Proton Pump Inhibitor Use in Patients with Helicobacter Gastritis Increases the Risk for Corpus-Predominant Gastritis and Preneoplastic Lesions of the Proximal Stomach
Kirthi R Kumar, Ramiz Iqbal, Elizabeth Coss, Christina Park, Byron Cryer, Robert M Genta. Miraca Life Sciences Research Institute, Irving, TX; UT Southwestern Medical School, Dallas, TX; Dallas VAMC, Dalllas, TX; Dallas VAMC, Dallas, TX
Background: Experimental studies have shown that proton pump inhibitors (PPI) use may cause a shift from H.pylori antrum-predominant (AP) gastritis to a corpus-predominant (CP) pattern. It is unclear whether in the clinical setting therapeutic PPI use affects the topography of gastritis. This study was designed to test the hypothesis that the patterns of gastritis in H. pylori-infected patients are different in PPI users and non-users.
Design: Topographically defined biopsies (2 each from corpus and antrum, and 1 from incisura) were obtained from patients recruited into a novel therapeutic trial for H. pylori. History of PPI and Histamine2-receptor blockers (H2-B) use was collected. Two blinded pathologists used the Updated Sydney System to evaluate the biopsies. Patients were assigned to one of 3 categories based on their gastritis scores: AP-gastritis (inflammatory scores of antrum and incisura were greater those of the corpus); CP-gastritis (corpus scores were greater than antrum and incisura scores); and pangastritis (two sets of scores were identical). PPI and H2-B use were then disclosed and the topographic distribution of the components of gastritis was analyzed.
Results: There were 97 patients with H. pylori gastritis (median age 66 years, 89% men, 52% white). CP gastritis was found in 40% of PPI users versus 15% in non users (OR 4.19; 95% CI 1.47-11.9; p<0.01). PPI use was also associated with increased atrophy and intestinal metaplasia (IM) in the corpus (16.4% in users versus 7.3% in non-users) and IM in the incisura (18.8% vs. 9.7%), but the differences did not attain statistical significance. These associations remained similar for PPI use shorter or longer than one month. H2-blocker use was unrelated to the topography of gastritis. Age, sex, and race had no influence on the topography of gastritis.
Conclusions: Even short-term PPI use can affect the distribution of inflammation in H. pylori gastritis and may induce or accelerate the development of preneoplastic lesions in the transitional and oxyntic mucosa. Our results provide support for the Maastricht guidelines, widely followed in Europe but not formally espoused by the American College of Gastroenterology, that recommend eradication of H. pylori prior to long-term PPI use.
Wednesday, March 6, 2013 1:00 PM
Poster Session VI # 75, Wednesday Afternoon