Effect of long-term treatment with corticosteroids on adrenocortical function studies in rheumatoid arthritis in the light of the response of plasma-free and total 17,21-dihydroxy-20 ketosteroids to intravenous corticotropin.

It is well known that prolonged treatment with corticosteroids interferes with normal adrenocortical function, causing involvement or atrophy of the gland. This was first demonstrated in animals by Ingle and Kendall (1937) with adrenocortical extracts. Since the introduction of cortisone in clinical medicine, a great deal of evidence has accumulated concerning adrenocortical hypofunction or atrophy after the administration of this agent (e.g. Sprague, Power, Mason, and six others, 1950; O'Donnell, Fajans, and Weinbaum, 1951). These effects are assumed to be due to suppression of the release of ACTH from the adenohypophysis. The degree and duration of adrenocortical hypofunction produced by the administration of corticosteroids has considerable clinical significance. Certain aspects of the problem have been discussed in earlier studies (Engleman, Krupp, Johnson, Welsh) Wrenn, and King, 1953; Fredell, Johnson, Krupp, Engleman, and McGrath, 1955; Hansen, Fischer, and Brochner-Mortensen, 1955; Christy, Wallace, and Jailer, 1956; Larzelere, Barthold, Willett, Feichtmeir, Wilson, and Engleman, 1957). The purpose of the investigation now reported was to determine the adrenocortical function in a group of patients with rheumatoid arthritis after prolonged treatment with corticosteroids, and to follow up the restoration of function after the withdrawal of therapy. The ability of intramuscular ACTH administration to promote the normalization of adrenocortical function was also studied.