autoimmuunigastritis

Autoimmune gastritis, also known as autoimmune metaplastic atrophic gastritis (AMAG), is a chronic immune-mediated inflammatory disease of the stomach lining. It primarily affects the gastric body and fundus, leading to loss of parietal cells, reduced acid production (hypochlorhydria or achlorhydria), and impaired intrinsic factor production.

The condition is driven by autoantibodies against gastric parietal cells and intrinsic factor, with T-cell–mediated injury contributing to glandular atrophy. AMAG often coexists with other autoimmune diseases, such as autoimmune thyroid disease, type 1 diabetes, or vitiligo.

Most cases are asymptomatic or present with nonspecific dyspepsia. Pernicious anemia may develop due to vitamin B12 malabsorption from intrinsic factor loss, causing fatigue, pallor, and neuropathy. Laboratory findings can include macrocytic anemia and low serum B12; gastrin levels may be elevated due to reduced acid secretion.

Diagnosis relies on a combination of serology and histology. Serologic tests may detect anti-parietal cell antibodies or anti-intrinsic factor antibodies. Biochemical markers include low serum pepsinogen I with a reduced pepsinogen I/II ratio. Endoscopy shows atrophy of the corpus and fundus, and gastric biopsies reveal lymphoplasmatic inflammation with mucosal atrophy and often intestinal metaplasia.

Complications include pernicious anemia and an elevated risk of gastric neoplasia, including intestinal-type gastric cancer and neuroendocrine tumors from ECL cell hyperplasia. Management centers on treating B12 deficiency (usually with parenteral B12) and monitoring for other autoimmune conditions; cancer surveillance remains individualized. Prognosis depends on timely recognition and treatment of B12 deficiency, with ongoing risk for gastric cancer in long-standing AMAG. Regular follow-up is recommended.