Helicobacter pylori infection in patients with celiac disease

V Villanacci, G Bassotti, B Liserre… - Official journal of the …, 2006 - journals.lww.com
V Villanacci, G Bassotti, B Liserre, A Lanzini, F Lanzarotto, RM Genta
Official journal of the American College of Gastroenterology| ACG, 2006journals.lww.com
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 …
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.
Lippincott Williams & Wilkins