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February 7, 1925


Author Affiliations

From the University of Kansas School of Medicine, Kansas City, Kan., and the Deaner Institute, Kansas City, Mo.

JAMA. 1925;84(6):409-413. doi:10.1001/jama.1925.02660320001001

The etiology of peptic ulcer is an undetermined question. It is agreed that the fundamental change is a localized impairment of nutrition of the mucosa of the stomach or duodenum with subsequent digestion of the damaged tissue. There is no agreement, however, as to what causes the initial injury. The corrosion, mechanical, nerve, thrombosis and embolism, and bacterial theories each have their exponents. That hemorrhage, lesion and ulceration of the gastric and duodenal mucosa may be produced by a large number of agents has been long recognized. Hemorrhage and ulcer of the duodenum occur frequently after severe body burns. Here the damage is due to the action of toxic products formed in the destruction of protein by heat. Similar lesions may occur in animals on the removal of the suprarenals. Industrial poisons, as benzene (benzol, C6H6), may also cause lesions in this location.

The recognized methods for