THE RELATIONSHIP OF GASTRIC ACTIVITY AND ADRENOCORTICAL FUNCTION: A CORRELATIVE STUDY*

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Abstract
INTRODUCTION STUDIES on human subjects reported previously from this laboratoryhave indicated that the administration of corticotropin or adrenal glucocorticoids may induce a marked increase in basal and nocturnal gastric acid and pepsin secretion, with a concomitant increase in urinary uropepsin (1–5). The administration of adrenal glucocorticoids has resulted in the development of epigastric pain or peptic ulcer in patients without previous gastrointestinal disease, and has led to reactivation of quiescent peptic ulcer in others (5–7). In patients with Addison's disease, in whom peptic ulceration is exceedingly rare, the administration of cortisone in the small replacement dosage of 25 to 50 mg. daily has been followed by documented gastric and duodenal ulcer formation (8, 9). Further indirect evidence favoring the hypothesis that gastric and adrenal activity are closely related is derived from study of the uropepsin and urinary steroid excretion in patients with hypofunction or hyperfunction of the adrenal and pituitary glands. A markedly diminished uropepsin excretion in patients with adrenal hypofunction (panhypopituitarism and Addison's disease) and a definite increase in uropepsin excretion in adrenal hyperfunction (Cushing's disease) have been noted, with parallel alterations in the urinary corticoid and ketosteroid excretions (5).