Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. PMID:29095917Īutoimmune gastritis: Pathologist's viewpoint.Ĭoati, Irene Fassan, Matteo Farinati, Fabio Graham, David Y Genta, Robert M Rugge, Massimo PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects. pylori-induced atrophic gastritis were associated with different gastric microbial profiles. pylori-induced atrophic gastritis versus autoimmune atrophic gastritis, and that both these groups showed increases in fumarate reductase. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. Patients with autoimmune atrophic gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). pylori-induced atrophic gastritis and autoimmune atrophic gastritis) were selected from a cohort of 1400. 95 patients (in groups representing normal stomach, PPI treated, H. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. Helicobacter pylori-induced atrophic gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Comparison of the human gastric microbiota in hypochlorhydric states arising as a result of Helicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor useĮccles, Richard Duckworth, Carrie A.

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