Lack of specific binding of prostaglandin E2, prostaglandin F2 alpha, and 6-keto prostaglandin F1 alpha to serum in patients with peptic ulcer disease and in healthy subjects.
Rabbits immunized against prostaglandins develop antibodies to prostaglandins and peptic ulcer disease (duodenal and gastric ulcers). We have evaluated the hypothesis that idiopathic gastric or duodenal ulcer disease in humans may be associated with the spontaneous occurrence of serum antibodies directed against endogenous prostaglandins. We found that serum from 45 ulcer patients (34 duodenal, 11 gastric) had a low degree of binding of radiolabeled prostaglandin E2, prostaglandin F2 alpha, or 6-keto prostaglandin F1 alpha. The extent to which prostaglandins were bound to serum of ulcer patients was not statistically different from prostaglandin binding to serum from 25 normal subjects. Therefore, we conclude that spontaneous occurrence of circulating antibodies against endogenous prostaglandins is an unlikely cause of gastroduodenal ulceration in humans.
Redfern
J S
JS
Feldman
M
M
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000906:Antibodies / Q000032:analysis; D015237:Dinoprost; D015232:Dinoprostone; D006801:Humans; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000097:blood / Q000378:metabolism*; D011458:Prostaglandins E / Q000097:blood / Q000378:metabolism*; D011460:Prostaglandins F / Q000097:blood / Q000378:metabolism*
D000906:Antibodies; D011458:Prostaglandins E; D011460:Prostaglandins F; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D015232:Dinoprostone