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• W4233361928 abstract "IN LATE 1964 a sudden increase in the occurrence of circumferential ulcerating, stenosing lesions of the small bowel was noted both in Europe and the United States. Lindholmer et al¹in Sweden and Baker et al²in this country first suggested the association of these lesions with enteri-coated thiazide diuretic potassium chloride preparations. Extensive experimental and clinical investigations^3-6quickly identified enteric-coated potassium chloride as the responsible agent, and led to recognition of perforating areas of necrosis as a more severe form of the same lesion. The mechanism of damage is believed to be the release and absorption of high concentrations of potassium chloride over short segments of small bowel acting upon submucosal and mural veins to produce venous spasm or paralysis. The resultant venous stasis causes segmental hemorrhagic infarction of varying severity with ulceration and stenosis.⁷ Recognition of this complication of enteric-coated potassium chloride ingestion has" @default.
• W4233361928 created "2022-05-12" @default.
• W4233361928 creator A5019365294 @default.
• W4233361928 date "1967-01-16" @default.
• W4233361928 modified "2023-10-18" @default.
• W4233361928 title "Potassium citrate and potassium gluconate versus potassium chloride. Experimental evaluation of relative intestinal toxicity" @default.
• W4233361928 doi "https://doi.org/10.1001/jama.199.3.215" @default.
• W4233361928 hasPublicationYear "1967" @default.
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