The problem of the etiology of ulcer of the stomach has recently been approached from the point of view of that older problem—the nondigestibility of the stomach by its own digestive juice. For instance, Frentzel,1 in 1891, and Katzenstein,2 in 1908, showed that living stomach and duodenum implanted in the stomach were not influenced in any way, while small intestine and spleen under similar conditions were promptly digested. Katzenstein believed that the resistance of the stomach and duodenum to peptic digestion was due to the presence in the stomach wall of a specific inhibiting body—antipepsin.
In a more recent contribution, Katzenstein,3 by reducing the antipepsin content of the stomach and blood (by methods not altogether clear), succeeded in producing chronic experimental ulcers in dogs' stomachs. He concluded that gastric ulcer is a sequence to a local injury of the stomach wall, whereby the normal balance between
HAMBURGER WW. THE INACTIVATION OF PEPSIN BY SODIUM CHLORID: ITS CLINICAL SIGNIFICANCE. Arch Intern Med (Chic). 1915;XVI(3):356–362. doi:10.1001/archinte.1915.00080030017002
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