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Helicobacter Pylori Infection in Celiac Disease Patients
http://www.celiac.com/articles/1124/1/Helicobacter-Pylori-Infection-in-Celiac-Disease-Patients/Page1.html
Scott Adams

In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I created The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

 
By Scott Adams
Published on 03/26/2007
 
Celiac.com 03/26/2007 - In is known that increased duodenal intraepithelial lymphocytes (IEL) are

Celiac.com 03/26/2007 - In is known that increased duodenal intraepithelial lymphocytes (IEL) are more common in celiac patients with Helicobacter pylori gastritis (H. pylori) than in those celiacs without Helicobacter pylori. It is also known that the elimination of Helicobacter pylori can reverse this problem.

The study was motivated by the following two hypotheses:

  • Celiac patients with Helicobacter pylori might present different clinicopathological profiles from those celiacs without H.pylori.
  • Celiac patients with Helicobacter pylori might show different histopathological responses to a gluten-free diet than those celiacs without H.pylori.

The research team compared the duodenal and gastric biopsies of 80 adults who had histologically and serologically confirmed CD. The biopsies were taken both before and after patients had adhered to a gluten-free diet for 12 to 18 months.

The team classified and scored gastritis using the Updated Sydney System. They classified duodenal biopsies using both the Marsh-Oberhuber and a simplified classification developed by the team.

Three test subjects who were positive for Helicobacter pylori, and 12 who were negative (a total of 15 test subjects), presented with lymphocytic gastritis.

Overall, a greater proportion of Helicobacter pylori-negative patients had severe villous atrophy (p < 0.01), while the Helicobacter pylori-positive patients more commonly showed milder forms (p < 0.01).

Regardless of their initial Helicobacter pylori status, all subjects showed marked improvement of duodenal aspects following a gluten-free diet (p < 0.001).

With the exception of the intraepithelial lymphocytes (IEL), which returned to normal in two Helicobacter pylori-positive patients, and in ten Helicobacter pylori-positive patients, gastric variables remained unchanged.

The study concludes that Helicobacter pylori gastritis is not related to the clinical features of celiac disease, and that a gluten-free diet is equally effective for both groups.

The study also notes that the inflammatory and structural changes to the mucosal architecture that are associated with celiac disease might eclipse some of the signs of lymphocytosis induced by Helicobacter pylori gastric infection.

The study also further documents the pathogenic connections between celiac disease and lymphocytic gastritis.

Am J Gastroenterol. 2006;101(8):1880-1885.