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New approach to celiac testing identifies more at risk new
      #370107 - 08/30/13 12:11 PM
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New approach to celiac testing identifies more at risk

Full Text
ScienceDaily, 08/30/2013

Australian researchers have developed a new approach to detecting coeliac disease, revealing this immune disorder is far more common than previously recognised. In a study of more than 2500 Victorians the researchers combined traditional antibody testing (measuring the immune response to gluten) with an assessment of specific genetic risk markers. They found more than half of Australians had genetic risk factors for developing coeliac disease. The research is published online today in the journal BMC Medicine. Dr Jason Tye–Din from the Immunology division at the Walter and Eliza Hall Institute and Dr Bob Anderson, chief scientific officer at US biotechnology company ImmusanT, worked with Barwon Health, Deakin University, Healthscope Pathology and the University of Queensland Diamantina Institute to develop and trial the new diagnostic approach. Dr Tye–Din said the new approach of combining the genetic test with a panel of antibody tests would increase the accuracy of testing, decrease overall medical costs by reducing invasive diagnostic tests, and avoid medically unnecessary use of a gluten–free diet.

http://www.mdlinx.com/gastroenterology/newsl-article.cfm/4799402/ZZ956160859472514387259/?news_id=522&newsdt=083013&subspec_id=155&utm_source=Newsletter&utm_medium=DailyNL&utm_content=General-Article&utm_campaign=Article-Section

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Evidence points to Monsanto Roundup as culprit in rise of gluten intolerance & IBS new
      #370918 - 02/19/14 01:30 PM
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Nancy Swanson
Seattle GMO Examiner

February 18, 2014

New evidence points to glyphosate, the active ingredient in Roundup, as the culprit in the rise of gluten intolerance, celiac disease and irritable bowel syndrome. A study just published in the Journal of Interdisciplinary Toxicology (Vol. 6(4): 159–184 ) by Anthony Samsel and Stephanie Seneff explains how the nearly ubiquitous use of glyphosate as a crop desiccant is entering our food chain and making us ill.


Pre-harvest application of glyphosate to wheat and barley as a desiccant was suggested as early as 1980 and its use as a drying agent 7-10 days before harvest has since become routine. It is now used on all grain crops, rice, seeds, dried beans and peas, sugar cane, sweet potatoes, and sugar beets. According to the Pulse Growers Association in Canada (legume growers), "Desiccants are used worldwide by growers who are producing crops that require 'drying down' to create uniformity of plant material at harvest. These products may also assist in pre-harvest weed control. In Canada, products such as diquat (Reglone) and glyphosate (Roundup) have been used as desiccants in pulse crops in the past, and there are new products on the way. "

The percentage of the total acreage of wheat in the US treated with glyphosate in 1998 and 2012 is shown in Table 1 (slide show).

Samsel & Seneff state that in 2004 glyphosate was used to treat 13% of the wheat in the UK and by 2006, 94% of UK growers used glyphosate on 40% of cereal and 80% of oilseed crops for weed control or harvest management. According to a 2012 report on glyphosate residues in food in the UK, residues as high as 1.1 parts per million [ppm] were detected in whole wheat flour. Lesser residues were detected in a wide range of breads. Residues of 0.6 ppm were found in dried lentils and peas, 2.7 ppm in dried beans, and 11 ppm in dried chickpeas.

Despite multiple letters and documents submitted in protest, just last July the EPA raised the maximum allowable residues of glyphosate in our food, most likely to accommodate levels already present. Allowed levels for various crops where desiccants are routinely used are shown in Table 2 (slide show).

In 2009 Gasnier et al. published an article in the journal Toxicology citing evidence that glyphosate-based herbicides are endocrine disruptors in human cells. They reported toxic effects to liver cells "at 5 ppm, and the first endocrine disrupting actions at 0.5 ppm."

Samsel & Seneff have meticulously researched the known (published) effects of glyphosate along with the known (published) pathologies associated with celiac disease, gluten intolerance and irritable bowel syndrome. They have identified chemical and biological pathways where glyphosate can be the cause. These are: disruption of the gut bacteria; breakdown in the junctions of the intestinal wall; depletion of vital minerals, vitamins and nutrients; and impairment of cytochrome enzymes that aid the liver in detoxifying environmental toxins, thus multiplying the deleterious effect of other environmental toxins to which we are exposed in increasing amounts.

The increase in the amount of glyphosate applied to wheat correlates with the rise of celiac disease, peritonitis, and deaths due to intestinal infection (see slide show). Samsel and Seneff argue that

the increases in these diseases not only have an environmental factor, but not all patient's symptoms are alleviated by eliminating gluten from the diet, which points to another cause.

http://www.examiner.com/article/is-it-the-gluten-or-is-it-the-glyphosate

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Delays in gluten introduction, onset of celiac disease in at-risk infants linked new
      #371524 - 10/07/14 02:23 PM
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Delays in gluten introduction, onset of celiac disease in at-risk infants linked
October 3, 2014

Among infants at-risk for celiac disease, delayed introduction of dietary gluten was associated with delayed onset of disease, according to new research data.

To explicate the correlation between age of introduction to dietary gluten and risk for celiac disease (CD), Elena Lionetti, MD, PhD, department of pediatrics at the University of Catania, Italy, and colleagues conducted a multicenter, prospective intervention trial (CELIPREV) between 2003 and 2008. They compared outcomes of infants with familial risk for CD who either had early or delayed introduction of gluten to their diet.
Elena Lionetti, MD, PhD

Elena Lionetti

Participants were randomly assigned to introduce gluten at age 6 months (group A) or 12 months (group B), and daily intake was assessed by a questionnaire. HLA genotype was determined at 15 months, CD serology was performed at 15, 24 and 36 months and at 5, 8 and 10 years. Patients who were seropositive for CD also had biopsy performed.

Among children (n=707) still participating at 36 months (group A, n=379; 49.6% girls; median age at study completion, 7.9 years), 553 had standard-risk or high-risk HLA genotypes and completed the study. At 2 years 16% of group A had CD autoimmunity and 12% had overt CD, compared with 7% and 5%, respectively, of group B (P=.002; P=.01). CD autoimmunity differences were no longer significant at 5 years (21% vs. 20%), nor was overt disease (16% vs. 16%). At 10 years risk for CD autoimmunity was 37.9% in high-risk HLA genotypes compared with 19.2% for standard-risk genotypes (HR=0.5; 95% CI, 0.3-0.7). Risk for overt disease was 25.8% among high-risk HLA genotypes vs. 15.8% for standard-risk genotypes (HR=0.6; 95% CI, 0.3-1).

"Postponing the introduction of gluten had two potentially positive consequences," the researchers concluded. "First, it delayed the development of celiac disease, which might reduce the negative effect of the disease on vulnerable organs such as the brain. Second, it reduced the prevalence, albeit nonsignificantly, of celiac disease autoimmunity at any age among children carrying the high-risk HLA genotype."
Jonas F. Ludvigsson, MD, PhD

Jonas F. Ludvigsson

In an accompanying editorial, Jonas F. Ludvigsson, MD, PhD, from Karolinska Institutet and Örebro University Hospital, Sweden, and Peter H.R. Green, MD, from the Celiac Disease Center at Columbia University, College of Physicians and Surgeons, wrote that this and related studies "will change the conceptual landscape" of celiac disease. The CELIPREV researchers, they said, found "first, the timing of introduction of gluten in high-risk children does not appear to influence the development of CD in childhood. Second, there is no evidence that the duration of breast-feeding or the maintenance of breast-feeding when gluten is introduced influences the risk of CD later in life. Finally, the only identified risk factor for CD later in life is the HLA genotype."

For more information:

Lionetti E. N Engl J Med. 2014;371:1295-1303.

Ludvigsson JF. N Engl J Med. 2014;371:1341-1343.


http://www.healio.com/gastroenterology/malabsorption/news/online/%7B92a0c67d-41ee-44ad-862a-4106de0039c3%7D/delays-in-gluten-introduction-onset-of-celiac-disease-in-at-risk-infants-linked

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Children with silent celiac new
      #372193 - 06/19/15 03:06 PM
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"Silent" celiac disease (CD), or CD without gastrointestinal symptoms, was present in 2.0% of children presenting for initial pediatric rheumatology evaluation, researchers from the Hospital for Special Surgery, New York City, report in an article published online June 15 in Pediatrics. The authors say celiac testing should be included in the standard initial laboratory workup for pediatric rheumatology patients, as they found that initiation of a gluten-free diet led to resolution of musculoskeletal symptoms in many of the affected patients.

Yekaterina Sherman, BA, and a research team led by Thomas J. A. Lehman, MD, retrospectively reviewed medical charts and data from standardized serologic screening for 2125 patients (age, 2 - 16 years) who presented for care at the Hospital for Special Surgery, Division of Pediatric Rheumatology, between June 2006 and December 2013. The researchers found that 36 patients had previously unsuspected CD. Together with the eight patients known to have CD at study entry, the prevalence of CD during the 6.5-year study period was 2.0%, or about 1 in 48 patients. Prevalence in the general population was 0.7%.

Thirty of the 36 "silent CD" cases were confirmed by endoscopy. Six refused endoscopy but had significant reduction of symptoms with a gluten-free diet.

"The majority of the newly diagnosed CD cases, 22 out of 36 (61.1%), presented with musculoskeletal complaints alone and none of the classic symptoms of CD, such as abdominal pain, short stature, weight loss, and failure to thrive," the authors write. "In fact, only 12 patients reported a history of [gastrointestinal]-related complaints." They note that these data provide further evidence that symptom-based case finding will miss the majority of CD cases in children.

Pediatric CD Guidelines Need a Rewrite

The researchers suggest that current clinical guidelines for CD screening published by the American College of Gastroenterology and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition be revised to include children with musculoskeletal complaints.

Current guidelines do not consider such patients to be a high-risk group and do not specifically recommend screening of this population. The guidelines recommend CD screening for children with failure to thrive, persistent diarrhea, recurrent abdominal pain, constipation and vomiting, dermatitis herpetiformis, dental enamel hypoplasia, osteoporosis, short stature, delayed puberty, iron-deficient anemia, asymptomatic diabetes mellitus, autoimmune thyroiditis, Down syndrome, Turner syndrome, Williams syndrome, selective immunoglobulin A deficiency, and a history of a first-degree relative with CD.

Clinicians using the current guidelines rather than screening all children with musculoskeletal complaints would have missed all but six of the asymptomatic CD cases in the study population. The authors note that prompt detection of CD would not only enable the patient to achieve the benefits of early initiation of a gluten-free diet but also avoid the dangers of unnecessary immunosuppressive therapy.

If CD Is Present, Is This Really Idiopathic Arthritis?

The association between CD and musculoskeletal complaints raised a further interesting question: Is this really "idiopathic arthritis" if it resolves with treatment of CD?

"Our data suggest that there may be a subset of patients with 'silent' CD who present with isolated musculoskeletal symptoms and that perhaps [juvenile idiopathic arthritis] is not an appropriate diagnosis in these cases. Clinicians must be vigilant in cases such as these to evaluate appropriately for CD," the authors note.

The authors have disclosed no relevant financial relationships.

Pediatrics. Published online June 15, 2015.

http://www.medscape.com/viewarticle/846467

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Relatives, spouses of celiac disease patients at risk for autoimmune disease new
      #372206 - 07/09/15 03:39 PM
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Relatives, spouses of celiac disease patients at risk for autoimmune disease

Emilsson L, et al. Clin Gastroenterol Hepatol. 2015;doi:10.1016/j.cgh.2015.01.026.

A recent study found first-degree relatives and spouses of individuals with celiac disease have increased risk for nonceliac autoimmune diseases.

"The prevalence of celiac disease is about 10% in first-degree relatives of celiac patients compared to about 1% in the general population. …However, very little is known about the risk of developing other autoimmune diseases in relatives of celiac patients," Louise Emilsson, MD, PhD, from Oslo University and primary care research unit, Värmlands Nysäter, told Healio Gastroenterology. "The main finding of the study is that both first-degree relatives (+28%) and spouses (+20%) are at increased risk of other autoimmune diseases."

Louise Emilsson

Aiming to determine the risk of several autoimmune diseases in first-degree relatives and spouses of patients with celiac disease, Emilsson and colleagues performed a nationwide, population-based, longitudinal cohort study in Sweden involving 29,096 patients with celiac disease and 144,522 controls matched for sex, county, age and birth year, all identified using national database records from 1969 to 2008. They also identified all first-degree relatives and spouses of the celiac patients (n = 84,648) and controls (n = 430,942) and calculated hazard ratios for Crohn's disease, ulcerative colitis, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis and systemic lupus erythematosus.

After a median follow-up period of 10.8 years, 4.3% of celiac patient relatives and spouses had a nonceliac autoimmune disorder compared with 3.3% of relatives and spouses of controls. Compared with controls, celiac patient relatives (HR = 1.28; 95% CI, 1.23-1.33) and spouses (HR = 1.2; 95% CI, 1.06-1.35) had increased risk for nonceliac autoimmune diseases, both of which were statistically similar. The excess risk for nonceliac autoimmune diseases was 79 per 100,000 person-years in relatives and 63 per 100,000 person-years in spouses. Risk for developing a nonceliac autoimmune disease was greatest in the first 2 years after the celiac patient's diagnosis (HR = 1.42; 95% CI, 1.28-1.57), but HRs were still significant after 2 years. Risk was higher in female spouses (HR = 1.33; 95% CI, 1.12-1.59) compared with male spouses (HR = 1.09; 95% CI, 0.92-1.29), but risk was not different between sexes among relatives. The highest HRs were for systemic lupus erythematosus, type 1 diabetes mellitus and sarcoidosis.

"There are several plausible explanations for these findings," Emilsson said. "One is of course that individuals with celiac disease and their first-degree relatives share a genetic autoimmune predisposition. Another potential explanation involves shared environment (relevant for both first-degree relatives and spouses), but finally we cannot rule out that a certain degree of increased awareness of signs and symptoms in both first-degree relatives and spouses might lead to more examinations and thereby diagnoses (so-called ascertainment bias). Probably all of these mechanisms contributed to the finding. Clinicians could benefit from knowing that the genetic predisposition for celiac disease in celiac first-degree relatives also implies a higher risk of other autoimmune diseases." – by Adam Leitenberger

Disclosure: The researchers report no relevant financial disclosures.

http://www.healio.com/gastroenterology/malabsorption/news/online/%7Beb7e22e3-edcf-4cec-93a5-65a6e0800b88%7D/relatives-spouses-of-celiac-disease-patients-at-risk-for-autoimmune-disease?utm_source=maestro&utm_medium=email&utm_campaign=gastroenterology%20news

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Fructans Suspect in Non-Celiac Gluten Sensitivity new
      #373676 - 03/19/18 02:44 PM
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Gastroenterology > General Gastroenterology

Fructans Suspect in Non-Celiac Gluten Sensitivity

Randomized double-blind trial casts doubt on need for gluten-free diets in NCGS


by Diana Swift, Contributing Writer
March 08, 2018

Note that this small study found that fructans, not gluten, promote the worst symptoms in patients with self-reported non-celiac gluten sensitivity.

Be aware that the effect of placebo is very strong in studies of this type, potentially adding noise to the outcome data that make these estimates less reliable.

A Norwegian study has found that fructan is somewhat more likely than gluten to induce the symptoms of non-celiac related gluten sensitivity (NCGS), a term first used in 1978.

In a randomized, double-blind crossover trial of 59 patients with self-reported intolerance to wheat, rye, and barley, but no celiac disease, the overall symptom score was highest after challenge with the carbohydrate fructan. Fructan is a member of the fermentable oligo-di-monosaccharides and polyols (FODMAPs) family, and is often found in gluten-containing foods such as wheat.

The study, published in Gastroenterology and led by Gry I. Skodje, MSc, RD, a PhD student at Oslo University Hospital, found that gluten challenge had no effect at the overall group level and triggered the highest level of symptomatic response in just 13 of the 59 participants.

Skodje and colleagues pointed out that NCGS symptoms often improve after gluten withdrawal even though no celiac disease is present, and that gastrointestinal symptoms often improve on low-FODMAP diets. Currently the mechanisms of NCGS remain unclear; the disorder has no known biomarkers.

The study was conducted at the hospital during 2014-2016; the patients with self-reported NCGS, were mostly female (n=53), and had a mean age of approximately 44. Participants were randomized to the following dietary arms based on a 7-day challenge with different muesli bars: gluten 5.7 g, fructan 2.1 g, and placebo -- all in the roughly 400-kcalorie range. After a 7-day washout period, participants crossed over into a different group until they had completed all three challenges; the reported compliance was high.

Symptoms were measured using the Gastrointestinal Symptom Rating Scale-Irritable Bowel Syndrome (GSRS-IBS). Overall scores differed moderately across the gluten, fructan, and placebo challenges, with mean respective values of 33.1±13.3, 38.6±12.3, and 34.3±13.9 (P=0.04).

The mean scores for bloating specifically were 9.3±3.5, 11.6±3.5, and 10.1±3.7, respectively (P=0.004). The overall score for participants consuming fructan was higher than for those consuming gluten (P=0.049), as was the GSRS bloating score (P=0.003). Just 13 participants had the highest overall GSRS-IBS score after consuming gluten, 24 had the highest score after consuming fructan, and, interestingly, 22 had the highest score after consuming placebo -- due perhaps, the researchers said, to the nocebo effect of anticipating negative outcomes after any intervention, which has been as high as 40% in other research.

"The large placebo response, as seen in previous studies, demonstrates how difficult it is to correctly identify which patients should be gluten-free."

The authors pointed out that the respective muesli bars were carefully formulated to contain no other potential triggers, and when pretested on biopsy-tested celiac patients, the gluten bars induced a strong duodenal immune response.

In secondary findings, the fructan effect was not restricted to abdominal symptoms, the team found. The Short Form (36) Health Survey vitality scale was significantly lower, and the Visual Analog Scale weakness significantly increased in response to fructan compared with to gluten and placebo: mean 44.3, 38.2, and 44.4, respectively (P=04). Using the Giessen Subjective Complaint List, the highest weakness was found after the fructan challenge versus gluten and placebo: 32.8, 42.5, and 33.5, respectively (P=0.02).

"The findings weaken the role of gluten as a symptom inducer in patients with self-reported NCGS," Skodje and colleagues wrote." They pointed to Australian research showing that NCGS patients placed on a low-FODMAP diet with tight control of background confounders had no response to rechallenge with gluten.

Javier Molian-Infante MD, of Hospital San Pedro de Alcantara in Caceres, Spain, who was not involved with the study, commented that other research has found that gluten plays only a minor role in self-diagnosed NCGS sensitivity.

"The term would be better changed to 'wheat and/or cereal sensitivity,'" Molina-Infante told MedPage Today. "Aside from gluten, a protein, fructans, which are carbohydrates, [other protein] components are under suspicion as symptom triggers in non-celiac, non-wheat sensitivity."

Writing in an accompanying editorial, Kristin Verbeke, PhD, Pharm, of the University of Leuven in Brussels, Belgium, noted that current research is homing in other problematic components. One is α−amylase/trypsin inhibitors (ATIs), pest-proofing proteins that are potent promoters of inflammation through activation of the innate immune system, including dendritic cells, monocytes, and macrophages via stimulation of the toll-like receptors. The need for ever-greater crop yields and greater pest resistance has led to the development of wheat cultivars higher in ATIs, she explained.

In addition, Verbeke continued, while fructans and other FODMAPs likely contribute to NCGS, they may only explain the gastrointestinal symptoms and not the disorder's extraintestinal symptoms such as neurologic dysfunction, psychological disturbances, fibromyalgia, and skin rash -- "Therefore, it is unlikely that they are the sole cause of NCGS."

Studies such as Skodje et al's disentangle the contribution of different suspect components in cereal grains and are very much needed, Verbeke said. "They might stimulate the food industry to develop adapted food products, eliminating the need for gluten-free diets for NCGS patients." And that would be desirable since a gluten-free diet tends to reduce consumption of whole grains and cereal fiber and whole grains, potentially raising cardiovascular risk, she said.

Study limitations, the team said, included a relatively small sample, the heterogeneity of NCGS populations, the potential for recall bias during recording of symptoms, and the possibility of unreported dietary changes during the course of the study.

This study was funded by the Extra Foundation Health and Rehabilitation, the Norwegian Celiac Association, the Throne Holst Foundation for Nutrition Research, and the Wedel Jarlsberg Foundation.

One of the co-authors has published an information/recipe book on the low-FODMAP diet, and his institution receives royalties from the sale of The Monash University Low-FODMAP Diet App. Skodje and the other authors reported having no competing interests.

Neither Molian-Infante nor Verbeke reported having any conflicts of interest in regard to their comments.

Reviewed by F. Perry Wilson, MD, MSCE Assistant Professor, Section of Nephrology, Yale School of Medicine

last updated 03.08.2018

Primary Source
Gastroenterology
Source Reference: Skodje GI, et al "Fructan, Rather Than Gluten, Induces Symptoms in Patients with Self-Reported Non-Celiac Gluten Sensitivity" Gastroenterology 2018; 154(3): 529–539.
Secondary Source
Gastroenterology
Source Reference: Verbeke K "Non-Celiac Gluten Sensitivty: What is the Culprit?" Gastroenterology 2018; 154(3): 471–473.


https://www.medpagetoday.com/gastroenterology/generalgastroenterology/71617?xid=nl_mpt_%20SRCardiology_2018-03-18&eun=g379602d0r&pos=3333

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Antibiotics Before Age 1 Tied to Celiac Disease Risk new
      #373827 - 03/13/19 01:34 PM
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Antibiotics Before Age 1 Tied to Celiac Disease Risk

Results from Scandinavian study differ from TEDDY trial

by Diana Swift, Contributing Writer
March 05, 2019

Exposure to systemic antibiotics in the first year of life was modestly associated with later diagnosis of celiac disease, a national study of Danish and Norwegian children found.

In the observational study of two independent cohorts numbering more than 1.7 million children, a dispensed systemic antibiotic in the first year of life consistently correlated with diagnosed celiac disease, with a pooled odds ratio (OR) of 1.26 (95% CI 1.16-1.36), according to Stine Dydensborg Sander, MD, PhD, of Hans Christian Andersen Children's Hospital in Odense, Denmark, and colleagues.

And a dose-dependent relationship emerged as the number of antibiotic prescriptions increased (OR 1.08, 95% CI 1.05-1.11), they reported in Gastroenterology.

"These findings indicate that childhood exposure to systemic antibiotics may be a risk factor for celiac disease," the authors stated.

Other studies have found no such association, including the 2017 TEDDY study, a multinational cohort of children at high genetic risk of type 1 diabetes and celiac disease. TEDDY "found no association between parentally reported antibiotic exposure and persistently positive celiac disease," at age 4 years, Sander and colleagues noted.

"In contrast to population-based cohort studies that do not include cases of undiagnosed children, screening for celiac disease autoimmunity as the outcome captured all the children with celiac disease and some who never will develop celiac disease. Our findings may be affected if factors related to being diagnosed as opposed to remaining undiagnosed are related to the use of antibiotic," they stated.

Neither a specific type of antibiotic nor age at exposure were prominent factors in celiac disease, suggesting there is no particularly vulnerable age and no differing effect among antibiotic classes. The association was at least as strong for exposure from 0 to 24 months as for 0 to 12 months, Sander's group reported.

The study cohorts consisted of children born in Denmark from 1995 to 2012 (the Danish National Birth Cohort) and followed until May 2015, and children born in Norway from 2004 to 2012 (the Norwegian Mother and Child Cohort Study) and followed until December 2013. The mothers answered questionnaires, sometimes aided by computer-assisted telephone interviews, on infectious diseases and feeding.

The final analysis in the Danish cohort included 1,168,656 children with a median age at end of follow-up of 11.6 years. A diagnosis of celiac disease was registered for 1,427 of these children (0.12%). Systemic antibiotics in the first year of life were dispensed to 451,196 participants without celiac disease (38.7%) and to 622 with celiac disease (43.6%).

The final Norwegian cohort consisted of 537,457 children, with a median age at end of follow-up of 5.4 years. Celiac disease was diagnosed in 1,919 (0.36%) of participants. Systemic antibiotics in the first year of life were dispensed to 98,538 without celiac disease (18.4%) and to 390 with celiac disease (20.3%).

Data from two large subgroups within the final cohort looked at the potentially confounding impact of adjustment for the number of children's maternally reported infections as well as the duration of breastfeeding, examined 6 and 18 months postpartum for 55,082 Danish children (100 with celiac disease) and 53,257 Norwegian children (464 with celiac disease). Neither variable had a measurable impact, nor did prescriptions for topical antifungal drugs, although these were more common in those registered for systemic antibiotics.

The authors pointed out that the intestinal microbiota is considered a player in pathogenesis of celiac disease and one strongly influenced by systemic antibiotics, especially in early life. Early-life infections have been proposed as promoters of celiac disease development and important potential confounders. Some studies have reported associations with types of infection, as well as the number of hospital admissions for infectious diseases, medically attended infectious diseases, and parentally reported infectious diseases.

Jocelyn A. Silvester, MD, of Boston Children's Hospital and Harvard Medical School, commented that understanding the potential ties between antibiotics and celiac disease poses a challenge.

"This is a very difficult question to answer, even though this is one of the largest datasets we have to look at," said Silvester, who was not involved in the study.

She added that it is difficult to tease out the true relationship because of potential confounding factors, noting that not all antibiotic types have the same effect on the microbiota, and not all the infections treated with antibiotics were bacterial but may have included viral and fungal.

Underlying infection rather than antibiotics may have been driving the celiac risk. "But having large well-done studies that try to answer difficult questions is always a step in the right direction," Silvester said.

Study limitations included the difficulty of disentangling the effect of infections and antibiotics in an observational study lacking details of the infections and indications for antibiotic use.

The authors concluded that the findings could have resulted from reverse causality, in which the symptoms of celiac disease can mimic infection, exaggerate infectious symptoms, or raise the risk of infectious diseases, thereby increasing the propensity for prescriptions for antibiotics.

The study was funded by the Novo Nordisk Foundation, the A.P. Møller Foundation, and Odense University Hospital's Research Grants.

The Danish National Birth Cohort was supported by multiple agencies including the Danish National Research Foundation, the Pharmacy Foundation, the Egmont Foundation, the March of Dimes Birth Defects Foundation, and the Health Foundation.

Sander and co-authors disclosed no relevant relationships with industry. Silvester disclosed consulting for Takeda.

last updated 03.06.2019


Source Reference: Sander SD, et al "Association between antibiotics in the first year of life and celiac disease" Gastroenterology 2019; DOI:10.1053/j.gastro.2019.02.039.

https://www.medpagetoday.com/gastroenterology/generalgastroenterology/78384?xid=nl_mpt_SRGastroenterology_2019-03-10&eun=g379602d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=GastroUpdate_031019&utm_term=NL_Spec_Gastroenterology_Update_Active

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