intrinsic-factor and Scleroderma--Systemic

We examined 51 sera from patients with pernicious anaemia for their capacity to block maximal gastrin stimulation of acid secretion by isolated rodent gastric parietal cells. 14C-aminopyrine accumulation was used as the index of acid secretion in vitro. Sera from patients with pernicious anaemia gave significantly (P less than 0.005) more block of maximal gastrin stimulation of acid secretion (61.7 +/- 37.8%) than sera from 10 patients with systemic lupus erythematosus (19.6 +/- 17.7%), 10 with scleroderma (34.2 +/- 22.3%), five with rheumatoid arthritis (22.4 +/- 15.6%) or 30 from healthy persons (27.4 +/- 12.8%). Maximal histamine stimulation of acid secretion was not inhibited. The blocking factor was present in serum IgG fractions, and serum and IgG fractions gave parallel dose-response and dilution curves. The serum block was abolished by absorption with gastric mucosal cells and correlated with the presence of parietal cell surface autoantibody. We conclude that serum immunoglobulin in pernicious anaemia can block gastrin stimulation of acid secretion and suggest that this block may be mediated by competition with gastrin for surface receptors on parietal cells.

Topics: Adult; Aged; Aminopyrine; Anemia, Pernicious; Animals; Arthritis, Rheumatoid; Autoantibodies; Binding, Competitive; Dose-Response Relationship, Immunologic; Female; Gastric Acid; Gastrins; Humans; Immunoglobulin G; In Vitro Techniques; Intrinsic Factor; Lupus Erythematosus, Systemic; Male; Middle Aged; Parietal Cells, Gastric; Rats; Rats, Inbred Strains; Scleroderma, Systemic

Topics: Anemia, Pernicious; Autoimmune Diseases; Child; Colitis, Ulcerative; Crohn Disease; Dermatomyositis; Digestive System Diseases; Hepatitis; Humans; Intrinsic Factor; Lupus Erythematosus, Systemic; Scleroderma, Systemic