BACKGROUND AND AIMS: Patients with Helicobacter pylori gastritis are more likely to have increased duodenal intraepithelial lymphocytes (IEL); this can be reversed by H. pylori eradication. We hypothesized that: (1) H. pylori-infected celiac disease (CD) patients could have different clinicopathological features from noninfected subjects; and (2) the histopathological responses to a gluten-free diet could be different in H. pylori-infected and noninfected patients. METHODS: Duodenal and gastric biopsies obtained from 80 adults with histologically and serologically confirmed CD before and after 12-18 months of a gluten-free diet were retrospectively evaluated. Gastritis was classified and scored according to the Updated Sydney System; duodenal biopsies were classified using both the Marsh-Oberhuber and a simplified classification proposed by our group. RESULTS: At baseline, 30 patients had H. pylori infection and 50 did not; at follow-up five new infections were detected. Fifteen patients (3 H. pylori-positive and 12 negative) had lymphocytic gastritis. At baseline, a greater proportion of H. pylori-negative patients had severe villous atrophy (p < 0.01), but milder forms were more prevalent in H. pylori-positive patients (p < 0.01). After a gluten-free diet, significant improvement occurred in all duodenal features (p < 0.001), irrespective of H. pylori status; gastric variables did not change, except for lymphocytic, which resolved in 2 infected and 10 noninfected patients. CONCLUSIONS: The clinical features of CD patients are unrelated to H. pylori gastritis, and a gluten-free diet is equally effective in infected as in uninfected patients. The higher prevalence of milder duodenal lesions in CD patients with H. pylori infection suggests that lymphocytosis induced by H. pylori gastric infection becomes less obvious as profound inflammatory and structural changes alter the mucosal architecture. This study also provides further support for a pathogenetic relationship between CD and lymphocytic gastritis.
BACKGROUND AND AIMS: Patients with Helicobacter pylorigastritis are more likely to have increased duodenal intraepithelial lymphocytes (IEL); this can be reversed by H. pylori eradication. We hypothesized that: (1) H. pylori-infected celiac disease (CD) patients could have different clinicopathological features from noninfected subjects; and (2) the histopathological responses to a gluten-free diet could be different in H. pylori-infected and noninfected patients. METHODS: Duodenal and gastric biopsies obtained from 80 adults with histologically and serologically confirmed CD before and after 12-18 months of a gluten-free diet were retrospectively evaluated. Gastritis was classified and scored according to the Updated Sydney System; duodenal biopsies were classified using both the Marsh-Oberhuber and a simplified classification proposed by our group. RESULTS: At baseline, 30 patients had H. pyloriinfection and 50 did not; at follow-up five new infections were detected. Fifteen patients (3 H. pylori-positive and 12 negative) had lymphocytic gastritis. At baseline, a greater proportion of H. pylori-negative patients had severe villous atrophy (p < 0.01), but milder forms were more prevalent in H. pylori-positive patients (p < 0.01). After a gluten-free diet, significant improvement occurred in all duodenal features (p < 0.001), irrespective of H. pylori status; gastric variables did not change, except for lymphocytic, which resolved in 2 infected and 10 noninfected patients. CONCLUSIONS: The clinical features of CDpatients are unrelated to H. pylorigastritis, and a gluten-free diet is equally effective in infected as in uninfected patients. The higher prevalence of milder duodenal lesions in CDpatients with H. pyloriinfection suggests that lymphocytosis induced by H. pylorigastric infection becomes less obvious as profound inflammatory and structural changes alter the mucosal architecture. This study also provides further support for a pathogenetic relationship between CD and lymphocytic gastritis.
Authors: Benjamin Lebwohl; Martin J Blaser; Jonas F Ludvigsson; Peter H R Green; Andrew Rundle; Amnon Sonnenberg; Robert M Genta Journal: Am J Epidemiol Date: 2013-10-11 Impact factor: 4.897
Authors: Kamran Rostami; David Aldulaimi; Geoffrey Holmes; Matt W Johnson; Marie Robert; Amitabh Srivastava; Jean-François Fléjou; David S Sanders; Umberto Volta; Mohammad H Derakhshan; James J Going; Gabriel Becheanu; Carlo Catassi; Mihai Danciu; Luke Materacki; Kamran Ghafarzadegan; Sauid Ishaq; Mohammad Rostami-Nejad; A Salvador Peña; Gabrio Bassotti; Michael N Marsh; Vincenzo Villanacci Journal: World J Gastroenterol Date: 2015-03-07 Impact factor: 5.742
Authors: Jennifer M Noto; Jennifer A Gaddy; Josephine Y Lee; M Blanca Piazuelo; David B Friedman; Daniel C Colvin; Judith Romero-Gallo; Giovanni Suarez; John Loh; James C Slaughter; Shumin Tan; Douglas R Morgan; Keith T Wilson; Luis E Bravo; Pelayo Correa; Timothy L Cover; Manuel R Amieva; Richard M Peek Journal: J Clin Invest Date: 2012-12-21 Impact factor: 14.808