The etiologic role of potassium in the development of characteristically circumferential, stenosing ulcers of the small bowel has been previously inferred and is now established as fact. Precisely how the potassium effects ulcerogenesis is the subject of this communication. The conclusion that an orally administered agent ulcerates the intestine by a topical, escharotic action is the natural one but the morphological and physiological evidence does not substantiate it. In our judgment, the lesion is essentially a hemorrhagic infarct which, depending on its extent and fulminance, produces edema, hemorrhage, erosion, perforation, or cicatrizing stenosis. In the majority of instances, an antedating or perhaps, concomitant organic change in the appertaining vessels may contribute to the vascular insufficiency. In other instances, the vascular insufficiency in both humans and in the experimental animal appears to occur on a functional, probably venomotor, basis and is reflected in segmental hemorrhagic infarctions.
|Original language||English (US)|
|Number of pages||6|
|Journal||JAMA: The Journal of the American Medical Association|
|Publication status||Published - Sep 20 1965|
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