researchers found that eating certain foods, including apples, broccoli and cauliflower, might help stop the immune system from attacking normal intestinal flora, thereby removing the stimulus for inflammation and fibrosis formation in patients with inflammatory bowel disease. Though diet choices can help alleviate IBD symptoms, doctors may still recommend surgery to remove fibrotic or scarred areas of the intestine in some patients with IBD.

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Scientists find that while there is no cure for IBD, certain dietary changes can make it and resulting fibrosis more manageable.
By Anoopa Singh ' Jun 19, 2013 03:21 PM EDT


Four million Americans suffer from inflammatory bowel disease (IBD), an autoimmune disorder where the immune system attacks one's colon and intestines and leads to high levels of inflammation and digestive difficulties. Often, as a result of the constant inflammation, the intestines will form fibroids, or masses of cells that try to reinforce the intestinal walls to protect from further immune attack. This fibrosis is driven by the chronic inflammation but does not always work as the body hopes it will. Frequently, fibroids in the intestines can lead to large amounts of scar tissue that prevent the intestines from being as elastic as they once were and can narrow them, making digestion and elimination difficult or impossible.

Fixing these digestive issues caused by IBD often requires surgery. But, what if the fibrosis was reversible?

A new study indicates that the presence alone of the microbes that the immune system wishes to attack will begin the bodily response that sparks fibrosis. Previous studies have shown that when intestinal microbes are sent to the liver by accident, fibrosis will begin there as well. However, once the microbes are sent away from the liver, dangerous fibrosis ceases.

The researchers attempted to kill off all of the gut bacteria with antibiotics, but this can lead to other health issues as well as a worsening of IBD symptoms. They found that some foods have the potential to block the receptors in the body that recognize benign gut bacteria as invaders. This can ease a lot of the inflammation that is characteristic of IBD. In the same way, easing the inflammation can prevent further fibrosis. Some of these foods include broccoli, cauliflower, and apples.

It is clear that there is some promise in altering one's diet to manage IBD. But while the blockage of inflammation will stop fibrosis, the condition can progress if some inflammation still occurs. The researchers hope that fibrosis in other organs can regress the way it does in the intestines, but researchers still believe that in spite of their finding, surgical management of fibroids must be employed in order to ensure the health of those with IBD.


Source: Rieder F. The Gut Microbiome in Intestinal Fibrosis: Environmental Protector or Provocateur?. Science Translational Medicine. 2013.

http://www.medicaldaily.com/articles/16675/20130619/intestinal-bacteria-fibrosis-ibd-inflammatory-bowel-disease-dietary-change-autoimmune-disorder.htm

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Inflammatory Bowel Disease: Heat Waves Linked to Flares new
      #369994 - 08/16/13 12:58 PM
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Medscape Medical News
Inflammatory Bowel Disease: Heat Waves Linked to Flares

Joanna Broder
Aug 13, 2013

During a heat wave, there is more to worry about than just heat stroke: Flares of inflammatory bowel disease (IBD) and bouts of infectious gastroenteritis (IG) are things to consider as well, according to a study from Zurich, Switzerland, published online August 13 in the American Journal of Gastroenterology.

"There is evidence for an increase of IBD hospital admissions by 4-6 percent for each additional day within a heat wave period," Christine N. Manser, MD, from the Division of Gastroenterology and Hepatology, Department of Internal Medicine, University Hospital, Zurich, and colleagues said in a new release. "Presence of a heat wave was estimated to increase the risk of [IG] by 4-7 percent for every additional day within a heat [wave] period. In the control group there was no evidence for a heat wave effect."

To conduct this retrospective, controlled observational study, researchers used data from 738 patients with IBD and 786 patients with IG who had been admitted to a Swiss hospital during the 5-year period from 2001 to 2005. They then compared this data, using other noninfectious chronic intestinal inflammations as the control. The Swiss Federal Office for Meteorology and Climatology provided climate data for 17 heat waves during the same period.

Results from the study showed that for every additional day within a heat wave, the risk for IBD flare ups increased by 4.6% (95% confidence interval [CI], 1.6% - 7.4%; P = .0035), and the risk for IG flares increased by 4.7% (95% CI, 1.8% - 7.4%; P = .0020). Members of the control group, in contrast, showed no significant effect (95% CI, &#8722;6.2% - 2.9%; P = .53). The analyses were adjusted for day of the week, long-term time trends, and seasonal pattern.

Results also suggest that the risk for IG increased per day and was strongest "when lagged by 7 days" (risk increase per day, 7.2%; 95% CI, 4.6% - 9.7%; P < .0001). The risk for IBD did not require such a transformation: The model fit was not improved by using formulations that had additional adjustments for daily average temperature, the authors note.

"[W]e found a substantial increase in hospital admissions because of flares of IBD and IG during heat wave periods," they write. "Whereas the effect on IG is strongest with a delay of 7 days, the effect on IBD flares is immediate, suggesting different mechanisms."

One of the reasons heat waves might affect IBD flare-ups and IG is because they can cause physical stress, Dr. Manser said in the press release. "Physical as well as mental stress has been shown to cause flares of IBD and may explain the increase in IBD hospital admissions during heat."

The growth of bacteria may be another factor affecting how heat waves affect digestive symptoms, the authors write. "During a heat wave, changes in bacterial composition of food, skin, soil, and water may occur. This has never been investigated in much detail. However, recent research suggests that temperature plays a crucial role for the expansion of enterohemorrhagic Escherichia coli and other pathogenic bacteria," they write.

"This study ties heat stress to digestive symptoms supporting the observed seasonal variation in the clinical course of [IBD] and suggests that microbial infections of the gut might be additionally influenced by climate changes," Dr. Manser said in the news release.

In conclusion, the authors warn that the public should be aware of an increased risk for flare-ups from IBD and IG during a heat wave. "[M]itigation and adaptation strategies are needed to reduce current vulnerability to climate change and to address the health risks projected to occur over the coming decades," they write.

This study was supported by the Swiss National Science Foundation. The authors have disclosed no relevant financial relationships.

Am J Gastroenterol. Published online August 13, 2013. Abstract

http://www.medscape.com/viewarticle/809363

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Breathing exercises, meditation improved inflammatory markers, quality of life in IBD patients new
      #370525 - 10/23/13 04:20 PM
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Breathing exercises, meditation improved inflammatory markers, quality of life in IBD patients

October 18, 2013

SAN DIEGO — Patients with mild-to-moderate inflammatory bowel disease who participated in a program of breathing, movement and meditation exercises experienced significant improvement to inflammatory markers and quality of life in a study presented at the American College of Gastroenterology Annual Scientific Meeting.

Researchers randomized 30 patients with mild-to-moderate IBD to participate in either a breathing, movement and meditation workshop (BBMW) or a control group undergoing a parallel educational seminar (ES). Inflammatory and psychometric markers were assessed via brief symptom inventory (BSI), Beck anxiety inventory (BAI), Beck depression index and IBD questionnaire (IBDQ) at baseline, with changes after 6 weeks as the primary endpoint and after 6 months as the secondary endpoint. Both groups received similar access to health care professionals.

Patients in the BBMW group experienced significant improvements to BSI after 6 weeks compared with the ES group (P=.02 for difference). Similarly, quality of life as measured by the IBDQ (P=.01) was significantly improved in the BBMW group, as were symptoms of anxiety (P=.02). These improvements all persisted after 6 months (P=.04 for BSI score, P=.03 for BSAI and P=.01 for IBDQ), and investigators noted additional improvements to perceived stress (P=.01), perceived disability (P=.001) and depression (P=.01).

At 6 weeks, fecal calprotectin levels had improved significantly in the ES group (P=.04), and numerically in the BBMW group. These changes were not maintained at the 6-month evaluation.

"Many of our young patients with IBD have a decreased quality of life from many symptoms, including diarrhea, bleeding and abdominal pain," researcher Vinita E. Jacob, MD, assistant clinical professor of medicine at New York Presbyterian Hospital, Weill Cornell Medical College, told Healio.com. "… While we have excellent medical therapy, it's important to be broad-minded about other techniques that can be helpful in decreasing the inflammatory state in these particular patients. There are so many young patients who do not want to be on lifelong medication therapy; there is a role for stimulating the parasympathetic nervous system in these patients to help them feel better."

For more information:

Jacob VE. P1064: Impact of Breathing and Education Programs on Inflammatory Bowel Disease (IBD) Quality of Life (QOL) and Inflammatory Biomarkers. Presented at: The American College of Gastroenterology Annual Scientific Meeting; Oct. 11-16, San Diego.

http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7B65ae4fe2-c79a-4a82-9e7f-4e62c9d0b6bc%7D/breathing-exercises-meditation-improved-inflammatory-markers-quality-of-life-in-ibd-patients


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Stool test distinguishes between IBD and IBS new
      #371087 - 04/07/14 01:40 PM
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Stool emissions test distinguished between IBD, IBS

Shepherd SF. J. Breath Res. 2014;doi:10.1088/1752-7155/8/2/026001.

April 1, 2014

Analysis of volatile organic compounds emitted from stool samples distinguished patients with either inflammatory bowel disease or irritable bowel syndrome, according to new data from researchers in the UK.

Investigators coupled a gas chromatograph to a metal oxide sensor with pattern recognition software. The volatile organic compounds (VOCs), acting as a proxy for conditions in the gastrointestinal tract, produced a unique profile for each bowel disease with 76% overall accuracy.

The system required 40 minutes to obtain a chromatogram which then was assessed "in seconds" by artificial neural network software, according to researchers.

Stool samples were collected from 182 patients with inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) between October 2010 and October 2011. After being frozen, the samples were compared to control samples from healthy patients. The system was able to distinguish IBD from controls with 79% mean accuracy. But the method was less sensitive when distinguishing IBS from controls (mean accuracy, 54%). Sensitivity and specificity in differentiating IBS from IBD samples were 76% and 88%, respectively.

"Our work has demonstrated that a low-cost device based on VOC analysis could be used to potentially diagnose, and differentiate, IBS and IBD at the point of care," researcher Sophie F. Shepherd,BSc, Institute of Bio-sensing Technology, University of the West of England, said in a press release.

http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7B3331848c-73ad-4ab8-bbfc-ca6a876c2fee%7D/stool-emissions-test-distinguished-between-ibd-ibs

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Self-assessment scale developed for patients with IBD-fatigue new
      #371245 - 06/17/14 10:44 AM
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Self-assessment scale developed for patients with IBD-fatigue

Czuber-Dochan W. J Crohns Colitis. 2014;doi:10.1016/j.crohns.2014.04.013.

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June 9, 2014

Researchers from the United Kingdom have developed an inflammatory bowel disease fatigue patient self-assessment scale that is designed to more accurately and reliably measure the severity and impact of disease-associated fatigue.
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The IBD-F scale was developed and validated in a five-phase process between September 2010 and May 2013, and involved 567 patients with Crohn's disease or ulcerative colitis. Phase one entailed researcher-conducted interviews with patients (n=20) to qualitatively assess their experience with fatigue, its impact on their quality of life, and the efficacy of existing fatigue scales (Multidimensional Fatigue Inventory [MFI], Multidimensional Assessment of Fatigue [MAF]) in reflecting their specific experience and concerns. Phases two (n=16), three (n=30), four (n=36) and five (n=465) qualitatively and quantitatively assessed and refined the IBD-F scale. Participants completed drafts of the developing questionnaire, modifications were made based on commentary from subsequent interviews in phases two and three, and reliability was tested in phases four and five.

The final questionnaire entailed three sections, evaluating fatigue severity and frequency, its impact on daily activities, and duration of fatigue. The IBD-F scale was preferred over alternatives overall; patients interviewed reported it was "more attuned to their experience than the MAF and MFI." Agreement between scores associated with individual questions, measured through test-retest in phase four, was "relatively poor," but agreement between total scores was higher (ICC=0.74; 95% CI, 0.54-0.86).

Phase five revealed "moderate correlation" between sections one (ICC=0.73; P<.001) and two (ICC=0.78; P<.001) of the IBD-F scale and the MAF, along with the five MFI subscales (ICC=0.47-0.65; P<.001).

"The IBD-F scale consists of items generated specifically from the issues of importance to people with IBD fatigue," the researchers concluded, "and it has been found on initial testing to be valid and reasonably reliable."

http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7Bdbb71f02-1941-4695-abcd-3079eb60432a%7D/self-assessment-scale-developed-for-patients-with-ibd-fatigue

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Vitamin D and Cancer Risk in IBD new
      #371282 - 07/15/14 02:53 PM
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Vitamin D Blog: Cancer Risk in IBD

Published: Jul 8, 2014
By Ashwin Ananthakrishnan, MBBS, MPH , Massachusetts General Hospital

In this Guest Blog, Ashwin N. Ananthakrishnan, MBBS, MPH, a gastroenterologist at Massachusetts General Hospital in Boston, discusses his recent study on vitamin D and its relationship with cancer in patients with inflammatory bowel disease.

Vitamin D has pleiotropic effects on the immune system and has been associated with reduced risk of autoimmunity, cardiovascular disease, and cancer. Yet there are no data on the association between vitamin D and cancer in chronic immune-mediated diseases where mechanisms of cancer may be distinct and other competing factors may influence both vitamin D status and cancer risk.

My team at Massachusetts General Hospital in Boston is interested in uncovering the connection between vitamin D and inflammatory bowel disease (IBD). Although a third of IBD patients are vitamin D deficient and an equal proportion have insufficient levels, there has been only limited study of potential longitudinal consequences.

Cross-sectional studies suggested an association between vitamin D status and disease activity, a finding that was confirmed in a study from our group demonstrating an inverse association with IBD-related hospitalizations and surgery. We have also shown that normalization of vitamin D levels is associated with a reduction in the risk of IBD-related surgery.

Since no prior studies have examined the effect of vitamin D status on the risk of cancers in patients with IBD, we looked into the issue using a well-characterized, multi-institutional IBD cohort involving 2,809 patients. We assessed several types of cancers to see if the effect of vitamin D is specific to certain cancer subtypes in the IBD population.

This study, published in Clinical Gastroenterology and Hepatology, involved a follow-up period of 11 years, during which 169 patients (7%) developed cancer (excluding nonmelanoma skin cancer), with 41 cases of colorectal cancer.

We found that low vitamin D is associated with an increased risk of metastatic and nonmetastatic cancers -- and the association was strongest for colorectal cancer.

There were, of course, limitations. Our cohort is based primarily at two referral centers, so the population may be skewed toward greater severity of underlying IBD. Also, we did not have information on body mass index or smoking status, both of which have been associated with overall risk of malignancy and colorectal cancer -- although the effect of BMI and smoking on IBD-related cancers has not been noted previously.

Nor did we have information on medications such as aspirin and nonsteroidal anti-inflammatory drugs, both of which have been inversely associated with the development of colorectal cancer. However, long-term use of such medications is uncommon in patients with IBD because of their potential to trigger disease relapses.

Nevertheless, to our knowledge, this remains the largest cohort containing information on the vitamin D status of patients with IBD. Based on our findings, an assessment of vitamin D status should routinely be part of comprehensive care of patients with IBD.

I know from treating patients with IBD that controlling symptoms can be a daily struggle. Luckily, vitamin D is relatively easy to monitor and maintain and may offer long-term health benefits for those with the disease. However, we need much more rigorous data to examine the role of vitamin D, safety with various doses of supplementation, and clinical trials examining its effect on disease activity and other outcomes in patients with IBD.

http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/46665

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Fecal lactoferrin differentiated IBD from IBS new
      #371308 - 07/29/14 01:50 PM
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Fecal lactoferrin differentiated IBD from IBS

Zhou X-L. BMC Gastroenterol. 2014;doi:10.1186/1471-230X-14-121.


July 22, 2014

Fecal lactoferrin as a diagnostic biomarker effectively distinguished between inflammatory bowel disease and irritable bowel syndrome in a recent study.
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Seeking a less invasive and more economical alternative to standard endoscopy and radiographic imaging for discounting inflammatory bowel disease (IBD) in patients with symptoms of irritable bowel syndrome (IBS), researchers in China assessed the diagnostic utility of fecal lactoferrin (FL) levels in discriminating between IBD and IBS. They performed a meta-analysis of seven relevant studies sourced from Medline, Embase and other databases through November 2013.

After analyzing a cohort of 1,012 adult and pediatric patients (609 with IBD, 381 with IBS, 22 controls), sensitivities of FL in differentiating IBD from IBS ranged from 0.69 to 0.86, with a pooled sensitivity of 0.78 (95% CI, 0.75-0.82). Specificities ranged from 0.83 to 1, with a pooled specificity of 0.94 (95% CI, 0.91-0.96). Pooled positive likelihood ratio was 12.31 (95% CI, 6.05-25.07), pooled negative likelihood ratio was 0.23 (95% CI, 0.18-0.29), pooled diagnostic OR was 52.65 (95% CI, 25.69-107.91) and the pooled summary receiver-operating characteristic AUC was 0.94 (95% CI, 0.9-0.98).

"To our knowledge, this study is the first … to assess the diagnostic performance of FL in differentiating between IBD and IBS," the researchers wrote. "This meta-analysis showed that FL appears to have good diagnostic precision in distinguishing IBD from IBS both in adults and children.

"Owing to study limitations [including a small cohort with few controls], additional high-quality original studies (especially in patients stratified by disease type, severity and distribution) are required to confirm the predictive value of FL."

http://www.healio.com/gastroenterology/irritable-bowel-syndrome/news/online/%7Be8dae45a-dce9-4242-bab6-91552d932acc%7D/fecal-lactoferrin-differentiated-ibd-from-ibs

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Hormonal contraception improved menstrual-related IBD symptoms new
      #371462 - 09/15/14 12:43 PM
HeatherAdministrator

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Hormonal contraception improved menstrual-related IBD symptoms

Gawron LM. Inflamm Bowel Dis. 2014;doi:10.1097/MIB.0000000000000134.
August 18, 2014

Hormonal contraception improved cyclical menstrual-related symptoms of inflammatory bowel disease in some women, according to recent study data.

Researchers performed a cross-sectional survey of 129 women treated for inflammatory bowel disease (IBD) at the Northwestern Medical Faculty Foundation's academic gastroenterology practice between 2010 and 2012. Participants were identified by database and questioned by telephone between March and November 2013 regarding cyclical menstrual-related IBD symptoms and how their contraceptives affect them.

Sixty percent of participants (mean age, 34.3 years; 85% white) were diagnosed with Crohn's disease. Cyclical IBD-related symptoms were reported by 60% of participants, with 42% and 72% citing symptoms in the pre-menstrual and menstrual phases, respectively (both P=.02). A current contraceptive method was used by 68% compared with 43% using hormonal contraception. Among those using hormonal contraception, 20% reported improved cyclical IBD symptoms, while 75% reported no change in symptoms, the most common being diarrhea (48%), pain (44%) and cramping (41%).

"In this subset of women with IBD, the majority report either improvement or no significant change in their disease-related symptoms," the researchers concluded. "This finding has several implications as follows: (1) contraception is unlikely to worsen IBD symptoms, (2) for at least a subset of patients with IBD, contraception use might improve symptoms by reducing the impact of menses on intestinal function, and (3) there is justification to study the use of contraception for disease management purposes in future studies."

http://www.healio.com/news/online/%7B637f28e2-bf9f-45c7-859d-9caeb2fd55e5%7D/hormonal-contraception-improved-menstrual-related-ibd-symptoms

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7 recent developments in Crohn's disease new
      #371993 - 04/02/15 03:16 PM
HeatherAdministrator

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7 recent developments in Crohn's disease

Crohn's disease has been a hot topic recently, with an abundance of data being published in the journals this month. Here is a recap of the most trafficked news on Healio Gastroenterology about Crohn's disease.

1. Racial disparities exist among children with Crohn's disease

Jennifer Dotson

Disparities in hospital readmissions, complications and procedures in pediatric Crohn's disease patients are related to race, according to data from a recent retrospective review.

"We found racial inequalities exist among children and adolescents with Crohn's disease, likely due to a combination of genetic and environmental differences," Jennifer Dotson, MD, MPH, a gastroenterologist at Nationwide Children's Hospital in Columbus, Ohio, and principal investigator in the Center for Innovation and Pediatric Practice, said in a press release. "This is one of the first studies to investigate the rate of various health disparities in the Crohn's disease population in pediatrics, despite the fact that 25% of the time, Crohn's disease is diagnosed in childhood." Read more



2. Experts release international consensus statement on surveillance, management of dysplasia in inflammatory bowel disease

Tonya Kaltenbach

SCENIC, an international multidisciplinary group, has developed unifying consensus recommendations on surveillance and management of dysplasia in IBD.

"We recognized that there was variable practice in the surveillance methods for dysplasia detection in patients with IBD and there were also variable guidelines, both within the US and internationally," Tonya Kaltenbach, MD, MS, from the Veterans Affairs Palo Alto, who served on the panel, told Healio Gastroenterology. The need for an international consensus statement, she said, came from "an interest to provide a uniform recommendation" — namely on the use of chromoendoscopy for the detection of dysplasia. Read more



3. CRP, calprotectin, excludes IBD in patients with IBS symptoms

William D. Chey

Adding C-reactive protein and fecal calprotectin to symptom-based diagnostic criteria may help to rule out inflammatory bowel disease in patients with symptoms of irritable bowel syndrome, according to new research data.

"Though IBD is uncommon in patients with typical IBS symptoms and no alarming features, patients and providers remain concerned about this possibility," William D. Chey, MD, AGAF, FACG, FACP, from the University of Michigan Health System, told Healio Gastroenterology.

Adding C-reactive protein and fecal calprotectin to symptom-based diagnostic criteria may help to rule out inflammatory bowel disease in patients with symptoms of irritable bowel syndrome, according to new research data.

"Though IBD is uncommon in patients with typical IBS symptoms and no alarming features, patients and providers remain concerned about this possibility," William D. Chey, MD, AGAF, FACG, FACP, from the University of Michigan Health System, told Healio Gastroenterology.

William D. Chey

Chey and colleagues performed a systematic review and meta-analysis to assess the utility of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fecal calprotectin and fecal lactoferrin to aid in differentiating between IBS, IBD and healthy patients. After reviewing 1,252 relevant studies, 12 involving 1,059 IBD patients (52.7% male; mean age, 40.7 ± 13.3 years), 595 IBS patients (29.9% male; mean age, 40 ± 18.2 years) and 491 healthy controls (53.5% male; mean age, 38.7 ± 13.8 years) were included in the meta-analysis.

The researchers found that none of the biomarkers could distinguish patients with IBS from healthy controls, but CRP and calprotectin had some value in distinguishing IBD from IBS or healthy controls. High CRP was predictive of IBD, while low CRP indicated the absence of IBD; CRP &#8805; 1.7 mg/dl and > 2.7 mg/dl indicated > 52% and > 90% likelihood of IBD, respectively, while CRP &#8804; 0.5 indicated that the probability of having IBD was 1% or less.

Likelihood of IBD also increased with calprotectin level, which had a maximal predictive value of 78.7% at 1,000 µg/g. Patients with < 40 µg/g calprotectin had &#8804; 1% chance of having IBD. However, calprotectin level could not rule out IBS entirely; on both sides of the fecal calprotectin range (20 µg/g - 1,000 µg/g) there was an 11.6% and 7.6% predictive probability of IBS, respectively, with a peak predictive probability of 280 µg/g (18.8%).

"Serum CRP and fecal calprotectin provide a noninvasive means by which to exclude IBD in patients with IBS symptoms and no alarming features," Chey said.

"Based upon these results, it may be reasonable for clinicians to consider ordering CRP or fecal calprotectin to improve their confidence in making a diagnosis of IBS," the researchers concluded, adding that "prospective studies to evaluate the clinical utility and cost effectiveness of adding CRP or fecal calprotectin to the evaluation of patients with suspected IBS in different populations would be of considerable interest." – by Adam Leitenberger

4. Slow IBD diagnosis in children leads to more advanced disease
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Slow diagnosis of inflammatory bowel disease in pediatric patients was associated with advanced bowel involvement at the time of diagnosis, according to recent data.

"Time from symptom onset to diagnosis for IBD among children and adolescents is too long: an average of 4 to 6 months," the researchers wrote. "The majority of pediatric IBD patients already have extensive involvement at diagnosis." Read more



5. FMT induces remission in pediatric patients with Crohn's disease

David L. Suskind

Children with Crohn's disease achieved remission after fecal microbiota transplant, recent study data found.

"The fecal microbiome is likely the cause or trigger of the immune response in IBD," David L. Suskind, MD, from the department of pediatrics, division of gastroenterology at Seattle Children's Hospital, told Healio Gastroenterology. "Therapies which affect the fecal microbiome such as FMT, have the potential to change our current treatment paradigm by altering the fecal microbiome instead of using medications which suppress the immune response." Read more



6. Smoking cessation programs for Crohn's improve outcomes, reduce costs

Stephanie Coward

Gilaad G. Kaplan

The integration of smoking cessation programs targeting patients with Crohn's disease is cost-effective for health care systems, recent study data found.

"Smoking is known to worsen the course of Crohn's disease, whereas individuals who quit have a similar prognosis to patients with Crohn's disease who never smoked," Stephanie Coward, MSc, and Gilaad G. Kaplan, MD, MPH, both from the University of Calgary in Alberta, Canada, told Healio Gastroenterology. "We conducted a cost-utility analysis to compare different smoking cessation strategies for patients with Crohn's disease." Read more



7. Mongersen appears to improve remission in Crohn's disease

Séverine Vermeire

Patients with Crohn's disease achieved remission and clinical response in greater proportions with mongersen, a novel oral SMAD7 antisense oligonucleotide, compared with placebo, according to recent study data.

"The impressive clinical effects of mongersen beg for follow-up studies to confirm that we have indeed entered a new phase of Crohn's disease treatment," Séverine Vermeire, MD, PhD, from the University Hospitals in Leuven, Belgium, wrote in an accompanying editorial.



http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7Bcb981f43-1d15-4ecd-9e0f-9bf44e650089%7D/7-recent-developments-in-crohns-disease

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Heather is the Administrator of the IBS Message Boards. She is the author of Eating for IBS and The First Year: IBS, and the CEO of Heather's Tummy Care. Join her IBS Newsletter. Meet Heather on Facebook!

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Fecal transplant induces remission in active ulcerative colitis new
      #372219 - 07/16/15 04:39 PM
HeatherAdministrator

Reged: 12/09/02
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FMT induces remission in active ulcerative colitis

Moayyedi P, et al. Gastroenterology. 2015;doi:10.1053/j.gastro.2015.04.001.
Grinspan AM, Kelly CR. Gastroenterology. 2015;doi:10.1053/j.gastro.2015.05.030.
June 29, 2015



Aiming to evaluate the safety and efficacy of FMT for treatment of active UC, Paul Moayyedi, MD, from McMaster University in Ontario, and colleagues performed a placebo-controlled, double-blind, randomized, parallel study. Adult participants were randomly assigned to receive 50-mL FMT from healthy anonymous donors (n = 38) or placebo (50 mL water; n = 37) via retention enema once a week for 6 weeks. Stool samples were collected weekly prior to enema for microbiome analysis, flexible sigmoidoscopy was performed at baseline and week 7, and the primary study outcome was remission at week 7.

The trial was stopped early for futility, but patients already enrolled were allowed to complete the trial. Of the 70 patients who completed the trial, 24% of the FMT group compared with 5% of the placebo group were in remission at week 7 (17% difference; 95% CI, 2%-33%) with comparable adverse events. Of the nine patients in remission after FMT, seven received FMT from a single donor. Of the four patients with UC for 1 year or less, three achieved remission, and of the 34 patients with UC for more than 1 year, six achieved remission (P = .04). Patients in the FMT group had greater diversity in their stool microbial composition vs. baseline compared with patients in the placebo group (P = .02).

"This is the first randomized, placebo-controlled trial, to evaluate the efficacy of FMT in active UC and suggests that this approach induces remission in a statistically significant proportion of cases," the authors wrote. "FMT may be more efficacious in patients with a recent diagnosis of UC, and this is biologically plausible, as a perturbation in the microbiome might be more easily restored early in the course of the disease. The efficacy of this approach may also be donor dependent and this may explain why some case series have shown promise, and other have had disappointing results."

Colleen R. Kelly

In a related editorial, Ari M. Grinspan, MD, from Icahn School of Medicine at Mount Sinai in New York, and Colleen R. Kelly, MD, from Brown University, explored the reasons why another recent randomized controlled trial of FMT for UC (Rossen, et al) was negative while this one was positive. First, Moayyedi and colleagues administered a higher number of FMTs per patient and via the lower rather than upper gastrointestinal route. "The upper GI route might render the active constituent of FMT ineffective by the time it reaches the diseased colon. It is also possible that there is a dose response or a threshold required for engraftment to be attained to alter effectively the gut microbiome and the downstream inflammatory cascade," they wrote. Moayyedi's study also permitted anti-tumor necrosis factor treatment, "and those subjects on immunosuppression did better, raising the question as to whether immune factors may have a role in successful FMT induction. These uncertainties make our ignorance clear; we still do not understand the active component of FMT."

Grinspan and Kelly concluded that for IBD, "based on the current data, FMT should remain in clinical trials and not clinical practice." – by Adam Leitenberger

Disclosure: Moayyedi reports he is a chair partly funded by an unrestricted donation given to McMaster University by AstraZeneca, and he has received honoraria for speaking and/or serving on the advisory board for AstraZeneca, Actavis and Shire. Grinspan reports he received research support from the Sinai Ulcerative Colitis Clinical, Experimental and System Studies. Kelly reports she has served as a consultant and site investigator for Seres Health and received research support from Assembly Biosciences.

http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7B9917554a-9c2a-4b0e-8ada-ded4a9028707%7D/fmt-induces-remission-in-active-ulcerative-colitis?utm_source=maestro&utm_medium=email&utm_campaign=gastroenterology%20news

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Probiotics not superior for maintaining ulcerative colitis remission new
      #372635 - 12/29/15 10:12 AM
HeatherAdministrator

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Probiotics not superior for maintaining ulcerative colitis remission
December 14, 2015

ORLANDO — A systematic review showed no significant difference in efficacy between probiotics and placebo or mesalazine for maintenance of remission in ulcerative colitis, according to a poster presentation at the 2015 Advances in IBD Meeting.

"Five years ago, a Cochrane review found only four studies and no evidence regarding the efficacy of probiotics [for preventing UC relapse], but much work has been published in recent years," Morris Gordon, PhD, from University of Central Lancashire and Blackpool Victoria Hospital in the UK, and colleagues wrote. They therefore performed an updated Cochrane systematic review of data published up to January 2015 to evaluate the safety and efficacy of probiotics for the maintenance of remission in UC.

The review included seven randomized controlled trials (n = 887), ranging in duration from 3 to 12 months and comparing probiotics to placebo or mesalazine. They found the efficacy of probiotics was not significantly different from placebo based on two small studies involving 92 patients, which had some risk of bias (OR = 0.56; 95% CI, 0.22-1.4).

They also found the efficacy of probiotics was not significantly different from mesalazine, based on four studies involving 638 patients (OR = 1.29; 95% CI, 0.92-1.8). Incidence of adverse events was also statistically comparable (OR = 1.16; 95% CI, 0.79-1.71).

"There is a trend in favor of mesalazine, but this is not statistically significant," Morris said during his poster presentation. "It seems very hard to draw any strong conclusions. … There is some evidence to suggest there may be a trend towards effectiveness [of probiotics] when compared to placebo, but this is not statistically significant. … It therefore appears that — for the moment — probiotics cannot be supported as a superior intervention either compared to placebo or mesalazine for the maintenance of remission in ulcerative colitis."

The investigators concluded that further research on the role of probiotics in maintaining remission in UC is warranted. – by Adam Leitenberger

Reference: Gordon M, Farrell M. Abstract P-054. Presented at Advances in Inflammatory Bowel Diseases; Dec. 10-12, 2015; Orlando, Fla.

http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7B26ad66a8-794d-4a6b-bade-a17f76828504%7D/probiotics-not-superior-for-maintaining-ulcerative-colitis-remission?utm_source=maestro&utm_medium=email&utm_campaign=gastroenterology%20news

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Dietary fiber associated with reduced Crohn's disease flares new
      #372678 - 01/27/16 02:58 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Dietary fiber associated with reduced Crohn's disease flares

Brotherton CS, et al. Clin Gastroenterol Hepatol. 2015;doi:10.1016/j.cgh.2015.12.029.

January 25, 2016

Researchers suggested re-evaluating recommendations to limit dietary fiber due to recent evidence that disease flares in patients with Crohn's disease may be reduced with the intake of dietary fiber. However, in the study, the reduced flares were not observed in patients with ulcerative colitis.
Using the Crohn's and Colitis Foundation of America Partners Internet cohort, Carol S. Brotherton, PhD, of the School of Nursing, George Mason University, Fairfax, Va., and colleagues examined the association of dietary fiber intake with flares in patients with chronic inflammatory bowel diseases.

For the study, 1,619 patients were identified; 1,130 were patients with Crohn's disease (CD), and 489 were patients with UC/indeterminate colitis. Completed dietary surveys were collected from the patients at baseline and at 6-month follow-up. Consumption of fiber and whole grains was classified into quartiles and deciles. At the 6-month follow-up period, the researchers considered a disease flare to be a disease activity index score above remission cut-off values. IBD-related surgical procedures or hospitalizations that occurred from the time of the baseline survey to follow-up were also considered a disease flare.

The risk for disease flare differed by type of disease. Patients with CD were about 40% less likely to have a disease flare when they did not avoid high fiber foods compared to those who reported that they did avoid high fiber foods (adjusted OR, 0.59; 95% CI, 0.43-0.81). Patients with CD in the highest quartile of fiber intake were significantly less likely to have a flare (crude OR = 0.57; 95% CI 0.38-0.86). For patients with UC, researchers found no link between dietary fiber intake and disease flare (aOR, 1.82; 95% CI, 0.92-3.6).

"The results of this study support findings reported in investigations occurring in the 1980s – low fiber eating does not result in improved outcomes for individuals with CD compared to individuals with CD not restricting fiber intake," the researchers wrote. "More research is needed to explore the causes of fiber restriction in CD. More prospective studies are needed to explore the potential benefits of fiber-containing foods in the diet of individuals with IBD, especially in specific phenotypes. As suggested by the authors of a recent IBD diet review, it is unlikely that a single diet will be found to be sufficient to manage all IBD phenotypes; however, it will be remarkable progress if a diet is found to be sufficient alone for some and adjunctive therapy for others." – by Suzanne Reist


http://www.healio.com/gastroenterology/inflammatory-bowel-disease/news/online/%7Bbba2cce0-6133-43f9-9548-5d85bf529269%7D/dietary-fiber-associated-with-reduced-crohns-disease-flares?utm_source=maestro&utm_medium=email&utm_campaign=gastroenterology%20news



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Why cannabis relieves IBD symptoms new
      #373730 - 08/22/18 02:39 PM
HeatherAdministrator

Reged: 12/09/02
Posts: 7790
Loc: Seattle, WA

Why cannabis relieves IBD symptoms

Healthline/Medical News Today ' August 14, 2018

New research, published in the Journal of Clinical Investigation, reveals the molecular mechanism that explains why cannabis could help treat inflammatory bowel disease.

Inflammatory bowel disease (IBD) is an umbrella term that describes inflammatory conditions affecting the gastrointestinal tract, such as Crohn's disease and ulcerative colitis.

In the United States, approximately 1.6 million people are living with such disorders. Almost 70,000 new cases are diagnosed each year.

The chronic inflammation in IBD leads to often debilitating symptoms, such as abdominal pain, rectal bleeding, fatigue, and diarrhea.

Older studies and anecdotal reports have shown that people who use cannabis experience and maintain remission of the condition. Cannabis users say that the drug helps them to successfully manage "abdominal pain, joint pain, cramping, diarrhea, poor appetite, weight loss, and nausea."

What could explain this therapeutic effect? For the first time, researchers were able to find a biological mechanism that shows how cannabis relieves intestinal inflammation in IBD.

The scientists were led by Beth A. McCormick, vice chair and a professor of microbiology and physiological systems at the University of Massachusetts Medical School in Worcester.

How cannabinoids stop the inflammation

Prof. McCormick and her colleagues started their research by acknowledging an already known inflammation process that occurs when the body is infected with a pathogen.

The so-called neutrophil influx is a normal reaction of the immune system that sends neutrophilsâ€"a type of white blood cellâ€"to fight against foreign microorganisms such as viruses or bacteria.

However, if the immune cells react disproportionately, they can also destroy the epithelium, which is the protective layer of cells that lines the inside of the intestine.

So, in order to stop the overreaction of the immune response, special molecules are "dispatched" and transported across the epithelium to stop the inflammation.

The team found that the second process requires endogenous cannabinoids (endocannabinoids), which are naturally produced by our bodies and have a similar effect to the cannabinoids in cannabis.

By performing experiments in mice and human cell lines, the team found that if endocannabinoids are lacking or are insufficient, the body cannot control the inflammation process anymore and the neutrophils attack the protective intestinal layer.
The scientists believe that cannabis makes up for the natural cannabinoids, inducing the same anti-inflammatory effect that endocannabinoids would have.

Prof. McCormick comments on the findings, saying, "There's been a lot of anecdotal evidence about the benefits of medical marijuana, but there hasn't been a lot of science to back it up."

"For the first time, we have an understanding of the molecules involved in the process and how endocannabinoids and cannabinoids control inflammation. This gives clinical researchers a new drug target to explore to treat patients [with IBD]."

Prof. Beth A. McCormick

Study co-author Randy Mrsny, a professor in the Department of Pharmacy and Pharmacology at the University of Bath in the United Kingdom, also weighs in with a clarification.

According to him, "We need to be clear that while this is a plausible explanation for why marijuana users have reported cannabis relieves symptoms of IBD, we have thus far only evaluated this in mice and have not proven this experimentally in humans."

"We hope, however, that these findings will help us develop new ways to treat bowel diseases in humans," Prof. Mrsny concludes.

https://www.mdlinx.com/gastroenterology/top-medical-news/article/2018/08/14/7541445

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