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EPHRAIM P. ENGLEMAN, M.D.; MARCUS A. KRUPP, M.D.; HAROLD P. JOHNSON, Jr., M.D.; JOSEPH E. WELSH, M.D.; HAROLD T. WRENN, Ph.B.; WILBERT R. KING

AMA Arch Intern Med. 1953;91(1):1-7.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

SUPPRESSION of adrenocortical function and atrophy of the adrenal cortex have been described as following administration of cortisone.¹ Both effects, presumably, are due to suppression of secretion of corticotropin, with resulting inac- tivity of the adrenal cortex. Thus, the use of cortisone in interrupted courses, or of cortisone and exogenous corticotropin in alternating courses, has been recommended in order to produce periodic reactivation of the adrenal cortex. Obviously it is important to know whether the suppression of adrenocortical-activity which results from long-term treatment with cortisone is reversible. A number of studies¹ have suggested that this is the case, but this conclusion usually has been based on observations of patients who had received large doses of cortisone for relatively short periods. Furthermore, the eosinopenia following administration of corticotropin was often the sole criterion of adrenocortical responsiveness.

MATERIAL AND METHOD

The purpose of this study was to assess critically the . . . [Full Text PDF of this Article]

Author Affiliations
SAN FRANCISCO

From the Medical Service, Veterans Administration Hospital, and the Division of Medicine, University of California School of Medicine, and Stanford University School of Medicine.

Footnotes
Read before the meeting of the American Rheumatism Association, Chicago, June 6, 1952.

Reviewed in the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the authors are the result of their own study and do not necessarily reflect the opinion or policy of the Veterans Administration.

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