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Atrophic Body Gastritis: Distinct Features Associated with Helicobacter pylori Infection
Author(s) -
Annibale Bruno,
Marignani Massimo,
Azzoni Cinzia,
D’ambra Giancarlo,
Caruana Pietro,
D’adda Tiziana,
Fave Gianfranco Delle,
Bordi Cesare
Publication year - 1997
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.1997.tb00060.x
Subject(s) - atrophic gastritis , helicobacter pylori , gastritis , gastroenterology , medicine , parietal cell , achlorhydria , rapid urease test , gastric mucosa , population , pernicious anemia , atrophy , helicobacter , autoimmune gastritis , antrum , foveolar cell , pathology , stomach , anemia , environmental health
Background. Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus‐predominant atrophic gastritis. Patients and Methods. A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis 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 and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined. Results. Active H. pylori infection was present in 26.8% of our patients and allowed us to identify 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 subpopulation, a higher prevalence of gastric cancer familial history was found. Presence of parietal cell antibodies showed a similar prevalence in H. pylori –positive and H. pylori –negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia. Conclusion. Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one‐fourth of patients with newly diagnosed atrophic body gastritis.