PREVALENCE OF HELICOBACTER-PYLORI INFECTION IN PATIENTS WITH LARGE GASTRIC FOLDS - EVALUATION AND FOLLOW-UP WITH ENDOSCOPIC ULTRASOUND BEFORE AND AFTER ANTIMICROBIAL THERAPY

Citation
C. Avunduk et al., PREVALENCE OF HELICOBACTER-PYLORI INFECTION IN PATIENTS WITH LARGE GASTRIC FOLDS - EVALUATION AND FOLLOW-UP WITH ENDOSCOPIC ULTRASOUND BEFORE AND AFTER ANTIMICROBIAL THERAPY, The American journal of gastroenterology, 90(11), 1995, pp. 1969-1973
Citations number
18
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00029270
Volume
90
Issue
11
Year of publication
1995
Pages
1969 - 1973
Database
ISI
SICI code
0002-9270(1995)90:11<1969:POHIIP>2.0.ZU;2-V
Abstract
Objectives: Large gastric folds may result from infectious, inflammato ry, neoplastic, vascular, and infiltrative disorders involving a part or the entire gastric wall, Helicobacter pylori infection of the gastr ic mucosa is associated with an active gastritis characterized by infi ltration of the mucosa and submucosa with neutrophils, eosinophils, ma crophages, and lymphocytes. The purposes of the study were: 1) to stud y patients with large gastric folds noted on computed tomography, uppe r gastrointestinal series, or endoscopy, with endoscopy and biopsies a nd endoscopic ultrasound to determine the prevalence of H. pylori infe ction and the location of the thickening within the gastric wall; 2) t o reexamine H. pylori-infected patients with EUS after antimicrobial t herapy to determine whether resolution of the wall thickening accompan ied eradication of H. pylori and improvement of histological gastritis , Methods: Thirty-two patients with thickened gastric folds were studi ed. Eighteen patients had H. pylori infection and were treated with am oxicillin 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 gast ric biopsies were obtained Results: Eighteen of 32 patients had H. pyl ori infection and gastritis, In the H. pylori-infected patients with g astritis, EUS demonstrated diffuse thickening of the inner three layer s (mucosa-lumen interface, deep mucosa, submucosa) without thickening of the 4th and 5th layers of the gastric wall. After antimicrobial the rapy and resolution of gastritis, EUS demonstrated concomitant resolut ion of this thickening and normalization of layers 1-3. Conclusions: H . pylori gastritis is a common cause of gastric wall thickening. EUS a llows intrinsic localization of the gastric wall thickening in patient s with large gastric folds and H. pylori infection and documents the r esolution of this wall thickening upon eradication of H. pylori and re solution of gastritis.