Symptoms and diagnosis of autoimmune gastritis

Toh, 2014 Kulnigg-Dabsch, 2016

Autoimmune gastritis is an inflammatory condition associated with autoantibodies to parietal cells and intrinsic factor. It may occur alone or in association with other autoimmune disorders. Over time, the chronic inflammation may cause atrophy of the glandular mucosa of the stomach (the gastric body and fundus), leading to reduced secretion of acid (which may impair absorption of iron) and intrinsic factor (which may reduce vitamin B₁₂ absorption).

Autoimmune gastritis is asymptomatic, and most cases are suspected after blood tests are performed for unrelated reasons; any symptoms relate to the consequences of micronutrient malabsorption. If the condition is unrecognised and untreated, iron deficiency or vitamin B₁₂ deficiency megaloblastic anaemia (pernicious anaemia) may result. Advanced cases with neurological complications are rarely seen. Late sequelae include an increased risk of gastric cancer (estimated as 0.27% per person–years, a nearly 7-fold increase in relative risk)Vannella, 2013.

Gastric autoantibodies suggest, but do not confirm, the diagnosis. Antiparietal cell antibodies are less specific than anti-intrinsic factor antibodies. The Schilling test is no longer performed. The diagnosis is confirmed by histology of samples obtained at endoscopy; distal (ie antral) gastric mucosa is normal, while proximal histology (body and fundus) shows atrophy and inflammation. Helicobacter pylori infection is typically absent. Autoimmune gastritis can be distinguished from H. pylori gastritis, which usually causes pangastritis (ie involves the antrum as well as the body). However, there may be confusion when H. pylori infection has occurred but is no longer present; H. pylori serology is helpful in these cases.