Prevalence of Helicobacter pylori infection in patients with large gastric folds: evaluation and follow-up with endoscopic ultrasound before and after antimicrobial therapy.

Abstract

Large gastric folds may result from infectious, inflammatory, neoplastic, vascular, and infiltrative disorders involving a part or the entire gastric wall. Helicobacter pylori infection of the gastric mucosa is associated with an active gastritis characterized by infiltration of the mucosa and submucosa with neutrophils, eosinophils, macrophages, and lymphocytes. The purposes of the study were: 1) to study patients with large gastric folds noted on computed tomography, upper gastrointestinal series, or endoscopy, with endoscopy and biopsies and endoscopic ultrasound to determine the prevalence of H. pylori infection and the location of the thickening within the gastric wall; 2) to reexamine H. pylori-infected patients with EUS after antimicrobial therapy to determine whether resolution of the wall thickening accompanied eradication of H. pylori and improvement of histological gastritis. Thirty-two patients with thickened gastric folds were studied. Eighteen patients had H. pylori infection and were treated with amoxicillin 1 g b.i.d. and omeprazole 40 mg b.i.d. x 14 days. One month after antimicrobial therapy, patients were reexamined by EUS, and gastric biopsies were obtained. Eighteen of 32 patients had H. pylori infection and gastritis. In the H. pylori-infected patients with gastritis, EUS demonstrated diffuse thickening of the inner three layers (mucosa-lumen interface, deep mucosa, submucosa) without thickening of the 4th and 5th layers of the gastric wall. After antimicrobial therapy and resolution of gastritis, EUS demonstrated concomitant resolution of this thickening and normalization of layers 1-3. H. pylori gastritis is a common cause of gastric wall thickening. EUS allows intrinsic localization of the gastric wall thickening in patients with large gastric folds and H. pylori infection and documents the resolution of this wall thickening upon eradication of H. pylori and resolution of gastritis.