Why IBS Is NOT caused by Candida
#354094 - 01/06/10 11:00 AM
|
|
|
shawneric
Reged: 01/30/03
Posts: 1738
Loc: Oregon
|
|
|
Hopefully this post will help explain it and the actual diagnoses of IBS itself. There are some major misunderstanding about diagnosing IBS, the term IBS- a distint enity- A lower GI disorder of function. And people's frustration and looking for all the things that could cause it. However, some have already been ruled out, some important ones are being researched and some DON"T apply to begin with.
You can read it or not. But I hope it really helps some people. I will continue to add information to it, so its not all at once.
First its important to go over IBS itself. There are some 28 GI disorders of function, some examples are IBS, functional dyspepsisa, functional D, functional c, functional analrectal disorders ect..
The diagnoses of IBS is based on a specific cluster of symptoms. It is NOT a catch all diagnoses. "What Patients Know About Irritable Bowel Syndrome (IBS) and What They Would Like to Know. National Survey on Patient Educational Needs in IBS and Development and Validation of the Patient Educational Posted 09/18/2007
"The most prevalent IBS misconceptions included (% of subjects agreeing with the statement): IBS is caused by lack of digestive enzymes (52%), is a form of colitis (42.8%), will worsen with age (47.9%), and can develop into colitis (43%) or malnutrition (37.7%) or cancer (21.4%). IBS patients were interested in learning about (% of subjects choosing an item): (1) foods to avoid (63.3%), (2) causes of IBS (62%), (3) coping strategies (59.4%), (4) medications (55.2%), (5) will they have to live with IBS for life (51.6%), and (6) research studies (48.6%). Patients using the Web were better informed about IBS. Conclusion: (1) Many patients hold misconceptions about IBS being caused by dietary habits, developing into cancer, colitis, causing malnutrition, or worsening with age; (2) patients most often seek information about dietary changes; and (3) educational needs may be different for persons using the internet for medical information."
"The emerging research typifies IBS as a brain-gut disorder where psychosocial factors (e.g., stress, cognitions, coping, etc.) can alter the symptoms and illness experience for better or worse. Due to these and other disease specific characteristics, that are amenable to education, we believe effective educational interventions may significantly impact the management of this common disorder."
Patients Consider IBS a Diagnosis of Exclusion: Over 50% of the patients considered IBS to be a "catch all" diagnosis and another 22% were unsure. While this could reflect the information provided by their physicians (thus highlighting the need to also educate physicians about IBS), this misconception may motivate patients to seek more and more diagnostic studies to find "the cause." The use of the Rome criteria[17] permits the patient to have a positive diagnosis. With confidence in knowing that IBS is a specific entity , such behaviors are minimized. Thus it is important for the physician to provide proper education about the level of confidence in the diagnosis.
http://www3.interscience.wiley.com/journal/117956426/abstract?CRETRY=1&SRETRY=0
Hopefully also it will help when talking to your doctor.
NEVER self diagnose. The leading cause of misdiagnoses is self diagnoses. Some conditions that mimick some IBS symptoms are also very serious and even potentially deadly.
First though is the change in diagnosing IBS that has been made.
"In the past two decades, medical opinion has changed regarding how to diagnose IBS. The older view emphasized that IBS should be regarded primarily as a "diagnosis of exclusion;" that is, diagnosed only after diagnostic testing excludes many disorders that could possibly cause the symptoms. Because many medical disorders can produce the cardinal IBS features of abdominal discomfort or pain and disturbed bowel habit as well as other symptoms caused by IBS, this approach often led to extensive diagnostic testing in many patients. Since the era when such thinking about IBS was common, laboratory, motility, radiologic, and endoscopic tests have proliferated. Although each of these tests is useful in evaluating certain problems, their routine or indiscriminate use can cause unnecessary inconvenience and cost for patients, and complications even occur infrequently from some of the tests. Fortunately, physicians can now diagnose IBS in most patients by recognizing certain symptom details, performing a physical examination, and undertaking limited diagnostic testing. This simpler approach is grounded on recent knowledge of the typical symptoms of IBS, and it leads to a reliable diagnosis in most cases. Extensive testing is usually reserved for special situations."
http://www.aboutibs.org/Publications/diagnosis.html
Diagnosis Patients with IBS can be confidently and correctly diagnosed using the Rome criteria in conjunction with a complete history and thorough physical examination (reviewed by Lacy and De Lee The utility of routine laboratory testing is widely debated, however, especially in those presumed IBS patients with diarrhea predominance, because of concern regarding the possibility of missing the diagnosis of celiac disease or inflammatory bowel disease (IBD). During ACG 2006, studies were presented that evaluated the utility of tests commonly ordered in the evaluation of some IBS patients. Two separate studies[27,28] reported on the diagnostic accuracy of serologic markers for celiac disease and IBD in a prospective, multicenter, observational trial involving 323 patients with IBS symptoms (mean age = 39 years; 68% women) and 241 controls referred for routine colon cancer screening (mean age = 54 years; 43% women). Routine laboratory tests (complete blood count, thyroid-stimulating hormone, and electrolytes), testing for specialized IBD serologic markers (antineutrophil cytoplasmic antibodies, IgA, and IgG anti-Saccharomyces cerevisae antibodies, and anti-OmpC antibodies [outer membrane porin to Escherichia coli]), serologic tests for celiac disease (anti-gliadin, anti-endomysial, anti-tissue transglutaminase antibodies), and colonoscopy were performed in all patients. Patients with serologic evidence of celiac disease also underwent upper endoscopy with biopsies of the small intestine. In this large group of subjects, only 2 patients with IBS symptoms were diagnosed with IBD. In fact, IBD serologic markers had a false-positive rate of 30%, and this finding was similar in both control and IBS patients. Tests for celiac disease were more frequently positive in IBS patients (7.4%) than in controls (2.9%); however, biopsies confirmed the diagnosis of celiac disease in just 1.24% of IBS patients and 0.8% of controls. No single antibody test for celiac disease identified all patients with biopsy-proven celiac disease. This large, ongoing prospective study demonstrates that celiac disease is uncommon in patients with IBS, that no single antibody test can accurately diagnose all patients with celiac disease, and that serologic tests for IBD have a high false-positive rate. Testing for these disorders should thus be limited to those IBS patients with persistent symptoms who fail to respond to standard therapy and should not be routinely performed in all IBS patients.Two other studies presented during this meeting that discussed testing in IBS patients warrant mention. In the first of these studies, Whitlock and colleagues[29] measured lactoferrin, a marker of activated neutrophils, in stool specimens from 94 IBD patients, 22 IBS patients, and 27 healthy controls (mean age, race, and sex breakdown not provided). Although raw data were not included, the study authors reported that fecal lactoferrin differentiated active IBD from IBS patients and healthy controls with 100% sensitivity and specificity. In addition, the test appeared to be highly accurate in differentiating active IBD patients from inactive IBD patients. These preliminary results are very interesting and warrant confirmation in a multicenter, prospective trial. In the second study,
http://www.medscape.com/viewarticle/547772
Celiac disease is one of the conditions they are looking at in regards to a misdiagnoses.
However Celiac is NOT IBS and it has symptoms such as weight loss and other symptoms that can differentiate for IBS, by a knowledeable doctor.
Celiac does not always cause pain either. It is estimated in about 2 % percent of the population and is still some what underdiagnosed. It also has a close genetic relationship, so if family members have it is could be a very good idea to be screened.
If your looking for very accurate Celiac information this is one of the Doctors.
Dr Green is the Director of The Celiac Disease Center at Columbia University
http://www.celiacdiseasecenter.columbia.ed...3-StaffBios.htm
Further research showed a slightly higher celiac population.
So they are saying now that certain people should be tested for celiac.
Next I will post about the rome criteria hopefully used to diagnosed IBS. Als a little on researchers and the rome criteria and local gi doctors and the rome criteria.
Rome III Journal Articles: Gastroenterology, April 2006 The Rome III book was published in condensed form in a journal supplement that appeared in Gastroenterology (volume 20, issue 5, May 2006) the official journal of the American Gastroenterological Association. The Rome Foundation obtained permission to post the journal articles on our website for download by the American Gastroenterological Association Institute.
Table of Contents
The Functional Gastrointestinal Disorders and the Rome III Process D. A. Drossman
Fundamentals of Neurogastroenterology: Basic Science D. Grundy, E. D. Al—Chaer, Q. Aziz, S. M. Collins, M. Ke, Y. Taché, and J. D. Wood
Applied Principles of Neurogastroenterology: Physiology/Motility Sensation J. E. Kellow, F. Azpiroz, M. Delvaux, G. F. Gebhart, H. R. Mertz, E. M. M. Quigley, and A. J. P. M. Smout
Pharmacological and Pharmacokinetic Aspects of Functional Gastrointestinal Disorders M. Camilleri, L. Bueno, F. de Ponti, J. Fioramonti, R. B. Lydiard, and J. Tack
Gender, Age, Society, Culture, and the Patient's Perspective in the Functional Gastrointestinal Disorders L. Chang, B. B. Toner, S. Fukudo, E. Guthrie, G. R. Locke, N. J. Norton, and A. D. Sperber
Psychosocial Aspects of the Functional Gastrointestinal Disorders R. L. Levy, K. W. Olden, B. D. Naliboff, L. A. Bradley, C. Francisconi, D. A. Drossman, and F. Creed
Functional Esophageal Disorders J. P. Galmiche, R. E. Clouse, A. Bálint, I. J. Cook, P. J. Kahrilas, W. G. Paterson, and A. J. P. M. Smout
Functional Gastroduodenal Disorders J. Tack, N. J. Talley, M. Camilleri, G. Holtmann, P. Hu, J.-R. Malagelada, and V. Stanghellini
Functional Bowel Disorders G. F. Longstreth, W. G. Thompson, W. D. Chey, L. A. Houghton, F. Mearin, and R. C. Spiller
Functional Abdominal Pain Syndrome R. E. Clouse, E. A. Mayer, Q. Aziz, D. A. Drossman, D. L. Dumitrascu, H. Mönnikes, and B. D. Naliboff
Functional Gallbladder and Sphincter of Oddi Disorders J. Behar, E. Corazziari, M. Guelrud, W. Hogan, S. Sherman, and J. Toouli
Functional Anorectal Disorders A. E. Bharucha, A. Wald, P. Enck, and S. Rao
Childhood Functional Gastrointestinal Disorders: Neonate/Toddler P. E. Hyman, P. J. Milla, M. A. Benninga, G. P. Davidson, D. F. Fleisher, and J. Taminiau
Childhood Functional Gastrointestinal Disorders: Child/Adolescent A. Rasquin, C. Di Lorenzo, D. Forbes, E. Guiraldes, J. S. Hyams, A. Staiano, and L. S. Walker
Design of Treatment Trials for Functional Gastrointestinal Disorders E. J. Irvine, W. E. Whitehead, W. D. Chey, K. Matsueda, M. Shaw, N. J. Talley, and S. J. O. Veldhuyzen van Zanten
The Road to Rome W. G. Thompson
http://www.romecriteria.org/rome_III_gastro/
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
-------------------- Janey
Print
Remind Me
Notify Moderator
|
|
Thank you for the information. I admire your drive to clear up erroneous information about IBS. Unfortunately, the misinformation about Candida and IBS has taken on a life of its own almost like a religion and sometimes it is difficult to re-educate some individuals.
Keep up the great posts and excellent work promoting the on-line GI disorder chats.
-------------------- STABLE: ♂, IBS-D 50+ years - Science of IBS
The FODMAP Approach to Managing IBS Symptoms
Evidence-based Dietary Management of Functional GI Symptoms: The FODMAP Approach
FODMAP Chart & Cheatsheet
The Role of Food & Dietary Intervention in IBS
Print
Remind Me
Notify Moderator
|
|
No problem, I feel it is really needed at this point, because of the recent posts that cause more confusion on the actual diagnoses of IBS and the cause/causes.
People are posting IBS is an infections disease or food allergy, or toxins or bacterial infection, or fungus, or pathogens this is totally inaccurate. Those condition if some exist at all to begin with are not IBS, but there own seperate conditions.
Experts are working very hard to validate functional gi disorders as real seperate entities.
I will get to the candida in a bit here.
Next a history of the funtional Bowel disorders.
This is from the President of the Rome commitee to diagnosed functional disorders.
History of Functional Disorders
THE PAST HISTORICAL PRECEDENTS Historians and physicians have documented the presence of Functional GI disorders throughout recorded human history. However, until recently, limited attention has been granted to these disorders due to the lack of identifiable pathology and the absence of a conceptual framework to understand and categorize them. Systematic investigation of functional GI disorders did not begin until the middle of the 20th century, and prior to this time, only occasional reports of functional GI symptoms were published, the first appearing only 200 years ago. Over the past 25 years, scientific attention to understanding and properly caring for patients with functional GI disorders has grown progressively. With the understanding comes the rationale for use of medications directed at intestinal receptors as well as psychopharmacological, behavioral, and psychological forms of treatment. Additionally, there has been an increase in the rate of scientific publications and greater media exposure to the public through television, radio, and Internet. To understand the historical classification of these disorders, two differing theories relating to the interaction between the mind and body should be considered."
More explain in the document.
'THE PRESENT CONCEPTUAL BASES FOR THE STUDY OF FUNCTIONAL GI DISORDERS o The recent acceptance of functional GI disorders as legitimate medical entities is based on the following three developments: o The concept of the Biopsychosocial model of illness and disease o The development of new investigative methods for studying disease o The development of the Rome Criteria Biopsychosocial Model In 1977, the publication of the concept of the Biopsychosocial model by George Engel, and its later demonstration specifically for gastrointestinal disorders, marked an important change in thinking. A biopsychosocial model of illness and disease provides the needed framework to understand, categorize, and treat common GI symptoms. These symptoms are the integrated product of altered motility, enhanced visceral sensitivity, and brain-gut dysregulation and often are influenced by psychosocial factors. Figure 1 illustrates the proposed relationship between psychosocial and physiological factors with functional GI symptoms and the clinical outcome. Early in life, genetics and environmental influences (family attitudes toward bowel training or illness in general, major loss or abuse history or exposure to infection) may affect one's psychosocial development (susceptibility to life stress, psychological state, coping skills, social support) or the development of gut dysfunction (abnormal motility or visceral hypersensitivity). Additionally, the presence and nature of a functional GI disorder is determined by the interaction of psychosocial factors and altered physiology via the brain-gut axis. In other words, one individual afflicted with a bowel disorder but with no psychosocial disturbances, good coping skills and adequate social support may have less severe symptoms and not seek medical care. Another having similar symptoms but with coexistent psychosocial disturbance, high life stress, or poor coping skills may frequent his physician's office and have generally poor outcome.
DEVELOPMENT OF NEW INVESTIGATIVE METHODS The second concurrent process has been the expansion and refinement of investigative methods that allow the study of functional GI disorders in terms of biological, cultural, and psychosocial (i.e. brain) influences. These developments include: 1. the improvement of motility assessment, 2. the standardization of the barostat to measure visceral sensitivity, 3. the enhancement of psychometric instruments to determine psychosocial influences, 4. the introduction of brain imaging (PET, fMRI) to determine CNS contribution to symptoms, and 5. the molecular investigation of brain-gut peptides, which provide insight into how these symptoms become manifest. In less than ten years, these methods have produced new knowledge of the underlying pathophysiological features that characterize the age-old symptoms we now define as functional GI disorders.
ROME CRITERIA The Rome Criteria is an international effort to characterize and classify the functional GI disorders using a symptom-based classification system. This approach that has its precedents with classification systems in psychiatry and rheumatology. The rationale for such a system is based on the premise that patients with functional GI complaints consistently report symptoms that breed true in their clinical features, yet cannot be classified by any existing structural, physiological or biochemical substrate. The Rome Criteria was built upon the Manning Criteria, which was developed from discriminate function analysis of GI patients. The decision to develop diagnostic criteria by international consensus was introduced as part of a larger effort to address issues within gastroenterology that are not easily resolved by usual The UNC Center for Functional GI http://www.med.unc.edu/ibs & Motility Disorders 4 scientific inquiry or literary review. By 1992, several committees had met to discuss the criteria, which ultimately resulted in the publishing of many articles in Gastroenterology International and a book detailing the criteria titled "The Functional Gastrointestinal Disorders (Rome I)". Elaboration of the Rome I criteria led to a second edition of the Rome criteria (titled Rome II) in 2000 as well as the publication of a supplement to the journal Gut in 1999. Recently the Rome Coordinating Committee has met to begin Rome III, expected to be published in 2006. To learn more about the Rome Committees and to see a summary of the Rome II book: go to www.romecriteria.com.
PRESENT PATHOPHYSIOLOGICAL OBSERVATIONS Despite differences among the functional gastrointestinal disorders, in location and symptom features, common characteristics are shared with regard to: o motor and sensory physiology, o central nervous system relationships, o approach to patient care. What follows are the general observations and guidelines.
MOTILITY In healthy subjects, stress can increase motility in the esophagus, stomach, small and large intestine and colon. Abnormal motility can generate a variety of GI symptoms including vomiting, diarrhea, constipation, acute abdominal pain, and fecal incontinence. Functional GI patients have even greater increased motility in response to stressors in comparison to normal subjects. While abnormal motility plays a vital role in understanding many of the functional GI disorders and their symptoms, it is not sufficient to explain reports of chronic or recurrent abdominal pain.
VISCERAL HYPERSENSITIVITY Visceral hypersensitivity helps to account for disorders associated with chronic or recurrent pain, which are not well correlated with changes in gastrointestinal motility, and in some cases, where motility disturbances do not exist. Patients suffering from visceral hypersensitivity have a lower pain threshold with balloon distension of the bowel or have increased sensitivity to even normal intestinal function. Additionally, there may be an increased or unusual area of somatic referral of visceral pain. Recently it has been concluded that visceral hypersensitivity may be induced in response to rectal or colonic distension in normal subjects, and to a greater degree, in persons with IBS. Therefore, it is possible that the pain of functional GI disorders may relate to sensitization resulting from chronic abnormal motor hyperactivity, GI infection, or trauma/injury to the viscera.
BRAIN-GUT AXIS The concept of brain-gut interactions brings together observations relating to motility and visceral hypersensitivity and their modulation by psychosocial factors. By integrating intestinal and CNS central nervous system activity, the brain-gut axis explains the symptoms relating to functional GI disorders. In other words, senses such as vision and smell, as well as enteroceptive information (i.e. emotion and thought) have the capability to affect gastrointestinal sensation, motility, secretion, and inflammation. Conversely, viscerotopic effects reciprocally affect central pain perception, mood, and behavior. For example, spontaneously induced contractions of the colon in rats leads to activation of the locus coeruleus in the pons, an area closely connected to pain and emotional centers in the brain. Jointly, the increased arousal or anxiety is associated with a decrease in the frequency of MMC activity of the small bowel possibly mediated by stress hormones in the brain. Based on these observations, it is no longer rational to try to discriminate whether physiological or psychological factors produce pain or other bowel symptoms. Instead, the Functional GI disorders are understood in terms of dysregulation of brain-gut function, and the task is to determine to what degree each is remediable. Therefore, a treatment approach consistent with the concept of brain-gut dysfunction may focus on the neuropeptides and receptors that are present in both enteric and central nervous systems.
THE ROLE FOR PSYCHOLOGICAL FACTORS Although psychological factors do not define these disorders and are not required for diagnosis, they are important modulators of the patient's experience and ultimately, the clinical outcome. Research on the psychosocial aspects of patients with functional GI disorders yields three general observations: o Psychological stress exacerbates gastrointestinal symptoms in patients with functional GI disorders and can even produce symptoms in healthy patients (but to a lesser degree). o Psychological disturbances modify the experience of illness and illness behaviors such as health care seeking. For example, a history of major psychological trauma (e.g. sexual or physical abuse) is more common among patients seen in referral centers than in primary care and is associated with a more severe disorder and a poorer clinical outcome. Additionally, psychological trauma may increase painreporting tendency. o Having a functional GI disorder has psychological consequences in terms of one's general well-being, daily functional status, concerns relating to control over symptoms, and future implications of the illness (e.g. functioning at work and home). APPROACH TO TREATMENT The approach to treatment for all functional GI disorders is founded on a therapeutic physicianpatient relationship. The basis for implementing a strong physician-patient relationship is supported by evidence that patients with functional GI disorders have anywhere from a 30 to 80% placebo response rate regardless of treatment.
http://www.med.unc.edu/medicine/fgidc/historyfunctionaldisorders.pdf
This is important to notice and understand also
" functional GI disorders have anywhere from a 30 to 80% placebo response rate regardless of treatment."
This is an excellent new video.
An interview with Douglas A. Drossman, MD, Co-Director, UNC Center for Functional GI & Motility Disorders, University of North Carolina, Chapel Hill, NC. Dr. Drossman is a clinician, a clinical researcher, and an educator. In this video, Dr. Drossman explains continuing advances that help us understand and visualize these conditions.
http://www.youtube.com/watch?v=bm3gboLimvw
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
Syl, its a huge problem.
IF all the money, millions and millions spent on all the alternative junk and supplements and wasted money was given instead to the expert researchers we might have a cure or be a lot closer to one. Yes some help, but most do not.
Some will never give up there beliefs, but others after seeing the information might make better choises and understand IBS and what your really up against when you have it, or how they even diagnose it in the first place and why and how much progress has been made in it all.
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
I think it is easy for people to get caught up in something which may have a cure. It is difficult for many to discover that there is no magic pill or treatment that will cure their IBS. Once one can let go of the idea of a quick fix and deal with controling IBS symptoms life is a little easier and less stressful.
I agree that it is very important to provide the real facts about IBS. It is difficult to deal with something that you know nothing about.
Again, thank you for providing the information.
-------------------- Janey
Print
Remind Me
Notify Moderator
|
|
Janey
"I think it is easy for people to get caught up in something which may have a cure."
Even worse is some of the things they think they have Don't exist to begin with or don't have a cure either. But yes people go serching and find what fits their beliefs. A good number of people have bacteria phobias, or develop food phobias as well or don't have a simple understanding of how digestion works first, so they think its food or bacteria, which play parts as triggers. But logically a layman would wonder about those two first, as opposed to the millions of potential issues or even knowing about chemical reasons for dysfunction like serotonin for example.
The fact also that is a problem is IBS is not diagnosed on biomarkers, and the criteria is only 98% percent accurate as opposed to 100%.
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
maybe it went in your junk mail,don' know,but please read.
Print
Remind Me
Notify Moderator
|
|
Dr. Andrew Weil, bestselling author of Natural Health, Natural Medecine has to say about candidia...
Candidiasis
Candida albicans is a kind of yeast that normally lives in the gastrointestinal tract and vagina without causing any problems. Under certain circumstances it can reproduce wildly, causing symptomatic infections of the mouth (thrush) and vagina as well as intestinal upsets. A common cause of yeast overgrowth is antibiotic therapy, which can kill off the "friendly" bacteria that compete with candida for food and keep it in check. If you have to take broad-spectrum antibiotics, it is a good idea to take supplemental acidophilus; to reduce the possibility of yeast infections. Candidiasis also tends to occur in people with suppressed immunity, such as patients with cancer and AIDS and those on long-term treatment with steroids and other immunosuppressive drugs.
In recent years Candida albicans has received much notoriety in certain circles as a major cause of illness. Some holistic practitioners diagnose everyone coming through the door as having systemic yeast infections, and health-food stores make a great deal of money on supplements that claim to fight yeast. I have read books and pamphlets that give the impression that everyone who has ever taken an antibiotic or steroid now is infected with candida, and that undiagnosed yeast infections are responsible for fatigue, depression, anxiety, mood swings, behavioral problems in children, allergic reactivity, skin eruptions, and most chronic digestive problems. I have had patients who believed yeast was growing in their blood, lungs, and other vital organs and begged me to prescribe strong drugs to kill it. They shunned beer, wine, bread, vinegar, and even mushrooms in the belief that any food associated with yeast or fungus would contribute to their disease.
Most of these ideas are unsound. Diagnoses of systemic candidiasis usually have no scientific basis, and most treatments people take for it are a waste of time and money. If you had yeast growing in your blood or vital organs, you would be in an intensive care unit, critically ill. Since candida is a normal inhabitant of the human body, no objective test can prove it to be the cause of general symptoms. Culturing it from the throat of a depressed patient does not mean that yeast infection is the cause of the depression.
Most of the treatments prescribed for this faddish disease are harmless except to the pocketbook. One that is not is the prescription drug ketoconazole (Nizoral). It can be toxic to the liver and should not be used except on the advice of an infectious disease specialist. The more commonly used drug nystatin (Mycostatin) is usually safe because it is not absorbed from the gastrointestinal tract.
Women who have recurrent vaginal yeast infections should see the entry on that subject. Others who worry about yeast in their system would do well to eat raw garlic every day; since it is a very effective antifungal agent. Take a course of nystatin if you wish (it must be prescribed by a doctor), and try to cut way down on sugar in the diet. Pau d'arco, an herbal remedy made from the bark of a South American jungle tree (species of Tabebuia, also known as palo de arco, lapacho, and taheebo) is often recommended for candidiasis, but I do not prescribe it. Much of the bark that comes into this country is contaminated with pesticides.
Candidiasis is a wonderful example of a fashionable disease. It appeals to our fears of being vulnerable to foreign invaders and satisfies a need to blame our vague and general symptoms on a specific causative agent. ten years from now it may be out of fashion. In the meantime, if you have used antibiotics and steroids for a long time and have clear symptoms and signs of yeast infection, by all means follow the recommendations above and see what happens. If after a reasonable trial, say four to six weeks, you have not experienced dramatic improvement, consider another diagnosis.
The recomended anti-candida diet is VERY similar to the specific carbohydrate diets that are recomended for both IBS and IBD by the alternative therapy community.
Real Candidiasis which is "Systemic Candidiasis are "systemic infections"
Systemic Candidiasis is rare and usally found in highly compromised immune systems such as AIDS and Cancer and can be life threatening.
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
Dr Drossman's comments on foods for IBS Health.
Shawn, To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, since the gut will over react to stressors of all types including food (high fat or large volumes of food in particular). Furthermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse.
However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature.
The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps. Doug
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
Its funny there is no test for a proliferation of an OVERGROWTH of candida in the gi tract that can't even be seen with a microscope?
Nobody finds that odd?
Again this is a problem, people call their IBS candida overgrowth syndrome.
You don't want people with IBS to be misdiagnosed do you?
Both the USA and Australasian Society of Clinical Immunology and Allergy and the leading fungus doctors in the world have never found this condition in 20 YEARS. They have looked hard for it, that you might have a altered bacterial gut flora is not Candida overgrowth syndrome. There is no amount the gi tract has millions, so its how the "Doc" personally interprets the tests. It would also be in your blood work.
Unorthodox Techniques for the Diagnosis and Treatment of Allergy, Asthma and Immune Disorders
Advice needs to be "evidence based" When considering testing and treatment, advice needs to be "evidence based". In other words, there needs to be evidence that a particular test or treatment is reliable, based on studies of other patients with the same condition. Reliable tests need to be able to distinguish between those with illness and those without. Therapeutic trials are designed to show that any improvement seen is due to the treatment, and not just due to chance or coincidence.
Inappropriate Testing
Tests for 'dysbiosis' Use: Diagnosis of food sensitivity / allergy and other non-specific symptoms
Method: Some laboratories offer pathology tests including stool bacterial/chemical analysis, urine metabolite profiles, intestinal permeability assays, trace metal analysis, Candida antibody / cellular proliferation assays and blood / urine fatty acid and amino acid profiles for assessment of "dysbiosis". The concept of 'dysbiosis' states that there is a balance of 'good' versus 'bad' bacteria in the bowel of each person, that imbalances result in disease, and that this can be assessed by various metabolic and bacteriological measurements. Such tests are often used by unorthodox practitioners as a rationale to guide (a) megadose nutritional supplementation; (b) 'probiotic' and/or antibiotic therapy; or (c) dietary modifications. These treatments are promoted as a means of restoring a 'healthy' balance of bowel flora.
Evidence: No evidence
Comment: There is no sound evidence to support the notion of 'dysbiosis' as a cause of allergic diseases or related clinical conditions. The clinical validity of the tests involved or treatments advocated has not been demonstrated.
Unorthodox Treatments
Chronic Candidiasis Use: Treatment of a variety of ailments including allergy, irritable bowel, food allergy and intolerance, autoimmunity, arthritis and psychological conditions.
Method: This approach is based on the concept that imbalance of gut flora results in overgrowth of Candida albicans within the gut. Release of fungal toxins results in a variety of symptoms including fatigue, arthritis, irritable bowel, food intolerance as well as psychological symptoms. These toxins weaken the immune system, predisposing to further symptoms from ingested foods and toxins. Treatment centres on dietary supplements, administration of antifungal drugs such as nystatin, and restriction of "Candida friendly" foods such as those containing sugars, yeast or molds.
Evidence: Level II
Comment: Candida is a normal gut organism, and immune responses (antibodies, cell mediated responses) to this organism are both expected and observed in healthy controls as well as those allegedly suffering from this condition. There is no evidence of overgrowth of Candida or altered immune responses to this organism in patients complaining of this syndrome. There is neither a scientific rationale nor published evidence that elimination of Candida with diets or anti-fungal therapy is useful for management.
http://www.allergy.org.au/content/view/322/271/
Why is there candida in the bowel in the first place in humans?
""Candida albicans, and other strains of Candida are yeast that normally inhabits our digestive system: the mouth, throat, intestines and genitourinary tract. Candida is a normal part of the bowel flora (the organisms that naturally live inside our intestines, and are not parasitic). It has many functions inside our digestive tract, one of them to recognize and destroy harmful bacteria. Without Candida albicans in our intestines we would be defenseless against many pathogen bacteria. Healthy person can have millions of Candida albicans."
"About chronic candidiasis An overgrowth in the gastrointestinal tract of the usually benign yeast (or fungus) Candida albicans has been suggested as the origin of a complex medical syndrome called chronic candidiasis, or yeast syndrome.1 2
Purported symptoms of chronic candidiasis are fatigue, allergies, immune system malfunction, depression, chemical sensitivities, and digestive disturbances.3 4 Conventional medical authorities do acknowledge the existence of a chronic Candida infection that affects the whole body and is sometimes called chronic disseminated candidiasis.5 However, this universally accepted disease is both uncommon, and decidedly more narrow in scope, than the so-called Yeast Syndrome"a condition believed by some to be quite common, particularly in people with a history of long-term antibiotic use. The term chronic candidiasis as used in this article refers to the as yet unproven Yeast Syndrome."
Real Candidiasis which is a "Systemic Candidiasis are "systemic infections"
http://www.emedicine.com/emerg/topic76.htm
IBS is NOT an infectious disease.
Infectious diseases have to be ruled OUT for a dignoses of IBS!!!!!!!!!
From the Dr Fungus website. An exppert on all fungi
Overview
It has been proposed that the asymptomatic colonization with Candida might be associated with a variety of symptoms and cause a "Candida Hypersensitivity Syndrome" [592] This concept was popularized by William Crook, MD in his book The Yeast Connection [485]. Previously, C.O. Truss, a physician from Birmingham, Alabama had proposed the existence of such a malady [2232, 2234]. Other names that have been given to this presumed condition include: Candida-Related Complex Polysystemic Candidiasis Chronic Candidiasis (This term should not be confused with Chronic Mucocutaneous Candidiasis) The syndrome is theoretically due to an overgrowth of Candida albicans in the gastrointestinal tract or in association with mucous membranes. The syndrome is said to occur in connection with some or all of the following risk factors: Use of broad spectrum antibiotics Use of oral contraceptives Ingestion of diets rich in yeast-containing foods or readily utilizable carbohydrates. Pregnancy Tremendous attention by public media and health magazines has created a large body of uncritical publications on this topic [395, 480, 484, 2024, 2231, 2232, 2233, 2234, 2425]. There are no rigorous data to support these concepts. The whole idea is based on historical controls and no working definition has been ever assessed [218]. Although brief communications by the proponents have appeared in major journals [477, 478, 479, 481, 482, 483, 486], the actual studies performed by these physicians do not appear to have been subjected to peer review. The American Academy of Allergy and Immunology published a position paper in 1986 stating that the concept was "speculative and unproven" [82]. Later, a carefully designed study on the topic by Dismukes et al. demonstrated that the condition does not appear to be reproducible or verifiable [592].
Clinical Manifestations
There is a broad range of symptoms that have been associated with this syndrome. They can be classified in the following groups, although it is not clear how many or which of them are required to make a diagnosis nor is there scientific data linking these multiple clinical manifestations with Candida albicans overgrowth [218, 260]: Vaginal. Recurrent episodes of Candida vaginitis associated with the classic symptoms of pruritus, burning and abnormal discharge. Gastrointestinal. Heartburn, bloating, diarrhea or constipation. Respiratory allergy. Rhinitis, sneezing and/or wheezing. Central nervous system. Anxiety, depression, memory deficits and/or loss of ability to concentrate. Menstrual abnormalities. Severe premenstrual tension and/or menstrual irregularities. Other Systemic Symptoms. Fatigue, headache and/or irritability. Specific Diagnostic Strategies
The proponents of the existence of this syndrome base their diagnosis on the clinical picture previously discussed [484, 485, 2425]. There is no laboratory test that allows a clear identification of patients affected with this presumed disorder. Actually, "no clear definition of the disease has ever been advanced" [218]. Considering these facts, it is impossible to set criteria to establish and identify patients affected with this supposed disease.
From a practical viewpoint, we recommend that all women with recurrent vaginitis be carefully evaluated for possible causative factors. Patients with more general complaints should receive a general physical examination. A CBC, general serum chemistries (including liver enzymes), and thyroid studies should be checked to eliminate the possibility of an anemia, subclinical hepatitis, and so forth. Finally, Renfro et al. reported that approximately two-thirds of patients with chronic fatigue had an underlying psychiatric diagnosis [1871].
Treatment
Proponents of this syndrome have recommended such therapies as: Long-term therapy with antifungal agents at increasing doses until resolution of symptoms. Oral and usually vaginal nystatin are recommended. Other azoles, such as ketoconazole have been also used [260]. Diet modification including restriction of sugar and other simple carbohydrates [481]. Candida allergy shots [218]. Avoidance of mouldy environments [218]. The value of these therapies is unknown. Dismukes et al. conducted a prospective double-blind study to assess the impact of antifungal therapy on this condition [592]. This study compared oral and vaginal nystatin with placebo in 42 premenopausal women with the presumed diagnosis of chronic candidiasis. The remarkable finding of this study was that nystatin did not "reduce systemic or psychological symptoms more than placebo did "[592]. One of the major proponents of the syndrome, Doctor William Crook criticized the study by saying that nystatin is no more than one of the components of the "comprehensive and multimodal therapy" required for this condition [481]. The same author agreed on the urgent need for more scientific studies on the topic. However, a recently done and detailed Medline search on the topic yielded only the data that we have discussed.
Chronic Candidiasis FAQ
We often receive inquiries about the diagnosis and treatment of chronic candidiasis. Here is our FAQ list: How can I decide if I have chronic candidiasis? Answer: We don't know. The syndrome has never been clearly defined and a workable diagnostic approach has never been put forth. While we have no doubt that there are individuals who suffer from some (or all) of the symptoms listed above, we are not aware of any testing procedure that can link these symptoms to a candidal infection.
My doctor cultured Candida from my stool. What does this mean? Answer: Candida spp. are frequent asymptomatic colonizers of the skin and bowel. Such cultures are of little significance unless you are critically ill in an ICU or are receiving cancer chemotherapy.
I took _______ (name of drug) or I altered my diet to include (or exclude) _______ (name of food) and now I feel better. Doesn't that mean I have (had) chronic candidiasis? Answer: The most common form of this question is "I took fluconazole and now I feel better--does this mean I had chronic candidiasis?" While we're glad you feel better, response to fluconazole is not a diagnostic tool. The various antifungal drugs have effects that go beyond the fungi (for example, fluconazole interacts with the enzyme systems of people, not just of fungi) and many diseases have a natural course of progression and regression. Similar concepts apply to changes in diet. If something makes you feel better, we're delighted for you. We just don't know what it means.
I still really think I might have chronic candidiasis. What should I do? Answer: At the risk of being repetitive, we'll say it again: We don't know of any useful approaches to diagnosing or treating chronic candidiasis. You should see a competent physician and be checked for the things that we do know how to diagnose (see discussion above). If these tests are negative, then we have nothing too specific to offer other than sympathy. We are not denying your symptoms. Rather, we honestly don't know what to do about them. If you can identify something that makes you feel better, then we'll cheer for you!
Is "yeast" the same as Candida? Answer: The term "yeast" is relatively imprecise. Medical mycologists use this term to describe fungi that reproduce predominantly by budding or fission. There are many genera of fungi that fit in this category. Beer and bread makers use the term to refer to Saccharomyces cerevisiae. Doctors sometimes use the term "yeast infection" to refer to Candida spp. and its diseases. For example, yeast vaginitis is the colloquial phrase for candidal vaginitis.
http://www.doctorfungus.org/
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
To those who then say they are NOT stuying candida, or know nothing about fungus they have already studied it a lot.
IBS is not caused by an infectious disease and will not progress into anything worse. IBS is a functional disorder, how the colon functions itself. The large colon, sigmoid colon, although functional disorders can overlap, which is also relatively common. IBS and GERD for example.
Infectious Diseases Treatment Updates Managing Fungal Infections in the New Millennium CME
Author: John H. Rex, MD Reviewer: Ronald Liteplo, MD Clinical Editor: Joan Solomon Zolot, RPA-C
Review Date: April 6, 2000 Release Date: April 7, 2000 Valid for CME until April 7, 2001
Overview of Fungal Infections: Where Have We Come From and Where Are We Going?
Invasive fungal infections are more prevalent than ever, due to an increasingly large populations of patients at high risk secondary to immunosuppression. Underlying disease or chronic conditions such as cancer, bone marrow or solid-organ transplantation, HIV infection, and chronic corticosteroid administration make patients vulnerable to opportunistic fungal pathogens. In the hospital, complicated surgical procedures, widespread use of implanted devices, and administration of broad-spectrum antibiotics have dramatically increased the incidence of nosocomial fungal infections. Clinicians of all specialties will have to contend with the growing threat of fungal pathogens, if they have not already.
At a recent symposium held on January 29, 2000, at the MD Anderson Cancer Center, noted experts in fungal infections gathered to present the latest information about diagnosis and treatment of fungal infections in the immunocompromised patient.
In an overview of fungal infections, Kenneth V.I. Rolston, MD, of the MD Anderson Cancer Center, Houston, Texas, stated that Candidaspecies are now the fourth most common cause of nosocomial bloodstream infection, and they are associated with an extremely high mortality rate of 40%.[1] From 1980 to 1990, the incidence of fungal infections in US hospitals nearly doubled, from 2.0 to 3.8 per 1000 patients discharged.[2]The most marked increase in fungal infection rates occurred not in transplant units or oncology centers, but on surgical services, with medical services also showing increases. These changing patterns demonstrate that fungal infections are no longer limited to the most severely immunosuppressed patients.
Nor are fungal infections limited to large teaching hospitals; small teaching hospitals and nonteaching hospitals of all sizes have also experienced increases in fungal infection rates. In addition, fungal infections are not occurring only in intensive care units (ICUs) housing the sickest patients: just over half are in ICUs, but 43% are among patients in medical or surgical units.[2] "Living Petri Dishes" -- Who Is at Risk?
Most fungi are harmless to healthy individuals. But to patients with underlying medical problems or immunosuppression, fungi can become devastating, opportunistic pathogens. Patients with multiple risk factors have been likened by Michael G. Rinaldi, MD, to petri dishes, into which any one of a number of microbes can fall and launch devastating infection, with minimal host resistance.
In his talk on emerging fungal pathogens, Dr. Rinaldi, of the University of Texas Medical Branch, Galveston, discussed a variety of factors that predispose to fungal infection. In fact, many hospitalized patients have several risk factors, with each one multiplying the risk of fungal infection. Prior or concurrent use of broad-spectrum antibiotics is an important risk factor, because the reduction of protective bacteria may permit the growth of colonizing fungi. The use of devices that breach protective barriers, especially central venous catheters used for hyperalimentation, enables fungal pathogens to access the vulnerable host. An ICU admission, especially when prolonged, increases the likelihood of fungal infection. Specific conditions or procedures that predispose to fungal infection include: major surgery, transplantation (both solid organ and bone marrow), the administration of antirejection therapy, steroid administration, the presence of graft-versus-host disease (GVHD), intubation, malnutrition, hemodialysis, azotemia, HIV infection or AIDS, and a variety of cancers. Spectrum of Historically Common Fungal Pathogens
Since the 1950s and 1960s and until recently, the key opportunistic fungal pathogens with which clinicians had to contend were Candida albicans, Aspergillus fumigatus, and the Zygomycetes, which cause mucormycosis (Table 1). Today, non-albicans Candida have become more frequent, as have other Aspergillus species.
Table 1. Well-Known Medically Significant Fungi
Cutaneous/Subcutaneous Infection Systemic Disease of Healthy Individuals Opportunistic Pathogens Dermatophytes Coccidioides Candida Agents of Mycetoma Histoplasma Cryptococcus Sporothrix Blastomyces Aspergillus
Paracoccidioides Zygomycetes
The Changing Epidemiology of Candidal Infections
During the past 2 decades, a substantial shift in the epidemiology of candidemia due to different Candida species has occurred. In the 1960s and 1970s, Candida albicans accounted for 85% to 90% of cases of candidemia. However, an MD Anderson Cancer Center study of the epidemiology of candidal infections from 1988 to 1992 found the incidence of non-albicans Candida had surpassed that of C albicans. Only 42% of candidemia cases were caused by C albicans, while non-albicans Candida accounted for the remainder, including C tropicalis (18%), C parapsilosis (17%), C glabrata (11%), C krusei (4%), and others.[3] The authors of the study surmised that fluconazole prophylaxis was largely responsible for the shift, in that it reduced the incidence of C albicans infections. Similar results have been reported by other groups in noncancer settings as well.[4]
Similar trends apply in the neonatal setting. There, recent data suggest that C albicans causes only about 50% of infections, with C parapsilosis now being seen as the dominant non-albicans species in this patient group.[5]
The emergence of Candida infections due to non-albicans species is particularly important to practicing clinicians, because candidal isolates resistant to azole therapy have appeared, making species identification and sensitivity testing crucial (Table 2). Microbiology labs should no longer be reporting results such as "Candida species," "Candida - nonalbicans," or "yeast." The species of the organism must be provided, because the species differ in their susceptibility to antifungal agents and present different implications for outcome. C tropicalis has been shown to cause invasive disease and disseminated infection.[3] C parapsilosis, however, is typically less virulent.[6] C krusei is problematic because it almost universally exhibits resistance to azole therapy (eg, fluconazole) and may have reduced susceptibility to other therapies.[7]
Table 2. Candida species: Human Pathogens
C albicans C glabrata C guilliermondii C krusei C lusitaniae C parapsilosis C pseudotropicalis C rugosa C stellatoidea C tropicalis
Candida: The Diagnostic Paradox
Localized manifestations of candidal infection, such as mucocutaneous candidiasis, esophagitis, and urinary tract infection (candiduria), are typically not life-threatening. And fortunately, such localized infections do not usually progress to hematogenous dissemination.[8] However, presence of Candida at any site is a risk factor for potentially lethal disseminated or systemic candidiasis. Presence of the organism is not enough -- the host must also be impaired in some fashion. Typical addditional risk factors are stay in an ICU, use of central venous catheters, use of broad-spectrum antibiotics, diabetes, and dialysis.
Diagnosing disseminated candidiasis is unfortunately not straightforward. The single best tool is the blood culture, but this tool has limited value. Even in patients with severe neutropenia or immunosuppression, in whom disseminated candidiasis is strongly suspected, blood cultures are positive only 50% of the time.[9] Non-culture-based strategies for diagnosing invasive candidiasis have been intensively studied, but a highly reliable technology has yet to emerge.
There are some additional clues that, while not common, may be useful in selected patients. Nodular cutaneous lesions may occur in very immunocompromised patients with candidemia, and clearly indicate that bloodstream invasion and dissemination have already occurred.. Biopsy of the lesions would confirm the diagnosis. Radiographic imaging, including CT scanning or MRI, is also useful in diagnosing disseminated lesions on the lung, liver, spleen, or kidney, although the radiographic findings may not be pathognomonic. cont.
Aspergillosis
Invasive primary Aspergillus is an important cause of mortality among neutropenic patients, particularly among patients with leukemia or solid-organ transplantation. Aspergillus species cause 70% of noncandidal fungal infections following bone marrow transplantation.[10] The most common pathogenic species is A fumigatus, although others can cause devastating opportunistic infection (Table 3).
Table 3. Aspergillus: Key Human Pathogens
A fumigatus A flavus A nidulans A niger A terreus
Aspergillosis manifests quite differently from Candida. Localized disease appears as cutaneous lesions, sinusitis, tracheobronchitis, and aspergilloma (a bronchopulmonary granuloma). Invasive pulmonary aspergillosis and invasive sino-orbital aspergillosis are more common than hematogenous aspergillosis. Sino-orbital disease can progress to fatal cerebral abscess.
Aspergillus is ubiquitous in the environment, and the portal of entry is most commonly the lungs. The organism has a predilection for vascular tissue, and often invades blood vessels to the extent that the supplied organ is infarcted. Radiologic findings in neutropenic patients with pulmonary aspergillosis include pleural wedge-shaped lesions, nodular densities, cavitary lesions, necrosis, diffuse bilateral infiltrates, and, less commonly, bloody pleural effusion. A "halo" lesion is sometimes seen on lung CT and is strongly suggestive of tissue necrosis due to an angiocentric mould. Blood cultures from patients with disseminated Aspergillus infection are rarely positive. Biopsy, culture, and histologic examination of tissue reveal the organism.
Primary cutaneous Aspergillus infection typically occurs at the site of insertion of an intravenous catheter, or it is associated with adhesive cutaneous dressings, where black eschar can form. Biopsy of the eschar reveals the organism. The lesion can invade local blood vessels and lead to vascular necrosis and infarction, a complication that does not occur with Candida. It must be treated with surgical debridement and antifungal therapy. Zygomycetes
A 60-year-old patient with poorly controlled diabetes and end-stage cirrhosis who underwent liver transplantation was recently reported in The New England Journal of Medicine.[11] Following the transplantation, he developed several complications, including poor graft function, intrahepatic cholestasis, hyperglycemia, progressive renal failure, vancomycin-resistant Enterococcus faecium bacteremia, and Candida parapsilosis fungemia. During his hospitalization, a lesion developed on his forehead. It rapidly enlarged and became necrotic. The lesion was biopsied and histopathology revealed a nonseptate hyphal fungus. Culture grew Rhizopus oryzae. The patient died 1 month after transplantation from complications of septic shock.
Classically referred to as mucormycosis, his infection is now called zygomycosis. The most common causative agent is Rhizopus, a common bread mould that lives on any organic material. Other pathogens include Mucor, Rhizomucor, and Absidia. Zygomycetes include 20 different fungi, all appearing the same histologically. All are treated similarly, with amphotericin B or a lipid formulation of amphotericin B.
The severely immunocompromised patient may become infected with Zygomycetes via respiratory inhalation. Clinical manifestations may be rhinocerebral (involving skin of the face), pulmonary, cutaneous, gastrointestinal, or neurologic. The disease manifests with vascular invasion and tissue necrosis, forming black eschar (Figure 1).
Figure 1. Infections are frequently fatal. Emerging Fungal Pathogens
A wide variety of fungi now isolated from neutropenic patients were not previously recognized as human pathogens. Many of these are soil or plant fungi -- organisms that clinicians have not been trained to recognize -- and present considerable challenges in diagnosis and treatment, especially if the appropriate antifungal agent is not known.
Fusarium
More than a dozen fungi have been identified that appear histologically identical to Aspergillus. Fusarium is one of these genera. It is the most prevalent plant fungus worldwide, and it is now recognized as a human pathogen as well. Fusarium is infecting neutropenic patients with increasing frequency. It manifests with fever and large ulcerative cutaneous lesions that progress to necrosis -- the appearance also complicates distinguishing this fungus from Aspergillus. However, and quite distinct from Aspergillus, patients with disseminated fusariosis will often have a positive blood culture for this fungus.
Fusarium infections can occur in immunocompetent or immunosuppressed individuals. Immunocompetent patients develop infection following trauma, burns, or major surgery. Infections are more devastating, however, in immune-suppressed patients, such as those with GVHD or neutropenia.
Hematogenous dissemination of Fusarium involves multiple sites and organs, including sinuses, lungs, skin, brain, bone, and joints. Fungemia from disseminated Fusarium infection is revealed by blood culture 50% of the time[12] or more, since Fusarium is quite angioinvasive and is actually present in the bloodstream in sufficient amounts to be detected by current blood culturing methods. Histopathology of Fusarium reveals filamentous fungus with branching septate hyphae -- indistinguishable from Aspergillus. Fusarium infection is life-threatening and associated with a poor prognosis.[13]
Paecilomyces
Paecilomyces lilacinus gained notoriety more than a decade ago as one of the moulds capable of causing fungal keratitis in wearers of soft contact lenses.[14] Deep invasive infection due to this organism now occurs more frequently in immunocompromised patients. The disease manifests with skin lesions. This mould appears histologically, as do both Aspergillus and Fusarium.
Phaeohyphomycosis
Phaeohyphomycosis is an infection that manifests as a chronic, tissue-destroying, sinus-forming process. As the infection usually follows traumatic inoculation, the most common site for disease is an extremity, most often the feet. Phaeohyphomycosis can be caused by a variety of fungal genera, including Bipolaris, Exserohilum (which grows on grass), and Exophiala, all of which are darkly pigmented fungi. All the fungi that can cause this appear identical in tissue. Therefore, they must be grown in culture and examined histologically. The infection is usually treatable with surgical resection of the lesion and antifungal therapy.
Trichosporon
Trichosporon beigelii is fungus that lives on hair shafts of the scalp, body, and pubic hair as part of the normal flora, and can cause a superficial fungal infection called white piedra. The prevalence of hematogenous trichosporonosis is increasing among neutropenic patients.[12] Disseminated disease manifests as multiple, erythematous papular or purpural skin lesions. Systemic Trichosporon infection is often fatal.[12]
Other Fungi
Many other fungi are gaining attention as human pathogens. Malassezia is part of the normal human flora and can cause infection in immunocompromised hosts. Penicillium marneffei and Pythiosis insidiosi are environmental fungi that can cause serious, life-threatening infections in immunosuppressed patients. P marneffei has gained particular attention during the AIDS pandemic, as it may produce disease that is clinically indistinguishable from disseminated histoplasmosis. Pseudallescheria boydii is a mould that lives in the soil and in vegetation and is an agent of mycetoma, a subcutaneous infection. In immunosuppressed patients, it causes pseudallescheriasis, a soft-tissue and pulmonary disease that resembles aspergillosis (clinically and histologically) and can spread hematogenously. The Importance of Thinking Fungus
In the 1970s and 1980s, gram-negative sepsis was the chief nosocomial infection of concern. The most clinically significant pathogens were Klebsiella, Escherichia coli, Enterobacter, and Pseudomonas. During the 1980s and 1990s -- and today -- hospital-acquired gram-positive sepsis is the overriding concern, most commonly due to Staphylococcus or Enterococcus. Now Candida has become the fourth leading cause of hospital-acquired sepsis, surpassing even E coli.
Mycology has developed into a field that demands the attention of all clinicians treating patients in the hospital. During the 1980s, the incidence of bloodstream infection due to Candida species increased almost 500%.[15] The proportion of nosocomial bloodstream infections due to Candida increased from 2% in 1980 to 5% in the late 1980s.[16] The trend continued in the 1990s, with 8% of hospital-acquired bloodstream infections attributed to Candida.[15] A study published in 1999 found 12% of nosocomial bloodstream infections in the ICU were due to fungi.[17]
Now that fungi represent a substantial proportion of the pathogens in "living human petri dishes," it is crucial to consider the possibility of a fungal infection in hospitalized patients -- and consider it early. The High Cost of Thinking Fungus Too Late
The mortality rate in neutropenic patients with fungal infections is high. Among neutropenic patients with Aspergillus infection, it can exceed 90%.[18,19] Neutropenic patients with Fusarium or Trichosporon infection have a mortality rate approaching 100%.[13,20] Even candidemia is associated with a mortality rate of 50%.[21-23]
Mortality is higher when the diagnosis of fungal infection is not made early. In one study, patients with lymphoma were housed in a protective environment -- single-patient rooms under positive pressure with high-efficiency particulate air filtration -- while undergoing bone marrow or peripheral stem cell transplantation.[24] Despite these protective measures, 5.2% of patients developed nosocomial invasive aspergillosis. Although mortality rates among the patients with localized or pulmonary disease were substantial (42%), they were better than those of the patients who began treatment after the disease was already disseminated. In fact, none of the patients with documented disseminated disease survived.
A multicenter study of Aspergillus infection in immunosuppressed patients, most of whom had bone marrow or solid-organ transplantation, leukemia, lymphoma, or AIDS, confirmed the importance of early diagnosis.[25] Patients with only pulmonary disease had greater rates of complete response and fewer treatment failures than patients with disseminated or central nervous system disease (Table 4).
Table 4. Response to Therapy by Site of Infection
Pulmonary Disseminated (Without CNS) CNS Complete Response 29 (19%) 8 (17%) - Treatment Failure 61 (39%) 29 (63%) 18 (78%) Other Failure 32 (20%) 5 (11%) 3 (12%) Partial Response 25 (16%) 3 (6%) - Stable 8 (5%) 1 (2%) 1 (4%) N/A 1 (1%) - 1 (4%)
Patterson, ICAAC, 1996 The High Cost of Thinking Fungus Too Late
The mortality rate in neutropenic patients with fungal infections is high. Among neutropenic patients with Aspergillus infection, it can exceed 90%.[18,19] Neutropenic patients with Fusarium or Trichosporon infection have a mortality rate approaching 100%.[13,20] Even candidemia is associated with a mortality rate of 50%.[21-23]
Mortality is higher when the diagnosis of fungal infection is not made early. In one study, patients with lymphoma were housed in a protective environment -- single-patient rooms under positive pressure with high-efficiency particulate air filtration -- while undergoing bone marrow or peripheral stem cell transplantation.[24] Despite these protective measures, 5.2% of patients developed nosocomial invasive aspergillosis. Although mortality rates among the patients with localized or pulmonary disease were substantial (42%), they were better than those of the patients who began treatment after the disease was already disseminated. In fact, none of the patients with documented disseminated disease survived.
A multicenter study of Aspergillus infection in immunosuppressed patients, most of whom had bone marrow or solid-organ transplantation, leukemia, lymphoma, or AIDS, confirmed the importance of early diagnosis.[25] Patients with only pulmonary disease had greater rates of complete response and fewer treatment failures than patients with disseminated or central nervous system disease (Table 4).
Table 4. Response to Therapy by Site of Infection
Pulmonary Disseminated (Without CNS) CNS Complete Response 29 (19%) 8 (17%) - Treatment Failure 61 (39%) 29 (63%) 18 (78%) Other Failure 32 (20%) 5 (11%) 3 (12%) Partial Response 25 (16%) 3 (6%) - Stable 8 (5%) 1 (2%) 1 (4%) N/A 1 (1%) - 1 (4%)
Patterson, ICAAC, 1996 The Challenge of Diagnosis
There are no rapid, accurate diagnostic tests that can confirm with certainty the presence of invasive fungal disease. Unless the clinician considers fungal disease early, disease can progress rapidly while the patient is treated aggressively with broad-spectrum antibiotics.
Not only are fungal infections difficult to distinguish from bacterial or other infections, but the clinical manifestations of many fungal infections are shared among a variety of fungal pathogens as well.
Standard microbiology is often adequate to provide a diagnosis. Short of tissue biopsies, fungal cultures are not always positive in the presence of invasive disease. Moreover, positive cultures do not definitively signify invasive disease; they may represent colonization. Nonetheless, in patients who are immunosuppressed, a positive culture and invasive disease are highly correlated.[26] A high-risk patient with a positive culture should be considered to have invasive disease until proven otherwise.
Radiographic imaging can be useful in certain situations. X-ray and CT can assist in identifying early Aspergillus infection.[27] Pulmonary aspergillosis may manifest as focal areas of patchy consolidation, pulmonary nodules, cavitary lesions, a crescent air sign, or a "halo" on computed tomography.[28] A halo sign, an area of low attenuation (increased density), surrounding a nodular pulmonary lesion in a neutropenic or bone marrow transplant patient is highly suggestive of aspergillosis[27]; in solid-organ transplant patients, however, the significance of the halo sign has not been established.
In one study, early CT scans performed in febrile neutropenic patients with x-ray infiltrates and probable invasive pulmonary aspergillosis (IPA) identified halo signs in 92% of patients, reducing the time to diagnosis of IPA from 7 to 1.0 days.[29] Following antifungal treatment with or without surgical resection of pulmonary lesions, 72% of patients were cured or improved. The improved response rates were attributed to earlier diagnosis and initiation of therapy.
Serologic methods based both on detection of fungal antigens and fungal DNA are being pursued and may assist in making earlier and more specific diagnoses. However, the clinical utility of serologic testing for fungal infection has not been established. Sensitivity and specificity are often inadequate, with false positives and cross reactivity occurring. For example, serum Aspergillus antigen testing by ELISA may be associated with a false-positive rate of almost 10%.[30] Sensitivity of PCR may depend on the extent of invasion of disease; a higher frequency of detection by PCR is seen for invasive aspergillosis than for pulmonary aspergilloma.[31]
Biopsy of the lesion, culture, and histologic examination remain important components in the work-up and diagnosis of fungal infection. An Overview of the Newer Antifungal Agents for Deep Mycoses
Several new antifungal agents have been developed because of limitations among the already available agents, according to Thomas F. Patterson, MD, of The University of Texas Health Science Center at San Antonio. Limitations of current therapeutic options include: inadequate spectrum of activity, lack of efficacy due to growing resistance, poor safety profile, multiple drug interactions, inadequate pharmacokinetic profile, and excessive cost.
The ideal antifungal would have a broad spectrum of activity, be fungicidal rather than fungistatic, be available in oral and injectable formulations, cause minimal drug interactions, be safe at efficacious doses, be cost-effective, and be stable to resistance. Development of antifungal agents is a challenge because there are very few potential drug targets unique to fungi -- and not present in humans. Also, because diagnosis and identification of fungal species is elusive, it may be difficult to find an adequate-sized patient population to test experimental agents in large-scale trials.
Treatment of deep fungal infections often begins empirically, since obtaining the diagnosis can be difficult and often is delayed. Amphotericin B remains a drug of first choice in many settings, although it may not always be effective for Aspergillus infections in highly immunosuppressed patients.[25] The triazoles are first- and second-line agents for a variety of infections, but emerging resistance may limit their role (Table 5). Newer agents include lipid amphotericin B, which is already available; new azoles, some of which are already on the market; and candins, which have not yet been released.
Table 5. Current Treatment Recommendations for Selected Deep Fungal Infections
Fungal Pathogen First-line Agent(s) Second-line Agent(s) Candida Amphotericin B, fluconazole Itraconazole Aspergillus Amphotericin B, Itraconazole
Zygomycetes Amphotericin B Itraconazole Fusarium Amphotericin B Itraconazole Phaeohyphomycosis Itraconazole
Trichosporon Fluconazole
Lipid Formulations of Polyenes
The parent drug of lipid amphotericin formulations is amphotericin B. Amphotericin B is an intravenous drug with a very narrow therapeutic index. Three lipid amphotericin formulations -are now available and have a greatly improved toxicity profile (Table 6).
Table 6. Polyenes
Generic Name Trade Names Amphotericin B deoxycholate Fungizone Liposomal amphotericin B Ambisome Amphotericin B colloidal dispersion (ABCD) Amphotec or Amphocil Amphotericin B lipid complex (ABLC) Abelcet
Legend: The names of the forms of amphotericin B are shown. When referring to the group of lipid formulations, the most appropriate general term is "lipid-associated formulation of amphotericin B," or LFAB. Use of the phrase "liposomal amphotericin B" should be avoided as it produces confusion: does the speaker mean Ambisome or just one of the LFABs?
Only one of the products is a true liposome. This compound has the generic name of liposomal amphotericin B and a trade name of Ambisome. The other two products, amphotericin B lipid complex (ABLC; trade name Abelcet) and amphotericin B colloidal dispersion (ABCD; trade names Amphotec, Amphocil), are not true liposomes. ABCD is associated with more administration toxicity and offers no advantages compared with the other two products.[32] All 3, however, are generally less nephrotoxic than amphotericin B. All lipid amphotericin B agents still cause increased creatinine levels and electrolyte disturbances. Because amphotericin B causes membrane permeability to increase, amphotericin B agents can destabilize the cardiac conduction system in the presence of hypokalemia or hypomagnesemia, causing ventricular fibrillation and death during infusion. Therefore, it is critical to monitor electrolytes in patients receiving any form of the drug.
A recent study published in The New England Journal of Medicine demonstrated comparable efficacy and survival rates among neutropenic patients randomized to receive liposomal amphotericin B or conventional amphotericin B as empirical antifungal therapy.[33] Patients who received the liposomal drug, however, had significantly fewer infusion-related reactions, such as fever (17% vs 44%) and chills or rigors (18% vs 54%). Nephrotoxicity was also significantly lower (19% vs 34%). In another study, standard amphotericin B was shown to be less effective than lipid amphotericin B against invasive Aspergillus infection in a highly immunosuppressed patient population.[34] Patients who received the lipid formulation had higher response rates (50% vs 20%, proven Aspergillus infection; 52% vs 29%, suspected or proven Aspergillus infection) and lower mortality rates (22% vs 38%). Amphotericin B lipid complex was studied in an open-label, single-patient, emergency-use study of patients refractory to or intolerant of standard amphotericin B (Figure 2). A complete or partial response was demonstrated in 42% of patients with aspergillosis, 67% of patients with disseminated candidiasis, 71% of patients with zygomycosis, and 82% of patients with fusariosis. While these data are not comparative, they suggest that lipid amphotericin B may be effective against several mycoses.
Figure 2. ABLC Historical Control Study
ABLC (n=151) Control (n=122) Complete Response Partial Response Stable Disease Failure N/A 23 (15%) 38 (25) 16 (11) 71 (47) 3 (2) 13 (11%) 15 (12) 5 (4) 83 (68) 6 (5)
Compared with amphotericin B, a much higher dose of the LFABs must be administered for therapeutic efficacy.[36,37] Amphotericin B is usually dosed up to 1 mg/kg/day. Because they are less potent, the doses of LFABs may range from 3 to 6 mg/kg/day. Antifungal activity improves with increasing doses of the agent.[38] But, the LFABs offer a much wider therapeutic index than amphotericin B and toxicity is less likely even with the highest doses administered for longer periods of time. These agents are indicated to treat invasive fungal infections in patients who are refractory to, or intolerant of, amphotericin B therapy. Liposomal amphotericin B (Ambisome) also carries a specific indication for use as empiric therapy for presumed fungal infections in neutropenic patients.
The LFABs are expensive. While a standard day's dose of amphotericin B costs $20, a lipid-associated form of amphotericin B may cost up to $1000 per day. The cost differential requires the clinician to weigh the benefits of the safety profile of lipid amphotericin B versus the increased expense. How likely is the patient to develop nephrotoxicity if standard amphotericin B is used? Can the risk be quantified?
When making the decision of whether to administer amphotericin B versus an LFAB, one should also consider the labeling of the product: In general, the LFABs are off-labeled for use in patients refractory to or intolerant of amphotericin B. But, nephrotoxicity can be predicted in some patients. For example, I believe that a diabetic patient with proteinuria and a preexisting creatinine of 2.5 mg/dL should certainly receive an LFAB. This concept is supported by a study of 239 immunosuppressed patients receiving amphotericin B for aspergillosis in which that a creatinine level greater than 2.5 mg/dL predicted nephrotoxicity and the need for dialysis, which in turn directly increased mortality.[39] A "New" Azole. Itraconazole in Cyclodextrin
Itraconazole is a triazole drug (Table 7) that has long been available as a capsule and, more recently, as a solution. It has a wide spectrum of activity with extensive efficacy and safety data gathered. It is no more effective than amphotericin B for Candida, but it is efficacious for other types of systemic fungal infections, such as histoplasmosis, blastomycosis, and aspergillosis.[40,41]
Table 7. The Azoles
Imidazoles Triazoles 2nd-Generation Triazoles Ketoconazole Fluconazole Voriconazole (fluconazole congener)
Itraconazole Ravuconazole (fluconazole congener)
Posaconazole (itraconazole congener)
Oral absorption of the capsule is variable and improved by intake with food, but now a liquid formulation is available that confers 30% greater bioavailability. This formulation, a solution in cyclodextrin, should now be administered preferentially to the capsule for all immunocompromised patients with systemic fungal disease. Cyclodextrin is a ring of glucose molecules that stabilizes the azole drug and increases its absorption, resulting in improved blood and tissue levels of itraconazole.
The clinical utility of itraconazole has previously been limited by lack of a parenteral formulation. An intravenous formulation of the drug, also solubilized in cyclodextrin, has recently become available that offers improved absorption and serum drug levels, compared with either oral preparation. The drug is indicated as a second-line agent against aspergillosis and as a first-line agent for histoplasmosis and blastomycosis.
Intravenous administration for 2 weeks followed by oral administration of itraconazole for 12 weeks was shown to yield complete or partial responses in about half of immunocompromised patients with invasive pulmonary aspergillosis.[42] Itraconazole levels exceeded 250 mg/mL in 91% of the patients. Because itraconazole is metabolized by the liver and cyclodextrin is excreted renally, the drug should be used with caution in patients with reduced renal function; data on the drug in patients with renal dysfunction will not be available immediately. Therefore, this drug is contraindicated in the presence of nephrotoxicity (creatinine clearance less than 30 mL/min).
Adverse effects of itraconazole include dose-related nausea and abdominal pain, hepatic dysfunction, and, at very high doses, hypokalemia and edema. Because it is metabolized by the cytochrome P-450 enzyme system, itraconazole is associated with many drug interactions. Cont.
Truly New Azoles
New azoles -- a second generation of triazoles -- are currently in development. They will offer a broader spectrum of activity against many species of the key genera, compared with currently available triazoles. In particular, they are active against C krusei, one of the candidal species more frequently resistant to fluconazole.
Voriconazole is a second-generation congener of fluconazole active against a wide variety of candidal species.[43] Voriconazole may have more potent activity than fluconazole against some Candida species, including C krusei.[44] Voriconazole has also demonstrated in vitro activity against Aspergillus species resistant to amphotericin B[45] as well as against a variety of filamentous fungi.[46] One study in humans showed reasonable complete or partial response rates with intravenous followed by oral voriconazole administration for invasive aspergillosis (Figure 3). It also has a satisfactory safety profile. It will be available for twice-daily dosing by oral or intravenous administration.
Figure 3.
Ravuconazole (BMS-207,147) is also a second-generation fluconazole-based drug. It has a broad-spectrum of activity, and in particular is active against a wide spectrum of candidal species.[43] This drug has adequate oral bioavailability. Clinical trials of this agent are currently under way.
Posaconazole (SCH-56962) is a congener of itraconazole currently under investigation. It has an excellent safety profile and was efficacious in vitro against many candidal species[43] and was also very active against Fusarium in a murine model.[48] This agent is in advanced clinical trials.
New Classes: The March of the Peptides
For the first time in many years, a new class of drugs, the candins, is being developed to treat fungal infections. The candins inhibit fungal cell wall synthesis and therefore have been referred to as "penicillin for fungi." Their target in cell wall synthesis, (1,3)-beta-D-glucan synthase,[49] is not present in mammalian cells. By contrast, polyenes and azoles act on a cell membrane common to fungal and mammalian cells, accounting for the toxicity of these agents.
Candin agents in development include the pneumocandin caspofungin (formerly MK-991) and the echinocandins LY-303,366 and FK-463. All the candin agents are fungicidal against all species of Candida,[43] and they are also active against Aspergillus.[49]
The pneumocandin caspofungin is the agent furthest along in development. It is active against Candida species and Aspergillus species,[50] and was effective in vitro against azole-resistant candidal strains.[51] Caspofungin was also effective against Histoplasma and Pneumocystis in mice.[52] The agent was not active in vitro against Fusarium, Rhizopus, or Paecilomyces.[50] Because it has poor oral bioavailability, it will be available as a parenteral medication only. The agent is currently in late phase II and III clinical studies.
LY-303,366 and FK-463 are 2 echinocandins under investigation. Their spectra of activity are similar to that of caspofungin. The Future: What Is in Store for Mycology?
Infectious disease is entering a new era, the golden age of mycology. A new generation of antifungal treatments has begun to unfold. Lipid amphotericin compounds, intravenous azoles, and candins show promise. Future work will examine the role of these new agents both alone and potentially in combination.
Other possible future treatment options, now shiny specks in the distance, include the other types of peptide-based antifungal agents, the sordarins (which inhibit translation elongation factor 2), other amphotericin congeners, and combination therapies with cytokines. These are all in the early stages of exploration.
Significant investment is required for the next generation of antifungal agents. While discovery and development is a challenge, an unprecedented number of antifungal agents will ultimately join the clinician's armamentarium against emerging fungal pathogens.
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
an email you sent me?
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
Gastroenterology Expert Column Diagnosing Irritable Bowel Syndrome: What's Too Much, What's Enough? Posted 03/12/2004
Susan Lucak, MD
Introduction Irritable bowel syndrome (IBS) is the most common gastrointestinal disorder diagnosed in clinical practice in the United States. Because there is no biological marker to confirm the diagnosis of IBS, it is a diagnosis that has challenged clinicians for decades. In the past, IBS was a "waste-basket" diagnosis given to patients with unexplained gastrointestinal symptoms. It was considered to be "the diagnosis of exclusion" when extensive work-up for organic disease yielded no diagnosis.
In recent decades, it was recognized that patients with IBS experienced a constellation of specific gastrointestinal symptoms. Manning criteria were described in 1978,[1] followed by Rome I in 1989[2] and Rome II criteria in 1999.[3] Rome I and Rome II criteria were initially developed by multinational working groups to provide a framework for the selection of patients in diagnostic and therapeutic trials. These criteria are being continuously modified as we gain new knowledge about functional bowel disorders. Recently published diagnostic guidelines[4,5] recommend using symptom-based criteria in making the diagnosis of IBS in clinical practice. Using these criteria in conjunction with "alarm features" allows a physician to minimize the extent of diagnostic testing needed to make the diagnosis of IBS. Furthermore, recent systematic review of the literature indicates that performing a number of diagnostic tests did not result in a significant increase in the diagnosis of organic gastrointestinal disease.[6]
This column discusses novel approaches to the diagnosis of IBS."
""Alarm Features" An important aspect of making the diagnosis of IBS is the absence of "red flag" or "alarm features" ( Table 2 ).[4,11,12] Unexplained weight loss may reflect disorders such as malignancy, inflammatory bowel disease (IBD), or celiac disease. Persistent diarrhea or severe constipation may be associated with an organic disease.
IBS is generally an intermittent and recurrent disorder. Symptoms of IBS tend to disappear at night when the patient is asleep. Thus, nocturnal gastrointestinal symptoms warrant search for a diagnosis other than IBS. The onset of new gastrointestinal symptoms after the age of 50 should prompt the physician to look for organic disease, particularly colorectal cancer. Blood in stool may reflect IBD or an infectious process or colon cancer. Family history of IBD, celiac disease, or gastrointestinal malignancy requires evaluation for these diseases. Fever suggests the possibility of an infectious or inflammatory disorder. Anemia should alert the physician to look for IBD or colorectal cancer. Signs of bowel obstruction, malabsorption, extraintestinal signs of IBD, or thyroid dysfunction should all prompt organic disease work-up. Any laboratory test abnormalities should be pursued appropriately. Absence of these "alarm features" serves to support, not establish, the diagnosis of IBS."
Summary and Conclusions What's too much when we think about diagnosing IBS is to do exhaustive and duplicate testing. In a retrospective, community-based study in Olmsted County, Minnesota, two thirds of patients who consulted for gastrointestinal symptoms had to wait at least 2 years to have their IBS diagnosed, despite averaging nearly 5 healthcare visits per year.[20] Such an approach is not only costly and inefficient, but it delays treatment and fosters frustration on the part of the patient and the physician.
What's enough is to use symptom-based criteria, "alarm features," and guidelines proposed by the ACG IBS Task Force and the AGA Technical Review on IBS in making a more timely diagnosis of IBS. Although additional studies are necessary to validate Rome II criteria and to assess diagnostic testing in prospective studies, the expert guidelines allow the diagnosis of IBS to be made with greater efficiency, certainty, and confidence. Furthermore, once a diagnosis of IBS is made, it is retained in more than 93% of cases with a long-term follow-up. Considering legal aspects of IBS diagnosis, symptom-based criteria and guidelines set forth by the ACG and AGA are becoming key elements in establishing standard of care. It has become clear that the diagnosis of IBS can and should be made quickly so that treatment can be initiated as soon as possible. This promotes greater patient confidence in the physician."
Introduction Epidemiology Symptom-based Criteria "Alarm Features" Physical Examination Diagnostic Testing Differential Diagnosis and Durability of Diagnosis Legal Risks in Diagnosing IBS Summary and Conclusions
http://www.medscape.com/viewarticle/465760_1
Diagnosis, Pathophysiology, and Treatment of Irritable Bowel Syndrome
Diagnosis of IBS Symptoms of IBS can be common to any number of gastrointestinal disorders. Abdominal pain, bloating, and diarrhea or constipation can easily generate an extensive list of potential diagnostic possibilities. To adopt an open-ended approach to diagnosis and to value all diagnostic possibilities equally has never been an effective approach in the diagnosis of IBS. However, with the development and validation of the Rome II criteria for the diagnosis of IBS, our approach to the diagnosis of this traditionally perplexing disorder is rapidly changing.
Diagnosing the patient with IBS should include 3 steps. First, determine whether the patient at first encounter meets the Rome diagnostic criteria for IBS. Second, conduct a history and physical examination looking for so-called "alarm factors." Third, perform diagnostic testing.
Diagnostic Criteria The latest version of the Rome diagnostic criteria (Rome II) for IBS were first published in abbreviated form in 1999[7] and in full form in 2000.[8] See the Table below. The Rome criteria have been shown to be both sensitive and specific for the diagnosis of IBS[9] and can be used advantageously in clinical practice. If a patient presents with symptoms suggestive of IBS and epidemiologically fits the profile of a patient most likely to have IBS (ie, younger than 40 years of age and with typical symptoms), the Rome criteria can be used to validate the physician's initial impression. Starting with a "positive approach" to diagnosing IBS, as opposed to adopting a diagnosis of exclusion, sets the entire physician-patient encounter off in a positive and thoughtful direction. Providing the diagnostic framework presented by the Rome criteria gives the physician an intellectual basis for making an IBS diagnosis with confidence.[10]
History-Taking The key to history-taking in a patient with suspected IBS is first and foremost to look for the presence of so-called "alarm factors." It is clear that the symptoms of IBS can be typical of many other structural disorders of the gastrointestinal tract. Diarrhea, abdominal bloating, and constipation can all represent an extraordinarily wide spectrum of gastrointestinal pathology. The challenge using the framework provided by the Rome II diagnostic criteria is to rapidly exclude the possibility of other disorders. The key is to look for symptoms in the history that are atypical of IBS and suggestive of other disorders. The list of so-called "alarm factors" can certainly be open to debate and discussion.
Physical Examination After a patient history has been completed and the absence of "alarm factors" documented, a physical examination should always be performed. The physical examination should focus specifically on ruling out inflammatory bowel disease, colorectal or other gastrointestinal cancers, and malabsorption caused by luminal or pancreatic causes. Look for extraintestinal manifestations of inflammatory bowel disease, such as ophthalmic changes, Sicca syndrome, intraoral lesions (eg, aphthous ulcers), and skin or arthritic changes suggestive of inflammatory bowel disease. Likewise, signs of malabsorption, such as muscle wasting, nail or perioral changes, and weight loss should all be ruled out. Finally, the issue of colorectal cancer must be addressed. There is agreement in the functional bowel community that the best guide to help clarify this situation is to follow the colorectal cancer screening guidelines of the American Cancer Society. It is therefore recommended that patients 50 years of age or older who have never had a screening colonoscopy should have one performed as part of an IBS evaluation. Likewise, individuals 40 years of age or older who have a family history of colorectal cancer in a first-rank relative should also have a screening colonoscopy.[11] Finally, the use of sigmoidoscopy in individuals younger than 50 years old who have no family history is open to some discussion.[12]
Small bowel (to rule out Giardia or small bowel malabsorption) or colonic (to rule out microscopic colitis) biopsies may be indicated, particularly for patients with loose or watery stools.[13] These studies, although they include some diagnostic testing, may be considered part of the "physical examination" and initial evaluation of the patient with suspected IBS.
Diagnostic Testing The use of diagnostic testing in IBS has become an increasingly controversial topic. Traditionally, the "diagnosis of exclusion" approach encouraged extensive diagnostic testing to evaluate patients with suspected IBS to rule out other possible causes of the disorder. Given the high prevalence of IBS , this approach has been subject to considerable scrutiny over the last 5 years.[10] Numerous studies have shown that the use of routine lactase hydrogen breath-testing for sugar malabsorption,[14] abdominal ultrasound,[15] routine computed tomography scanning, particularly in younger patients, and more esoteric tests, such as screening for acute intermittent porphyria[16] or thyroid testing for hyper- or hypothyroidism,[17] rarely yield data that change the diagnosis of IBS. Testing for bacterial overgrowth has been recently proposed by 1 group as a possible cause of IBS-like symptoms.[18] However, the article supporting the reasonableness of this approach studied a cohort of patients who were specifically referred by their treating physician to a tertiary center specializing in bacterial overgrowth. These patients were specifically referred to the tertiary center to rule out the possibility of bacterial overgrowth. However, given the selection bias in this study, the applicability of these data to the universe of IBS patients is open to some question. Based on the available literature, routine testing for bacterial overgrowth in patients with suspected IBS cannot be routinely recommended at this time.
One additional issue that is rapidly evolving in the area of IBS diagnosis is the issue of celiac disease. A number of studies have recently demonstrated a higher prevalence of celiac disease in the North American population than was previously thought, as well as a possible higher prevalence among patients with IBS-like symptoms.[19] This issue is yet to be completely resolved. It would therefore seem prudent for physicians who have patients with suspected IBS who have subtle signs or symptoms of celiac disease, such as osteoporosis in a premenopausal female or male, infertility, mild anemia, or weight loss, to evaluate the patient by obtaining celiac disease markers. Endoscopy with small bowel biopsy can confirm any equivocal serologic results.
Given these data, it would seem reasonable for the patient with IBS who presents absent alarm factors and who has a normal physical examination to have a complete blood count and chemistry panel and perhaps erythrocyte sedimentation rate measurement and thyroid function testing in the form of thyroid-stimulating hormone (TSH) levels. As noted above, in patients with diarrhea, additional initial investigation may be warranted, particularly investigation for the possibility of microscopic colitis and perhaps celiac disease.[17] For the majority of patients, this should end the initial evaluation. It is at this point that the physician should begin treatment and follow the patient prospectively. Failure to respond to reasonable treatment for IBS after a period of 2-4 weeks should certainly invite the physician to question the validity of IBS diagnosis and to consider additional evaluation as indicated. See the Figure below for a schematic that outlines this approach.
Of course recently they have published the rome lll criteria.
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
Gastroenterology Expert Column Diagnosing Irritable Bowel Syndrome: What's Too Much, What's Enough? Posted 03/12/2004
Susan Lucak, MD
Introduction Irritable bowel syndrome (IBS) is the most common gastrointestinal disorder diagnosed in clinical practice in the United States. Because there is no biological marker to confirm the diagnosis of IBS, it is a diagnosis that has challenged clinicians for decades. In the past, IBS was a "waste-basket" diagnosis given to patients with unexplained gastrointestinal symptoms. It was considered to be "the diagnosis of exclusion" when extensive work-up for organic disease yielded no diagnosis. In recent decades, it was recognized that patients with IBS experienced a constellation of specific gastrointestinal symptoms. Manning criteria were described in 1978,[1] followed by Rome I in 1989[2] and Rome II criteria in 1999.[3] Rome I and Rome II criteria were initially developed by multinational working groups to provide a framework for the selection of patients in diagnostic and therapeutic trials. These criteria are being continuously modified as we gain new knowledge about functional bowel disorders. Recently published diagnostic guidelines[4,5] recommend using symptom-based criteria in making the diagnosis of IBS in clinical practice. Using these criteria in conjunction with "alarm features" allows a physician to minimize the extent of diagnostic testing needed to make the diagnosis of IBS. Furthermore, recent systematic review of the literature indicates that performing a number of diagnostic tests did not result in a significant increase in the diagnosis of organic gastrointestinal disease.[6]
This column discusses novel approaches to the diagnosis of IBS."
""Alarm Features" An important aspect of making the diagnosis of IBS is the absence of "red flag" or "alarm features" ( Table 2 ).[4,11,12] Unexplained weight loss may reflect disorders such as malignancy, inflammatory bowel disease (IBD), or celiac disease. Persistent diarrhea or severe constipation may be associated with an organic disease.
IBS is generally an intermittent and recurrent disorder. Symptoms of IBS tend to disappear at night when the patient is asleep. Thus, nocturnal gastrointestinal symptoms warrant search for a diagnosis other than IBS. The onset of new gastrointestinal symptoms after the age of 50 should prompt the physician to look for organic disease, particularly colorectal cancer. Blood in stool may reflect IBD or an infectious process or colon cancer. Family history of IBD, celiac disease, or gastrointestinal malignancy requires evaluation for these diseases. Fever suggests the possibility of an infectious or inflammatory disorder. Anemia should alert the physician to look for IBD or colorectal cancer. Signs of bowel obstruction, malabsorption, extraintestinal signs of IBD, or thyroid dysfunction should all prompt organic disease work-up. Any laboratory test abnormalities should be pursued appropriately. Absence of these "alarm features" serves to support, not establish, the diagnosis of IBS."
Summary and Conclusions What's too much when we think about diagnosing IBS is to do exhaustive and duplicate testing. In a retrospective, community-based study in Olmsted County, Minnesota, two thirds of patients who consulted for gastrointestinal symptoms had to wait at least 2 years to have their IBS diagnosed, despite averaging nearly 5 healthcare visits per year.[20] Such an approach is not only costly and inefficient, but it delays treatment and fosters frustration on the part of the patient and the physician.
What's enough is to use symptom-based criteria, "alarm features," and guidelines proposed by the ACG IBS Task Force and the AGA Technical Review on IBS in making a more timely diagnosis of IBS. Although additional studies are necessary to validate Rome II criteria and to assess diagnostic testing in prospective studies, the expert guidelines allow the diagnosis of IBS to be made with greater efficiency, certainty, and confidence. Furthermore, once a diagnosis of IBS is made, it is retained in more than 93% of cases with a long-term follow-up. Considering legal aspects of IBS diagnosis, symptom-based criteria and guidelines set forth by the ACG and AGA are becoming key elements in establishing standard of care. It has become clear that the diagnosis of IBS can and should be made quickly so that treatment can be initiated as soon as possible. This promotes greater patient confidence in the physician."
Introduction Epidemiology Symptom-based Criteria "Alarm Features" Physical Examination Diagnostic Testing Differential Diagnosis and Durability of Diagnosis Legal Risks in Diagnosing IBS Summary and Conclusions
http://www.medscape.com/viewarticle/465760_1
Diagnosis, Pathophysiology, and Treatment of Irritable Bowel Syndrome
Diagnosis of IBS Symptoms of IBS can be common to any number of gastrointestinal disorders. Abdominal pain, bloating, and diarrhea or constipation can easily generate an extensive list of potential diagnostic possibilities. To adopt an open-ended approach to diagnosis and to value all diagnostic possibilities equally has never been an effective approach in the diagnosis of IBS. However, with the development and validation of the Rome II criteria for the diagnosis of IBS, our approach to the diagnosis of this traditionally perplexing disorder is rapidly changing.
Diagnosing the patient with IBS should include 3 steps. First, determine whether the patient at first encounter meets the Rome diagnostic criteria for IBS. Second, conduct a history and physical examination looking for so-called "alarm factors." Third, perform diagnostic testing.
Diagnostic Criteria The latest version of the Rome diagnostic criteria (Rome II) for IBS were first published in abbreviated form in 1999[7] and in full form in 2000.[8] See the Table below. The Rome criteria have been shown to be both sensitive and specific for the diagnosis of IBS[9] and can be used advantageously in clinical practice. If a patient presents with symptoms suggestive of IBS and epidemiologically fits the profile of a patient most likely to have IBS (ie, younger than 40 years of age and with typical symptoms), the Rome criteria can be used to validate the physician's initial impression. Starting with a "positive approach" to diagnosing IBS, as opposed to adopting a diagnosis of exclusion, sets the entire physician-patient encounter off in a positive and thoughtful direction. Providing the diagnostic framework presented by the Rome criteria gives the physician an intellectual basis for making an IBS diagnosis with confidence.[10]
History-Taking The key to history-taking in a patient with suspected IBS is first and foremost to look for the presence of so-called "alarm factors." It is clear that the symptoms of IBS can be typical of many other structural disorders of the gastrointestinal tract. Diarrhea, abdominal bloating, and constipation can all represent an extraordinarily wide spectrum of gastrointestinal pathology. The challenge using the framework provided by the Rome II diagnostic criteria is to rapidly exclude the possibility of other disorders. The key is to look for symptoms in the history that are atypical of IBS and suggestive of other disorders. The list of so-called "alarm factors" can certainly be open to debate and discussion.
Physical Examination After a patient history has been completed and the absence of "alarm factors" documented, a physical examination should always be performed. The physical examination should focus specifically on ruling out inflammatory bowel disease, colorectal or other gastrointestinal cancers, and malabsorption caused by luminal or pancreatic causes. Look for extraintestinal manifestations of inflammatory bowel disease, such as ophthalmic changes, Sicca syndrome, intraoral lesions (eg, aphthous ulcers), and skin or arthritic changes suggestive of inflammatory bowel disease. Likewise, signs of malabsorption, such as muscle wasting, nail or perioral changes, and weight loss should all be ruled out. Finally, the issue of colorectal cancer must be addressed. There is agreement in the functional bowel community that the best guide to help clarify this situation is to follow the colorectal cancer screening guidelines of the American Cancer Society. It is therefore recommended that patients 50 years of age or older who have never had a screening colonoscopy should have one performed as part of an IBS evaluation. Likewise, individuals 40 years of age or older who have a family history of colorectal cancer in a first-rank relative should also have a screening colonoscopy.[11] Finally, the use of sigmoidoscopy in individuals younger than 50 years old who have no family history is open to some discussion.[12]
Small bowel (to rule out Giardia or small bowel malabsorption) or colonic (to rule out microscopic colitis) biopsies may be indicated, particularly for patients with loose or watery stools.[13] These studies, although they include some diagnostic testing, may be considered part of the "physical examination" and initial evaluation of the patient with suspected IBS.
Diagnostic Testing The use of diagnostic testing in IBS has become an increasingly controversial topic. Traditionally, the "diagnosis of exclusion" approach encouraged extensive diagnostic testing to evaluate patients with suspected IBS to rule out other possible causes of the disorder. Given the high prevalence of IBS , this approach has been subject to considerable scrutiny over the last 5 years.[10] Numerous studies have shown that the use of routine lactase hydrogen breath-testing for sugar malabsorption,[14] abdominal ultrasound,[15] routine computed tomography scanning, particularly in younger patients, and more esoteric tests, such as screening for acute intermittent porphyria[16] or thyroid testing for hyper- or hypothyroidism,[17] rarely yield data that change the diagnosis of IBS. Testing for bacterial overgrowth has been recently proposed by 1 group as a possible cause of IBS-like symptoms.[18] However, the article supporting the reasonableness of this approach studied a cohort of patients who were specifically referred by their treating physician to a tertiary center specializing in bacterial overgrowth. These patients were specifically referred to the tertiary center to rule out the possibility of bacterial overgrowth. However, given the selection bias in this study, the applicability of these data to the universe of IBS patients is open to some question. Based on the available literature, routine testing for bacterial overgrowth in patients with suspected IBS cannot be routinely recommended at this time.
One additional issue that is rapidly evolving in the area of IBS diagnosis is the issue of celiac disease. A number of studies have recently demonstrated a higher prevalence of celiac disease in the North American population than was previously thought, as well as a possible higher prevalence among patients with IBS-like symptoms.[19] This issue is yet to be completely resolved. It would therefore seem prudent for physicians who have patients with suspected IBS who have subtle signs or symptoms of celiac disease, such as osteoporosis in a premenopausal female or male, infertility, mild anemia, or weight loss, to evaluate the patient by obtaining celiac disease markers. Endoscopy with small bowel biopsy can confirm any equivocal serologic results.
Given these data, it would seem reasonable for the patient with IBS who presents absent alarm factors and who has a normal physical examination to have a complete blood count and chemistry panel and perhaps erythrocyte sedimentation rate measurement and thyroid function testing in the form of thyroid-stimulating hormone (TSH) levels. As noted above, in patients with diarrhea, additional initial investigation may be warranted, particularly investigation for the possibility of microscopic colitis and perhaps celiac disease.[17] For the majority of patients, this should end the initial evaluation. It is at this point that the physician should begin treatment and follow the patient prospectively. Failure to respond to reasonable treatment for IBS after a period of 2-4 weeks should certainly invite the physician to question the validity of IBS diagnosis and to consider additional evaluation as indicated. See the Figure below for a schematic that outlines this approach.
Of course recently they have published the rome lll criteria.
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
good resources for accurate info on IBS or to go see specialists in IBS.
THE JOHNS HOPKINS UNIVERSITY
Gastroenterology and Hepatology
IBS Information
http://www.hopkins-gi.org/GDL_Disease.aspx?CurrentUDV=31&GDL_Cat_ID=024CC2E1-2AEB-4D50-9E02-C79825C9F9BF&GDL_Disease_ID=F5E21D6B-A88E-44F9-900F-7E295C50D38B
Mind-Body Digestive Center Research and Treatment
http://mindbodydigestive.com/
IFFGD aboutibs
http://www.aboutibs.org/
The UNC Center for Functional GI & Motility Disorders was established in 1994 by its Co-Directors -- Douglas A. Drossman, MD and William E. Whitehead, PhD -- as a center of excellence within the Division of Gastroenterology & Hepatology, School of Medicine, University of North Carolina at Chapel Hill.
The Center has evolved into a multidisciplinary patient care, research, training, and public education initiative with an annual budget of $1.8 million and a base of 32 faculty, investigators and staff, in addition to visiting and collaborating scholars.
http://www.med.unc.edu/medicine/fgidc/
Mayo Clinic IBS
Gastroenterology and Hepatology at Mayo Clinic specializes in the prevention, diagnosis and treatment of diseases of the digestive tract and liver. It is the largest practice of its kind in the United States. In any given year, members of the Division perform approximately 30,000 minimally invasive, endoscopic procedures in state-of-the-art facilities.
Through a divisional infrastructure organized around interest groups oriented toward disease processes, organ systems, procedures or patient groups, clinical expertise is integrated with the newest forms of established and experimental diagnostic and therapeutic methods. Outpatients and patients in the hospital are cared for by teams of physicians and allied health personnel with broad expertise in all forms of gastroenterological and hepatobiliary diseases.
Because of our recognition that high-quality care depends upon scientific discovery, major research programs at the basic, applied, and translational levels exist to generate new knowledge that ultimately benefits patients.
http://www.mayoclinic.com/health/irritable-bowel-syndrome/DS00106/FLUSHCACHE=0&UPDATEAPP=false
The Cleveland Clinic: Gastroenterology and Hepatology:
(Best Hospitals 2004: U.S. News & World Report names The Cleveland Clinic one of the nation's top four hospitals in its annual "America's Best Hospitals" survey.)
The Center for Gastrointestinal Motility Disorders diagnoses and treats patients with motor abnormalities of the stomach, small intestine and large intestine (colon). Some of these problems are among the most common health concerns. It's estimated that constipation affects up to 10 million Americans, while approximately 20 million Americans suffer from the opposite problem, fecal incontinence.
The center provides the latest and most comprehensive diagnostic and treatment options for bowel incontinence. Diagnostic tests available include several types of manometric techniques, electrical recording from the stomach and nerve conduction tests. If necessary, additional tests are provided by the Radiology and Nuclear Medicine Departments.
Patients seen at the center are offered medical therapy and biofeedback training exercises, or surgical treatment in the departments of general surgery or colorectal surgery.
In addition to patient care, our staff participates in patient and medical education and clinical research. When appropriate, patients can participate in new treatment trials conducted at the Cleveland Clinic. overview
http://my.clevelandclinic.org/digestive_diseases/default.aspx?WT.mc_id=1125&utm_campaign=gastro-redirect&utm_medium=offline&utm_source=redirect
Medical Centers
USA
The UNC Center for Functional GI & Motility Disorders:
Established in 1994 by its Co-Directors -- Douglas A. Drossman, MD and William E. Whitehead, PhD -- as a center of excellence within the Division of Gastroenterology & Hepatology, School of Medicine, University of North Carolina at Chapel Hill.
Within ten years, the UNC Center has evolved into a multidisciplinary patient care, research, training, and public education initiative with an annual budget of $1.8 million and a base of 32 faculty, investigators and staff, in addition to visiting and collaborating scholars. News: UNC Receives NIH Grant
Five-Year NIH Grant on Mind-Body Interactions and Health September 2004
Chapel Hill, NC - The UNC Center for Functional GI & Motility Disorders has been awarded a five-year grant from the National Institutes of Health (NIH) to foster interdisciplinary research on the interactions among the mind and body in health and disease. The Center will receive a total of $4.3 million over a five-year period to establish a Gastrointestinal Biopsychosocial Research Center focused on the causes and treatment of functional gastrointestinal (GI) disorders.
UCLA/CURE Neuroenteric Disease Program
Past: The new Center has evolved from existing research programs at UCLA and at the Greater Los Angeles VA Healthcare System (GLAVAHS), in particular the CURE: Digestive Diseases Research Center, the UCLA/CURE Neuroenteric Disease Program under Dr. Emeran Mayer, and the Brain Gut Research Program under Y. Taché. Drs. Mayer and Taché are the P.I. and co-P.I. of the new center grant.
Present: The core of CNS/WH is the newly funded NIDDK P50 SCOR Center grant "Women's Health and Functional Visceral Disorders Center." The new center which closely links investigators based at UCLA and the VAGLAHS, is the only NIH-funded center in the area of brain-visceral interactions and the first DK Women's Center. It focuses on research into the bi-directional mechanisms by which the central nervous system and the viscera interact in health and disease. A particular focus is on the neurobiological mechanisms by which stress modulates these brain-visceral interactions, on mind/brain/body interactions and on sex-based differences in this modulation.
The grant has significant implications for a better understanding of such common gastrointestinal disorders as irritable bowel syndrome, Functional dyspepsia and common urological disorders such as irritable bladder syndrome ("interstitial cystitis"). In addition, a major research focus is on neurobiological mechanisms underlying the greater vulnerability of women to develop some of these disorders.
The center grant involves investigators and consultants from four different institutions: UCLA, VAGLAHS, Ohio State University and University of Pittsburgh who are interacting closely to accomplish the principal goals of the proposed studies.
http://www.ibs.med.ucla.edu/
with permission from the Internation Foundation of Functional Gastrointestinal disorders.
Facts About IBS Irritable bowel syndrome (IBS) is a disorder characterized by abdominal pain or discomfort, and altered bowel habit (chronic or recurrent diarrhea, constipation, or both – either mixed or in alternation).
•IBS affects between 25 and 45 million people in the United States (10 to 15% of the population).About 2 in 3 IBS sufferers are female. About 1 in 3 IBS sufferers are male. IBS affects people of all ages, even children. •Worldwide it's estimated that between 1 in 10 and nearly 1 in 4 people (9% to 23% of populations) has IBS. •Most persons with IBS are under the age of 50. But many older adults suffer as well. • The exact cause of IBS is not known. Symptoms may result from a disturbance in the way the gut, brain, and nervous system interact. This can cause changes in normal bowel movement and sensation. •Stress does not cause IBS. However, because of the connection between the brain and the gut, stress can worsen or trigger symptoms. •The impact of IBS can range from mild inconvenience to severe debilitation. It can control many aspects of a person's emotional, social and professional life. Persons with moderate to severe IBS must struggle with symptoms that often impair their physical, emotional, economic, educational and social well-being. •IBS is unpredictable. Symptoms vary and are sometimes contradictory. Diarrhea can alternate with constipation. Long-term symptoms can disrupt personal and professional activities, and limit individual potential. •Treatments are available for IBS to help manage symptoms. Not all treatments work for all people. Through research, better treatments may be found. •Although IBS is common in the general population, few seek medical care for their symptoms. •Nearly 2,000 patients with IBS reported in a survey by IFFGD that diagnosis of their IBS was typically made 6.6 years after the symptoms began. •Approximately 20 to 40% of all visits to gastroenterologists are due to IBS symptoms. •For those with IBS an additional burden comes from living in a society where the word "bowel" may scarcely be spoken. Individuals must cope with multiple symptoms that affect every aspect of their lives. Those around them may be unaware of the impact, or even the existence, of the disorder. •IBS can only be diagnosed by a medical professional.
http://www.aboutibs.org/site/about-ibs/facts-about-ibs
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
The Experts Speak
About IFFGD Learn about IFFGD on video
At IFFGD's 7th International Symposium on Functional Gastrointestinal Disorders in April 2007, we had the opportunity to talk to some of the international experts in functional GI disorders. Our discussions covered some of the most recent developments in this field.
Click the topic titles below to go to the video interviews!
Video Corner: Causes and TreatmentsA functional GI disorder such as irritable bowel syndrome (IBS) has very specific symptoms. Over the past 5–10 years we've developed an understanding that many different components contribute to these symptoms. Brain-gut interactions, changes in serotonin signaling, motility, inflammation, gut sensitivity, genetic predispositions, and bacterial flora all can contribute to varying degrees in an individual having this condition. Not only will this help with developing more effective treatments, but better understanding of the factors that underlie symptoms in each individual will enable more reliable treatments that will work earlier on rather than trying hit or miss one after another.
Functional GI disorders, such as IBS, present challenges to both the patient and the doctor or other healthcare provider. For the patient, education about their disorder is important to improving management of their condition. For the doctor, understanding the many facets involved with the condition and addressing those that are most evident in each individual is important.
Patients and many physicians alike will benefit from the recent and continuing advances, which not only further our understanding but also confirm the validity of the functional GI disorders.
http://www.aboutibs.org/site/learning-center/video-corner/causes
Video Corner: Gut Flora, Probiotics and Antibiotics Bacteria are germs that are normally in the gut. They are often referred to as the gut flora. Most bacteria are in the large intestine (colon). Some bacteria can cause infection; these are called pathogens. Other bacteria can be helpful. These helpful (or "good") bacteria are called probiotics. Medicines that destroy bacteria are called antibiotics.
During IFFGD's 7th International Symposium on Functional Gastrointestinal Disorders in April 2007, we had the opportunity to interview a leading researcher, Eamonn Quigley, MD, on the topics of probiotics and antibiotics. Dr. Quigley is Professor of Medicine and Human Physiology at University College, Cork (National University of Ireland). Brooks Cash, MD adds comments about issues of safety and effectiveness of antibiotics.
http://www.aboutibs.org/site/learning-center/video-corner/gutflora
Video Corner: Inflammation
In some people with IBS a subtle inflammation persists for some time after recovery from an initial infection and obvious inflammation. This can cause increased sensation in the intestines and changes in gut motility consistent with symptoms of IBS.
Inflammation Does inflammation have a role in generating IBS symptoms? An interview with Gary M. Mawe, PhD, Professor of Anatomy and Neurobiology, University of Vermont, Burlington, VT. Dr. Mawe is a basic scientist.
http://www.aboutibs.org/site/learning-center/video-corner/inflammation
Video Corner: Research Advances From mechanisms at the gut level and the micro flora to the spinal cord and brain our understanding to the functional disorders has grown tremendously over the past 5 years. In these videos Emeran Mayer, MD and Lin Chang, MD, both from UCLA, and Brooks Cash, MD from Bethesda, Maryland explain some of these advances.
On one end new techniques allow us to probe the living human brain to understand its structure, activity, and receptor systems. On the other end we are just beginning to view the universe of our gut micro flora and the cross-talk taking place between it and the brain. Growing understanding of the ways in which many systems within the body interact has implications for various disorders such as pain, irritable bowel syndrome, fibromyalgia, interstitial cystitis, gastroparesis, and others. Like a jigsaw puzzle, many pieces are beginning to emerge.
http://www.aboutibs.org/site/learning-center/video-corner/research
Video Corner: Serotonin
Increasingly our understanding of IBS is that it is a heterogeneous disorder – that is, multiple factors contribute to the well defined symptoms of the disorder. One of these suspected underlying dysfunctions involves serotonin, which is a neurotransmitter or messenger to nerves. Most serotonin in the body is in cells that line the gut where it senses what is going on and through receptors signals nerves that stimulate a response. The serotonin must then be reabsorbed (a process called re-uptake) into cells. This process appears to be disrupted in people with IBS.
Serotonin and SERT How does serotonin affect gut function? An interview with Gary M. Mawe, PhD, Professor of Anatomy and Neurobiology, University of Vermont, Burlington, VT. Dr. Mawe is a basic scientist.
http://www.aboutibs.org/site/learning-center/video-corner/serotonin
Video Corner: Overcoming Challenges There is growing recognition of the seriousness and the complexity of the functional GI disorders. Yet individuals affected by these disorders still face challenges in finding adequate care. Many physicians remain unprepared to diagnose and treat patients with functional GI disorders. Moreover, the burden of illness resulting from chronic pain or discomfort and other symptoms associated with functional GI disorders remains underappreciated by everyone it seems – except those who experience it, or those who are truly dedicated to finding solutions.
http://www.aboutibs.org/site/learning-center/video-corner/challenges
Video Corner: Kids and Teens
Many of the digestive disorders seen in adults begin in kids and teens. Providing better treatments early in life would not only help help children and their families, but would also help avoid much pain, suffering and expense later on in life. While we have seen many advances in understanding functional GI and motility disorders in kids and teens, much more remains to be done. Development of improved treatments in pediatrics is a particular challenge.
http://www.aboutibs.org/site/learning-center/video-corner/kids-and-teens
7th International Symposium on Functional GI Disorders
Report on the 7th International Symposium for Functional Gastrointestinal DisordersThe 7th International Symposium on Functional Gastrointestinal Disorders was held in Milwaukee on April 12–15, 2007. The meeting was sponsored by the University of Wisconsin School of Medicine and the International Foundation for Functional Gastrointestinal Disorders (IFFGD), in cooperation with the Functional Brain Gut Group (FBG).
This report highlights just some of the information presented at the Symposium. Nevertheless the information herein identifies several of the newer and more important research emerging in the field. Clearly many pieces of the puzzle are emerging, which will benefit patients with functional gastrointestinal (GI) and motility disorders.
http://www.aboutkidsgi.org/store/viewproduct/222
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
1992
"Postgrad Med J. 1992 Jun;68(800):453-4.
The role of faecal Candida albicans in the pathogenesis of food-intolerant irritable bowel syndrome. Middleton SJ, Coley A, Hunter JO.
Department of Gastroenterology, Addenbrooke's Hospital, Cambridge, UK.
Comment in:
Postgrad Med J. 1993 Jan;69(807):80.
Candida albicans was sought in stool samples from 38 patients with irritable bowel syndrome and 20 healthy controls. In only three patients with irritable bowel syndrome was C. albicans discovered and these patients had either recently received antibiotics or the stool sample had been delayed more than 24 hours in transit. C. albicans was isolated from none of the control stool samples. We conclude that C. albicans is not involved in the aetiology of the irritable bowel syndrome.
just fyi on real candida conditions in people with Aids and cancer and other diseases that highly compromise the immune system
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
Antifungal properties of 5-hydroxytryptamine (serotonin) against Candida species in vitro
"Our study revealed that 5 HT can inhibit and kill isolates of C. albicans, C. glabrata and C. tropicalis."
http://jmm.sgmjournals.org/cgi/content/full/52/2/169
-------------------- My website on IBS is www.ibshealth.com
Print
Remind Me
Notify Moderator
|
|
Print
Remind Me
Notify Moderator
|
|