Biomarkers in various types of atrophic gastritis and their diagnostic usefulness.

Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.