Pernicious anaemia (PA) is an autoimmune disease characterized by a chronic inflammatory infiltrate in the gastric mucosa, accompanied by the loss of gastric parietal cells and zymogenic cells. The immune response is directed against the intrinsic factor (IF) and the α and β subunits of H+/K+-ATPase (antigen of the anti-parietal cell antibodies). The IF is needed for the absorption of dietary cobalamin (vitamin B12). Hence, the anaemia in PA is caused by decreased IF production due to the loss of parietal cells. PA is commonly associated with macrocytosis neurological damage and hyperhomocysteinemia, the latter being a known risk factor for venous thrombosis. Chronic gastritis may favour the development of intestinal metaplasia, dysplasia, or gastric cancer. Thus, early identification of patients who may be carriers of premalignant lesions is important for proper monitoring.

Autoimmune gastritis affects the fundus and the corpus of the stomach, but spares the antrum; hyperplasia of gastrin-producing cells is observed in these patients, which leads to high serum gastrin concentration and a decrease in acid secretion and pepsinogen I concentrations. Gastrin and pepsinogen-I are representative biomarkers that influence the gastric physiology, acting as indicators of the functional state of its mucosa. Gastrin stimulates the secretion of gastric acid and mucosal cell growth. Pepsinogen I is secreted by chief cells from the mucosa of the gastric corpus, and its concentrations may reflect the mass and/or turnover of those cells in the mucosa. It has been reported that serum concentrations of these markers may suggest the presence of abnormalities such as atrophic gastritis or changes in gastric secretion.

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Mishita
Jornal co-ordinator
Journal of  Autoimmune Disorders