DRUG-INDUCED PEPTIC ULCER

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Abstract
The administration of certain therapeutic agents may be complicated by the development or reactivation of peptic ulcer, with hemorrhage and perforation. The compounds include mecholyl, priscoline, cinchophen, and especially salicylates. Use of ACTH and adrenal steroids may also be complicated by development of peptic ulcer and ulcer-type distress; many of the ulcers are gastric in location. Symptomatic relief and healing accompany antacid therapy despite continued administration of steroids. Other probable etiologic factors for ulcers occurring under such circumstances include those responsible for the natural incidence of peptic ulcer generally and in the diseases treated, emotional problems and concurrent ulcerogenic medication such as aspirin or butazolidin. Gastric secretion does not increase in most cases during the administration of ACTH and adrenal steroids; lowered tissue resistance may be a most important factor. Butazolidin orally or intramuscularly increases HCl concentration occasionally and may reactivate peptic ulcer or cause the new formation of peptic ulcer. The gastric stimulating effect is observed in patients with vagotomy and in individuals with bilateral adrenalectomy. Reserpine orally in doses of 1 mg daily usually does not increase gastric secretion; however, daily quantities of 2 mg or more may elevate volume of secretion and gastric acidity. The rise is especially pronounced following small amounts of intravenous reserpine. Drug-induced increases in gastric secretion and reactivation of peptic ulcer in occasional patients only suggest that individual susceptibility is an important factor determining the tendency to peptic ulcer.
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