Autoimmune metaplastic atrophic gastritis (AMAG) is a chronic progressive inflammatory condition cause by autoimmune destruction of the oxyntic mucosa and was replaced by atrophic and metaplastic mucosa that restricted to the corpus and fundus of stomach, sparing the antrum, and leading to progressive mucosal atrophy. Resulting in reduce or absent of acid production and loss of intrinsic factor may progress to a severe form of vitamin B12 deficiency anemia and iron deficiency anemia. Moreover, patients with AMAG have higher risks for gastric dysplasia, adenoma, adenocarcinoma, and gastric neuroendocrine tumor. The etiology and exact causal agent leading to the development of AMAG are unclear.

     The clinical presentation is usually non-specific signs or symptoms unless the degree of atrophy impairs the absorption of vitamin B12 and other substances, including folate and iron. Patients might have vague symptoms for many years before all reserves are depleted. Common clinical presentation is iron deficiency anemia and pernicious anemia

    The diagnosis of AMAG might be challenging and usually requires the combination of clinical and diagnostic tests such as laboratory tests, endoscopy, and histopathology. The management strategies are focused on the prevention of vitamin B12, folate and iron deficiencies. Rapid replenishment of vitamin B12 followed by lifelong maintenance on vitamin B12 is necessary when pernicious anemia is present. Patients should receive endoscopic follow-up every 3 - 5 years for surveillance of gastric cancer and neuroendocrine tumor.