Role of Helicobacter pylori and autoimmunity in serological atrophic corpus gastritis in a Dutch primary care community

Abstract

The seroprevalence of atrophic corpus gastritis in this primary care community is 3.4%. When compared with controls, the approximate relative risk of having atrophic corpus gastritis was significantly higher (P < 0.025) for antibodies to parietal cells (24.0) than to H. pylori (1.62). In view of the decreasing risk of H. pylori infection in the western world, it is likely that the impact of H. pylori on the development of atrophic corpus gastritis will further diminish.

The Diagnostic Value of Anti-Parietal Cell and Intrinsic Factor Antibodies, Pepsinogens, and Gastrin-17 in Corpus-Restricted Atrophic Gastritis

“…Gastrin-17 (G-17) is expected to be high in CRAG as a result of the compensatory mechanism when hydrochloric acid secretion in the corpus decreases due to parietal cell depletion but atrophy in the antrum is lacking, a situation in which production of G-17 increases [ 14 ]. PGI/II and G-17 are well-established biomarkers for gastric atrophy with a high correlation with gastric biopsy [ 15 , 16 ]. All of the above-listed markers have been reported to be of value for the detection of atrophic autoimmune gastritis; however, we are lacking clear diagnostic algorithms based on the routinely available serological tests.…”