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  • Jefferson Adams
    Jefferson Adams

    Patients with Active Celiac Disease At Slightly Higher Risk for Eosinophilic Esophagitis

    Celiac.com 09/09/2015 - Some researchers and clinicians suspect a connection between eosinophilic esophagitis (EoE) and celiac disease, but prior studies have shown conflicting results

    Image: Wikimedia Commons--Ed Uthman, MD.A team of researchers recently set out to determine the relationship between EoE and celiac disease among patients with concomitant esophageal and duodenal biopsies. The research team included Elizabeth T. Jensena, Swathi Eluria, Benjamin Lebwohl, Robert M. Gentab, and Evan S. Dellon.

    For their cross-sectional study, they team used data covering the period from January 2009 through June 2012 from a U.S. national pathology database.

    They defined esophageal eosinophilia as the presence of ≥15 eosinophils per high-power field. The crude and age and sex adjusted odds of esophageal eosinophilia for patients with active celiac disease were compared with those without celiac disease.

    Sensitivity analyses were performed by using more stringent case definitions and by estimating the associations between celiac disease and reflux esophagitis and celiac disease and Barrett’s esophagus.

    Out of 292,621 patients in the source population, the team looked at data from 88,517 patients with both esophageal and duodenal biopsies. Four thousand one hundred one (4.6%) met criteria for EoE, and 1203 (1.4%) met criteria for celiac disease. Patients with celiac disease had 26% higher odds of EoE than patients without celiac disease (adjusted odds ratio, 1.26; 95% confidence interval [CI], 0.98–1.60).

    The strength of the connection varied according to EoE case definition, but all definitions showed a weak positive association between the two conditions.

    Interestingly, this study showed no connection between celiac disease and reflux esophagitis (adjusted odds ratio 0.95; 95% CI, 0.85–1.07) or between celiac disease and Barrett’s esophagus (adjusted odds ratio 0.89; 95% CI, 0.69–1.14).

    Overall, this study showed only a weak increase in EoE in patients with celiac disease. The connection strengthened in direct relation to the strength of definitions of EoE, and was not seen with other esophageal conditions.

    Doctors should consider concomitant EoE in patients with celiac disease where clinical indications support it.

    Disclosures: Dellon reports receiving research funds from Meritage Pharma, consulting for Aptalis, Novartis, Receptos and Regeneron, and receiving an educational grant from Diagnovus.

    Source:



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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Jefferson Adams
    Celiac.com 10/12/2012 - What is the relationship between breastfeeding, the age of gluten introduction and rates of celiac disease?
    A number of studies have shown that increased breastfeeding may provide some protection against celiac disease. However, one study found no change in the overall prevalence of celiac disease in breastfed infants compared to controls, suggesting that breastfeeding may only delay the presentation of the disease but, does not prevent it. Other studies show no significant difference in the prevalence of celiac disease between breastfed and non-breastfed patients.
    Data from the Swedish celiac disease epidemic suggest a 3% prevalence of celiac disease in the children born during the epidemic. An analysis by Ivarsson et al. of children born during the epidemic, found that children under 2 years of age had a lower risk of celiac disease if they were still being breastfed when dietary gluten was introduced (odds ratio 0.59, 95, with a confidence interval 0.42–0.83). Children who continued breastfeeding after gluten was introduced to their diet showed a further decrease in the risk for celiac disease (OR 0.36, 95% CI 0.26–0.51).
    A meta-analysis that included the Ivarsson data, showed celiac disease risk was significantly lower in infants who were breastfed at the time of gluten introduction (pooled OR 0.48, 95% CI 0.40–0.59), compared to infants who were not breastfed at the time of first gluten exposure.
    A later study, by Akobeng and others, estimated that breastfeeding all babies in the UK at the time of gluten introduction, would prevent 2500 cases of celiac disease every year.
    The best data currently available on celiac disease and the age of gluten introduction comes from a prospective study by Norris et al. The study followed 1560 children in Denver between 1994 and 2004. This study showed that children exposed to gluten in the first 3 months of life had a fivefold increased risk of having celiac disease than children exposed to gluten between 4 and 6 months of age, while children exposed to gluten at 7 months old or later had an almost twofold increased risk compared with those exposed at 4 to 6 months (hazard ratio 1.87, 95% CI 0.97–3.60).
    When the analysis was limited to biopsy-diagnosed celiac disease, the hazard ratio was 23.97 (95% CI 4.55–115.9) for children exposed to gluten during the first 3 months of life compared to the 4–6 months exposure group, and 3.98 (95% CI 1.18–13.46) in the group exposed at 7 months or later
    What remains unclear, is whether breastfeeding and the age of introduction of gliadin prevent celiac disease or merely delay its onset.
    To clarify the relationship between breastfeeding, the age at which gluten is introduced into the diet, and celiac disease, the EU has funded a prospective study, called PREVENTCD, FP6, in 10 European centers. The PREVENTCD study recruited pregnant women with a family history of celiac disease, and determined HLA4 of the newborn at birth.
    By the end of December 2010, researchers had recruited a total of 1345 children at birth and enrolled 986 with positive HLA DQ status.
    Researchers instructed mothers to breastfeed for 6 months, if possible. Beginning at the age of 4 months, the researchers placed the infants into randomized study groups, and fed them 100 mg of gliadin or a non-gliadin placebo every day.
    The full data won't be available until all children reach the age of 3 years of age, but the researchers hope that the study will offer definitive answers on the relationship between breastfeeding and the age of gluten introduction and rates of celiac disease.
    Until new information become available, the ESPGHAN Committee on Nutrition recommendations remain in effect. This recommendations state that gluten should be introduced to infants no earlier than 4 months of age, and no later than 7 months, and that the introduction should be gluten be made while the infant is still being breastfed.
    This information was compiled by researcher R. Shamir of the Institute for Pediatric Gastroenterology, Nutrition and Liver Diseases, at the Schneider Children's Medical Center of Israel, Petah Tikva, affiliated with Sackler Faculty of Medicine, Tel Aviv University in Ramat Aviv, Israel.
    Source:
    Isr Med Assoc J. 2012 Jan;14(1):50-2.

    Jefferson Adams
    Celiac.com 07/27/2015 - First-degree relatives of individuals with celiac disease are at increased risk for this disorder, but little is known about their risk for other autoimmune diseases.
    A research team recently set out to assess the risk of non-celiac autoimmune disease in first-degree relatives and spouses of people with celiac disease.
    The research team included Louise Emilsson, Cisca Wijmenga, Joseph A. Murray, and Jonas F. Ludvigsson. They are variously affiliated with the Primary Care Research Unit, Vårdcentralen Värmlands Nysäter, Värmland County, Sweden, the Department of Health Management and Health Economy, Institute of Health and Society, University of Oslo, Oslo, Norway, the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, the Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    The team found individuals with celiac disease by searching computerized duodenal and jejunal biopsies, collected from 1969 through 2008, at 28 pathology departments in Sweden.
    The team found 29,096 patients with celiac disease based on biopsy reports of villous atrophy of Marsh grade 3 or higher and matched individuals with celiac disease with up to 5 of 144,522 non-celiac control patients based on sex, age, county, and calendar year.
    Through Swedish health care registries, the team identified all first-degree relatives (fathers, mothers, siblings, and offspring) and spouses of 84,648 individuals with celiac disease, and 430,942 control subjects. The team used Cox regression analysis to calculate hazard ratios (HRs) for non-celiac autoimmune disease, such as Crohn’s disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis, within these groups.
    Cox analysis showed that during the follow-up period averaging just under 11 years, nearly 3333, or 4%, of the first-degree relatives of patients with celiac disease, and 12,860 relatives of controls (3.0%), had an autoimmune disease other than celiac disease.
    First-degree relatives of people with celiac disease had an increased risk of non-celiac autoimmune disease, compared with controls (HR, 1.28; 95% confidence interval, 1.23–1.33), as did spouses (HR, 1.20; 95% confidence interval, 1.06–1.35).
    Risk estimates for non-celiac autoimmune disease did not differ between first-degree relatives and spouses of individuals with celiac disease (interaction test: P = .11). Hazard Ratios for non-celiac autoimmune disease were highest in the first 2 years of follow-up evaluation.
    First-degree relatives and spouses of individuals with celiac disease have a significantly higher risk of non-celiac autoimmune disease.
    In addition to genetic factors, environmental factors and better awareness, testing and diagnosis might influence rates of autoimmune disorders in first-degree relatives of individuals with celiac disease.
    Source:
     Clinical Gastroenterology and Hepatology. DOI: http://dx.doi.org/10.1016/j.cgh.2015.01.026

    Jefferson Adams
    Celiac.com 08/17/2015 - In an interesting update, researcher Giuseppe Mazzarella, of the Immuno-Morphology Lab at the Institute of Food Sciences of the National Council Research in Avellino, Italy recently set out to examine the role of effector and suppressor T cells in celiac.
    Celiac disease is a T-cell-mediated immune disorder in which gliadin-derived peptides activate lamina propria effector CD4+ T cells.
    This activation triggers the release of cytokines, compatible with a Th1-like pattern, which play a crucial role in the development of celiac disease, and which control many aspects of the inflammatory immune response.
    Previous studies revealed that a novel subset of effector T cells, marked by expression of high levels of IL-17A, termed Th17 cells, plays a key role in celiac disease.
    Although these effector T cell subsets produce pro-inflammatory cytokines, which cause significant tissue damage in celiac sufferers, recent studies have suggested the existence of additional CD4(+) T cell subsets with suppressor functions.
    These subsets include type 1 regulatory T cells and CD25(+)CD4(+) regulatory T cells, expressing the master transcription factor Foxp3, which have important implications for the development and progression of celiac disease.
    Source:
    World J Gastroenterol. 2015 Jun 28;21(24):7349-56. doi: 10.3748/wjg.v21.i24.7349.

    Jefferson Adams
    Celiac.com 08/19/2015 - For the first time since it was described and named by 1st century Greek physician Aretaeus of Cappadocia, first linked to wheat in the 1940's, and specifically linked to gluten in 1952, scientists have discovered the cause of celiac disease.
    Professor Ludvig Sollid, and his team at the Centre for Immune Regulation at University of Oslo, have discovered that people with celiac disease suffer from one of two defective human leukocyte antigens (HLAs), which cause the immune system to see gluten molecules as dangerous, triggering the immune response that causes classic celiac-associated inflammation and other symptoms.
    To be true, the team was not working in the dark. They were armed with a complete map of the genes, an understanding that two types of HLA (HLA-DQ2 and HLA-DQ8) predispose a person for celiac disease, and the very crucial recent discovery by a team of German colleagues that celiac patients have antibodies for a very precise enzyme: transglutaminase 2.
    "We also found that the bits of gluten that were presented to the T-cells have some changes caused by an enzyme in the body – transglutaminase 2", says Sollid. HLAs are proteins which act as markers, binding to fragments of other proteins, and telling T-cells how to treat them.
    So it wasn't much of a stretch for Professor Sollid's team to determine that the defective HLAs bind to fragments of gluten, causing the T-cells to treat them as bacteria or viruses.
    Basically, two HLA types present gluten remnants to the T-cells, causing the T-cells to regard the gluten as dangerous, and to trigger immune reactions that cause inflammation in the intestines, and this is what causes celiac disease.
    "We think that this is huge," Sollid said. "We understand the immune cells that are activated and why they are activated."
    At present, Professor Sollid and his group are investigating how antibodies against transglutaminase are formed.
    This is a simple, but huge moment in the annals of medicine and in the annals of celiac disease. It's a discovery that will help researchers develop new approaches to treatment, and/or a cure for celiac disease in the future.
    Source:
    Med.uio.no

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    The celiac tests are: TTG IgA TTG IgG DGP IgA DGP IgG  EMA IgA And....Immunogobulin A (IgA).  This test is used only as a control test when checking for celiac disease.  If your body is not producing enough IgA, the IgA celiac tests are invalid or will not work.    You would also have a immune deficiency issues too.  But that is a separate issue.   The previous link I gave you spells out the test names which are long!  😆
    Guys, thanks so much for taking time out of your day to reply to me. I'm going to ask my doc for the test, she's super and I'm sure she will go for it. This whole thing has sure taken it's toll on me both mentally and physically the last couple of months... to be honest, I don't care if I have it or not, I just want to know what's going on
    Dziekuje bardzo for that information,, CyclingLady! And you are correct, at least in my case --- I have been EXTREMELY reluctant to eat out in restaurants since going gluten free last year, and have only done so a small handful of times, under very strict conditions and only after talking to both the serving staff and the chefs/cooks at some length.  Now, on the Fasano Diet, it is simply not an option. Honestly, I do not understand this recent mania for eating out ALL the time!  Not on
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