Autoimmune gastritis, with or without pernicious anemia: epidemiology, risk factors, and clinical management

Abstract

Autoimmune gastritis (AIG) is a chronic immune-mediated, inflammatory condition that involves the destruction of the gastric oxyntic mucosa through the autoimmune-mediated loss of parietal cells, with replacement by atrophic and metaplastic tissue. Diagnosing AIG is important, given the need for ongoing clinical management and vigilance with respect to downstream complications, the most serious of which is gastric adenocarcinoma. Other clinical consequences include gastric neuroendocrine tumors, consequences related to decreased gastric acid and decreased intrinsic factor due to parietal cell destruction and antibodies against intrinsic factor (e.g. micronutrient deficiencies), as well as concomitant autoimmune disorders. Considering the prevalence of AIG and the potential for severe clinical outcomes, it is important to engage in efforts to reduce practice pattern variability related to diagnosis and management. Accordingly, herein, we review of the epidemiology, pathogenesis, clinical presentation of AIG, including both gastric and extragastric manifestations, and provide an overview of clinical management.

Keywords: Helicobacter pylori; atrophic gastritis; carcinoid; gastric neoplasm; intestinal metaplasia; iron deficiency; neuroendocrine tumors; vitamin B12 deficiency.

Figure 1.

Endoscopic view of type-1 gastric neuroendocrine tumor on background of atrophic gastritis. The typical endoscopic features of atrophic gastritis are apparent, including loss of rugal folds and pallorous-appearing gastric mucosa; not as appreciated here is the increased prominence of submucosal blood vessels in the gastric body due to the thinned gastric mucosa. Endoscopic image is courtesy of Michelle K Kim, MD PhD.

Figure 2.

(a) Histopathological features of autoimmune gastritis (H&E stain, 100×, oxyntic mucosa). As characteristic of autoimmune gastritis, there is absence of parietal and chief cells. These are replaced by intestinal metaplasia and pseudopyloric metaplasia. There is background chronic inflammation. (b) Histopathologic image of type-I gastric neuroendocrine tumor. The tumor cells are well differentiated as evidenced by monomorphic round nuclei. These appear as “nests” infiltrating the lamina propria. Chromogranin A stain could be used to confirm neuroendocrine differentiation (stain not shown). Images are courtesy of Dr M Blanca Piazuelo.

Figure 3.

Clinical and histological manifestations of autoimmune gastritis.