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CHRONIC STRESS AND PEPTIC ULCER:  I. EFFECT OF CORTICOTROPIN (ACTH) AND CORTISONE ON GASTRIC SECRETION

Seymour J. Gray, M.D., Ph.D.; John A. Benson Jr., M.D.; Robert W. Reifenstein, M.D.; Howard M. Spiro, M.D.
JAMA. 1951;147(16):1529-1537. doi:10.1001/jama.1951.03670330021007.
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Since the advent of corticotropin (ACTH) therapy, a number of reports have appeared describing massive gastric hemorrhage or the development, reactivation, or perforation of peptic ulcers during prolonged corticotropin administration.

The purpose of this communication is to present evidence that the chronic administration of corticotropin produces an increase in gastric acidity and gastric pepsin with subsequent peptic ulceration, perforation, or hemorrhage. The studies to be presented indicate, moreover, that chronic stress affects the stomach by a hormonal mechanism which is mediated through the adrenal gland.

It is well established that chronic physical and emotional stress leads to the release of corticotropin by the pituitary and that corticotropin in turn stimulates the adrenal cortex to secrete a variety of steroid hormones including cortisone and closely related compounds.1 The repeated administration of corticotropin over a period of time simulates chronic stress, since it elicits many of the same responses as those

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