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    Decreased Risk of Celiac Disease in Patients with Helicobacter Pylori Colonization


    Jefferson Adams

    Celiac.com 02/06/2014 - One theory that has emerged to account for the rise in celiac disease in recent decades is the "hygiene hypothesis," which proposes that decreased exposure to bacterial antigens may trigger celiac autoimmunity.

    Photo: CC--Eric SkiffA team of researchers recently set out to determine whether one such bacterial antigen, Helicobacter pylori infection and celiac disease were associated among patients undergoing upper gastrointestinal endoscopy.

    The research team included Benjamin Lebwohl, Martin J. Blaser, Jonas F. Ludvigsson, Peter H. R. Green, Andrew Rundle, Amnon Sonnenberg and Robert M. Genta.

    Team members are are variously affiliated with the Celiac Disease Center, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York; Department of Medicine, Langone Medical Center, New York University; Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital and Karolinska Institutet in Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medicine, Oregon Health & Science University, Portland, Oregon; Department of Pathology, UT Southwestern Medical Center, University of Texas, Dallas, Texas; and Miraca Life Sciences Research Institute, Irving, Texas.

    The team conducted a cross-sectional study of patients who received esophago-gastroduodenoscopy with submission of gastric and duodenal biopsies to commercial US pathology laboratory Miraca Life Sciences, Inc., in Irving, Texas, from January 2008 to June 2012. They compared the rates of H. pylori in celiac patients with rates for people without celiac disease. They conducted multiple logistic regression analysis, and adjusted odds ratios based on patient age, gender, and racial, ethnic, and socioeconomic factors.

    Of 136,179 patients, a total of 2,689 (2.0%) had celiac disease. Interestingly, H. pylori rates were significantly lower in patients with celiac disease than in those without celiac disease. In all, just 4.4% of celiac patients had H. pylori, compared with 8.8% of patients without celiac disease (P < 0.0001).

    Even after the team adjusted for the above variables, the inverse relationship remained strong (adjusted odds ratio (OR) = 0.48, 95% confidence interval (CI): 0.40, 0.58). The relationships were similar in both men (unadjusted OR = 0.51, 95% CI: 0.38, 0.69) and women (unadjusted OR = 0.46, 95% CI: 0.36, 0.58) and in all age groups.

    The results show that that H. pylori presence and celiac disease are inversely associated, even when adjustments are made for important socioeconomic factors. The team suggests that future studies address whether H. pylori modulates immune responses to ingested gluten.

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    Guest Bob Kalkman

    Posted

    Anecdotal evidence of one: My celiac disease was triggered by a 3 week dosing of Augmentin, so I fully believe gut bacterial has an affect on this - and many other health issues. Gut bacteria is criminally misunderstood.

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    Guest Kristin Jordan

    Posted

    I lived in a Third World country as a child and did lots of Third World travel, and I don't have h. pylori. My celiac disease likely began in my first year of life, before I moved away from the U.S. I've wondered if my active celiac disease somehow prevented me from getting infected with h. pylori.

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    Guest Brittany

    Posted

    I believe I've always had allergies, as I had asthma from birth until 5 years old. DNA testing shows I have HLA DQ2 and HLA DQ8. My health began to deteriorate after a battle with Mono when I was 21, I was placed on multiple antibiotics to clear the ongoing infection in my tonsils, which resulted in a tonsillectomy 2 months later. I didn't have the energy to even leave my bedroom. After the birth of my daughter, almost 2 years ago, when I was 25, I developed many allergies and celiac. I do believe antibiotics and gut bacteria play an important role in the development of celiac disease, as well as, allergies. I've also read that EBV (mono virus) is in essentially all people with Burkitt Lymphoma. Makes we wonder what kind of roles viruses play in the development of celiac.

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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, and science. He previously served as Health News Examiner for Examiner.com, and provided 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 Dangerous Grains by James Braly, MD and Ron Hoggan, MA.

  • Related Articles

    Jefferson Adams
    Iranian Study Finds Connection Between Helicobacter pylori and Celiac Disease
    Celiac.com 04/25/2011 - Research shows that celiac disease is associated with numerous gastric abnormalities. An international research team recently set out to examine the association between rates of celiac disease and Helicobacter pylori infection in an Iranian population of 250 patients.
    The research team included Mohammad Rostami Nejad BS1, Kamran Rostami MD PhD, Yoshio Yamaoka MD PhD, Reza Mashayekhi MD1, Mahsa Molaei MD, Hossein Dabiri PhD, David Al Dulaimi MD, Dariush Mirsattari MD, Homayoun Zojaji MD, Mohsen Norouzinia MD, and Mohammad Reza Zali MD FACG AGAF.
    The team members are variously affiliated with the Research Institute of Gastroenterology and Liver Disease, Shahid Beheshti University, M.C., in Tehran, Iran, the School of Medicine, University of Birmingham in the UK, the Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston, Texas, and the Department of Gastroenterology, Alexandra Hospital, Redditch, UK.
    For the study, the team took topsides from the gastric antrum and duodenum. They assessed morphology and histology using the updated Sydney system and modified Marsh criteria, respectively.
    In order to simplify the assessment of gastric lesions, the team classified gastritis in both macroscopic and microscopic stages. They screened for anti-tissue transglutaminase antibody to determine the presence of celiac disease.
    Of the 250 patients, 232 (93%) showed histological evidence of Helicobacter pylori infection, while 24 patients (10%) showed histological abnormalities (Marsh I to IIIc). Of the 24 patients with histological abnormalities 20 (83%) showed Helicobacter pylori infection.
    Of the total 250 patients, 25 patients (10%) showed positive anti-tissue transglutaminase antibody screens, nine (3.6%) of whom showed microscopic and macroscopic enteritis (Marsh I to IIIc).
    Clinically, there was no way to distinguish the presentation of celiac disease from those cases infected with Helicobacter pylori. Histology, even in patients with positive antibody screens, was non-specific and not useful.
    The results also showed a high prevalence of Helicobacter pylori infection and chronic gastritis in the study group. However, neither was associated with celiac disease, but rather, matched average rates in Western population studies.
    Source:

    Archives of Iranian Medicine, March 2011

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