Potassium Citrate and Potassium Gluconate Versus Potassium Chloride:  Experimental Evaluation of Relative Intestinal Toxicity

Scott J. Boley, MD; Leon Schultz, MD; Solomon Schwartz, MD; Armand Katz, MD; Arthur C. Allen, MD
JAMA. 1967;199(3):215-217. doi:10.1001/jama.1967.03120030119028.
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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 al1 in Sweden and Baker et al2 in this country first suggested the association of these lesions with enteri-coated thiazide diuretic potassium chloride preparations. Extensive experimental and clinical investigations3-6 quickly 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


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