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REVIEWS
Autoimmune atrophic gastritis pathogenesis, pathology and management
William L. Neumann, Elizabeth Coss, Massimo Rugge and Robert M. Genta
Abstract | Autoimmune gastritis is a chronic progressive inflammatory condition that results in the replacement ofthe parietal cell mass by atrophic and metaplastic mucosa. A complex interaction of autoantibodiesagainst the parietal cell proton pump and sensitized Tcells progressively destroy the parietal cells, inducing hypochlorhydria and then achlorhydria, while autoantibodies against the intrinsic factor impair the absorptionof vitaminB12. The resulting cobalamin deficiency manifests with megaloblastic anaemia and neurological and systemic signs and symptoms collectively known as pernicious anaemia. Previously believed to be predominantly a disease of elderly women of Northern European ancestry, autoimmune gastritis has now been recognizedin all populations and ethnic groups, but because of the complexity of the diagnosis no reliable prevalencedata are available. For similar reasons, as well as the frequent and often unknown overlap with Helicobacter pylori infection, the risk of gastric cancer has not been adequately assessed in these patients. This Review summarizes the epidemiology, pathogenesis and pathological aspects of autoimmune metaplastic atrophic gastritis. We also provide practical advice for the diagnosis and management of patients with this disease.
Neumann, W.L. et al. Nat. Rev. Gastroenterol. Hepatol. 10, 529541 (2013); published online 18 June 2013; http://www.nature.com/doifinder/10.1038/nrgastro.2013.101
Web End =doi:10.1038/nrgastro.2013.101
Introduction
Atrophy, derived from the Greek words and (literally meaning not fed), is used as a synonym for wasting (as, for example, in atrophy of muscles). When applied to the gastric mucosa, atrophy is defined as the reduction or disappearance of the native gastric glands, irrespective of whether they have been replaced by nothing, fibrosis, or a type of epithelium that should normally not be there (metaplasia).1 Both the antrum and corpus might be involved, but evident functional and clinical consequences occur only when atrophy affects the latter. The decrease or disappearance of parietal cells results in reduced or absent acid production (hypochlorhydria or achlorhydria) and loss of intrinsic factor. An increased gastric pH enables the colonization of the stomach by bacteria (normally deterred by the low physiological pH) that might produce nitrites and promote carcinogenesis; it interferes with the absorption of certain indispensable substances (such as iron and vitaminB12); and by continuously stimulating the gastrin-secreting cells of the antrum it induces...