Anti–Gastric Parietal Cell (PCA) Antibodies

Autoimmune chronic atrophic gastritis (AAG) is an organ-specific disease characterised by atrophy of the gastric body and fundus due to autoimmune aggression against the acid-secreting parietal cells lining the stomach wall. In AAG, laboratory findings may include microcytic anaemia, iron deficiency, elevated gastrin and a marked decrease in pepsinogen; serologically, anti–gastric parietal cell antibodies (PCA) target H+/K+-ATPase, a protein mainly involved in the production of hydrochloric acid and in the secretion of intrinsic factor, a glycoprotein required for vitamin B12 absorption.

AAG can lead to pernicious anaemia, where anaemia results from an intrinsic factor deficiency. In AAG associated with pernicious anaemia, in addition to APCA and anti–intrinsic factor antibodies, patients typically show macrocytic anaemia, vitamin B12 deficiency, elevated gastrin and low pepsinogen levels.

APCAs are considered the most sensitive biomarker for AAG and can be detected in 80–90% of patients. They are found mainly in the early stages of disease, often years before symptom onset. In advanced gastritis, APCAs become less frequent because the reduction in parietal cell number is accompanied by decreased antigen availability. Since APCAs are also associated with other autoimmune diseases—such as Hashimoto’s thyroiditis, type 1 diabetes, and coeliac disease—their specificity is limited.