Autoimmune
gastritis (AIG) is an increasingly prevalent, organ-specific, immune-mediated disorder characterized by the destruction of gastric parietal cells, leading to the loss of
intrinsic factor and reduced
acid output. These alterations result in malabsorption of
iron,
vitamin B12 (pernicious anaemia) and potentially other
micronutrients. For several years, most studies have focused on pernicious anaemia only, generating
confusion between the two entities. In AIG, the gastric
proton pump, H+/K+
ATPase, is the major
autoantigen recognized by autoreactive T cells. The T cell-dependent activation of B cells stimulates the production of anti-parietal cell
antibodies, the serological hallmark of AIG. The role of Helicobacter pylori
infection in activating or favouring the autoimmune process is still uncertain. Early histopathological alterations allowing a more precise and prompt recognition have recently been described. AIG is burdened by a substantial diagnostic delay as it can present with varied clinical signs including, among others, gastrointestinal symptoms and neuropsychiatric manifestations. In advanced stages, AIG might progress to neuroendocrine tumours and gastric
adenocarcinoma. Management includes early detection through a proactive case-finding strategy,
micronutrient supplementation and endoscopic surveillance. This Primer comprehensively describes the most important insights regarding the epidemiology, pathophysiology, diagnosis and management of AIG, focusing on the most controversial, outstanding issues and future directions.