Autoimmune Gastritis

Abstract

Context.— Autoimmune gastritis (AG) is a corpus-restricted chronic atrophic gastritis associated with intrinsic factor deficiency, either with or without pernicious anemia. Autoimmune gastritis is a microscopic disease because patients present with no or vague symptoms, and clinicians rarely find endoscopic changes. Autoimmune gastritis only becomes a clinical disease when pathologists diagnose it in gastric biopsies performed for a variety of clinical indications. Unfamiliarity with this disease can result in misdiagnosis of patients, and thus inadequate patient management. Objective.— To review the pathogenesis, clinical features, diagnostic criteria, differential diagnoses, sequelae, and surveillance recommendations for AG. Data Sources.— The sources of the study include a review of the pertinent literature for AG. Conclusions.— Autoimmune gastritis is an important disease characterized by a loss of oxyntic mucosa and presence of metaplastic epithelium and enterochromaffin-like cell hyperplasia. Awareness and proper diagnosis are critical to prevent mismanagement of patients.

Differences in image-enhanced endoscopic findings between Helicobacter pylori-associated and autoimmune gastritis

“…Histological findings of autoimmune gastritis differ according to early, florid and end phases [23,24]. In our study, the patients with autoimmune gastritis were younger than those with H. pylori-associated gastritis.…”

“…We explain the difference in micromucosal structure by different histological findings in the gastric mucosa in H. pylori-associated and autoimmune gastritis. H. pylori-associated gastritis showed diffuse infiltration of mononuclear inflammatory cells in the superficial layer of the lamina propria and neutrophils in the neck of the gastric glands [23,24] in response to colonization by H. pylori on the surface of the foveolar epithelium. Therefore, the surface of the foveolar epithelium may develop regenerative hyperplasia [23].…”

“…In contrast, autoimmune gastritis shows a basal-predominant, chronic inflammatory cell infiltrate in the lamina propria [23,24], thus the surface of the foveolar epithelium is less involved. Moreover, epithelial metaplasia seen in the early phase of autoimmune gastritis is usually pseudopyloric or pancreatic acinar cell metaplasia of the glandular epithelium, and intestinal metaplasia is not frequently seen until advanced phases of the disease [23,24]. These histological findings in autoimmune gastritis explain the unchanged foveola micromucosal pattern in magnifying NBI (▶ Fig.…”

The Role of Gastric Mucosal Immunity in Gastric Diseases

“…The noninfective gastric disease is mainly autoimmune gastritis. Autoimmune gastritis is a chronic gastritis characterized by gastric mucosa atrophy, which is closely related to the lack of intrinsic factors [63]. The main targets of autoimmune reaction are parietal cells and intrinsic factors, in which the parietal cell antibody (PCAs) can be found in the gastric mucosa of 90% patients with atrophic gastritis [64].…”

Association of MTHFR C677T polymorphism with severity and localization of chronic atrophic gastritis patients without Helicobacter pylori infection: a case control study

“…According to the Correa's theory, a series of precancerous lesions (atrophic gastritis [AG], intestinal metaplasia [IM], and dysplasia) is caused by chronic inflammation of the gastric mucosa, which leads to the evolution of stomach cancer [2]. AG is a chronic disorder losing the oxyntic glands, which is characterized by lamina propria fibrosis or their replacement with pseudo-pyloric or IM [3]. Therefore, early supervision of AG could reduce the incidence of gastric cancer [4].…”