ATROPHIC BODY GASTRITIS - DISTINCT FEATURES ASSOCIATED WITH HELICOBACTER-PYLORI INFECTION

Background. Usually, atrophic body gastritis has been considered an au toimmune disease characterized by the presence of parietal cell antibo dies. Previous investigations into the role of Helicobacter pylori inf ection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively i nvestigated population of patients with corpus-predominant atrophic ga stritis. Patients and Methods. A consecutive series of 67 newly diagno sed cases of atrophic body gastritis was derived from a screening of 3 26 patients with unexplained anemia or dyspepsia. Criteria for diagnos is were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay an d urease test. The gastritis status of both the fundic and antral muco sa were graded according to the Sydney system. Parietal cell and intri nsic factor antibodies also were determined. Results. Active H. pylori infection was present in 26.8% of our patients and allowed us to iden tify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this su bpopulation, a higher prevalence of gastric cancer familial history wa s found. Presence elf parietal cell antibodies showed a similar preval ence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histolog ical differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia. Conclu sion. Active H. pylori infection, a potential cause of oxyntic gland a trophy, is found in one-fourth of patients with newly diagnosed atroph ic body gastritis.