57Pinvestigate the role of autoimmunity in atrophic gastritis type B, 241 patients undergoing gastroscopy were examined carefully for the was the same as for conjugated B.A. recovery of B.A. (mean 2 S.E.M.) from BondelutPercentage ' was 92.6 + 1% (11-48) enzvmaticallv and presence of atrophic gastritis in the antrum.In 42 patients antral atrophic gastritis was diagnosed on the basis of visible veins, but only 32 had chronic atrophic gastritis histologically. Plasma gastrin concentrations and anti-parietal cells, anti-mitochondrial, antinuclear, anti-thyroid and anti-smooth muscle antibodies were measured. Two patients were then excluded because they had positive PCA and high levels of gastrins. Plasma samples from 26 of the patients with histologicallyproven atrophic gastritis type B were obtained. These were assayed for auto-antibodies to G-cells (at varying dilutions and incubation times) using indirect immunofluorescence on norma1,human antral mucosa, with sufficient numbers of G-cells as substrate. Plasma samples from 30 healthy subjects were used as controls. To detect circulating autoantibodies to gastrin, plasma from patients and controls was added to the standard gastrin RfA system minus gastrin antiserum. Results: No autoantibodies to 'G-cells' or-ating gastrin were found in plasma from patients or-controls. Atrophic gastritis type B was strongly correlated with'age, (p

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