Atrophic Body Gastritis: Clinical Presentation, Diagnosis, and Outcome

Abstract

Atrophic body gastritis is a chronic disorder characterised by atrophy of the oxyntic glands leading to reduced gastric acid and intrinsic factor secretion. Serological studies reported yearly prevalence and incidence rates between 3–9% and 0–11%, respectively. In atrophic body gastritis, the presence of parietal cells and/or intrinsic factor autoantibodies, and autoimmune diseases, such as autoimmune thyroid disease or Type 1 diabetes mellitus, are often observed. These cases are often diagnosed as autoimmune gastritis. This association has been included as part of the autoimmune polyendocrine syndrome. A frequent clinical presentation of atrophic body gastritis is pernicious anaemia, considered an autoimmune condition, arising from vitamin B12 malabsorption as a consequence of intrinsic factor deficiency. Another presentation may be an otherwise unexplained iron deficiency anaemia, as a result of iron malabsorption and consequence of reduced gastric acid secretion. To date, no universally accepted criteria are available to define autoimmune gastritis and to distinguish this clinical entity from chronic, Helicobacter pylori-driven, multifocal atrophic gastritis. In contrast with the classical perception of a silent condition, patients with atrophic body gastritis may complain of a spectrum of gastrointestinal symptoms, ranging from dyspepsia as early satiety, postprandial fullness, and epigastric pain, to gastro-oesophageal reflux symptoms such as regurgitation and heartburn. The timely diagnosis of atrophic body gastritis is important, as this condition puts patients at an increased risk of gastric cancer and other Type 1 carcinoids that may lead to micronutrient deficiencies crucial for erythropoiesis. The present review provides an update on epidemiological and clinical aspects as well as diagnosis and outcome of the disease.