: Autoimmune atrophic gastritis (AAG) is a non-self-limiting immune-mediated disorder exerting growing interest. The main autoantigen, the beta subunit of the proton pump (H+, K+-ATPase), is localised on the oxyntic mucosa parietal cells, limiting the autoimmune inflammatory damage to this stomach compartment. Clinical manifestations of AAG may occur late, once corpus-fundus atrophy occurs, and are characterised by loss of gastric acidity, impaired iron and/or cobalamin malabsorption, and increased risk of gastric type 1 neuroendocrine neoplasms and possibly gastric adenocarcinoma. Many topics regarding epidemiology, clinical features, pathogenesis, diagnosis, and management remain to be clarified. AAG patients are frequently misdiagnosed or diagnosed with delay. AAG still represents a clinical challenge and a great opportunity for advancing our knowledge on gastrointestinal autoimmune diseases and gastric precancerous conditions. The timely and correct diagnosis of AAG patients is clinically relevant to avoid potentially harmful consequences due to micronutrient deficiencies and related anaemia and neoplastic complications. The current position paper addresses AAG in adults and reflects the views of the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO) on its epidemiology, clinical features, pathogenesis, diagnosis, and management. Improving the understanding of AAG would facilitate timely and accurate diagnosis, enhance clinical management and patients' quality of life, and reduce the economic and social burden of this underrecognized condition.
Autoimmune gastritis: Diagnosis, clinical management and natural history. A position paper by the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO)
Zingone F.;Pelizzaro F.;
2025
Abstract
: Autoimmune atrophic gastritis (AAG) is a non-self-limiting immune-mediated disorder exerting growing interest. The main autoantigen, the beta subunit of the proton pump (H+, K+-ATPase), is localised on the oxyntic mucosa parietal cells, limiting the autoimmune inflammatory damage to this stomach compartment. Clinical manifestations of AAG may occur late, once corpus-fundus atrophy occurs, and are characterised by loss of gastric acidity, impaired iron and/or cobalamin malabsorption, and increased risk of gastric type 1 neuroendocrine neoplasms and possibly gastric adenocarcinoma. Many topics regarding epidemiology, clinical features, pathogenesis, diagnosis, and management remain to be clarified. AAG patients are frequently misdiagnosed or diagnosed with delay. AAG still represents a clinical challenge and a great opportunity for advancing our knowledge on gastrointestinal autoimmune diseases and gastric precancerous conditions. The timely and correct diagnosis of AAG patients is clinically relevant to avoid potentially harmful consequences due to micronutrient deficiencies and related anaemia and neoplastic complications. The current position paper addresses AAG in adults and reflects the views of the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO) on its epidemiology, clinical features, pathogenesis, diagnosis, and management. Improving the understanding of AAG would facilitate timely and accurate diagnosis, enhance clinical management and patients' quality of life, and reduce the economic and social burden of this underrecognized condition.Pubblicazioni consigliate
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