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An Appraisal of Its Safety and Mode of Action in Clinical Disorders, Including Rheumatoid Arthritis

William McK. Jefferies, MD

Arch Intern Med. 1967;119(3):265-278.

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

Such is the nature of medicine, that things which we have laid up in our minds as settled truths often require to be modified by our future experience.—Latham.¹

IN THE 18 years since the introduction of cortisone into medical therapy by Hench and his associates,² much has been learned about the effects of this and related steroids, but their basic mechanism of action remains obscure. In spite of their extensive clinical use, little has been added to the concept of their effects in the past 12 years³ and certain general impressions that prevailed then have persisted, including the following.

Clinical effects depend upon an excess of steroid in the tissues. Initial doses reported by Hench and his group were 300 mg of cortisone acetate daily, and subsequent early reports concerned starting dosages of 100 mg daily or greater. Because these doses produce an excess of steroid in . . . [Full Text PDF of this Article]

Author Affiliations
Cleveland

From the Department of Medicine, University Hospitals and Western Reserve University School of Medicine, and the Infertility Clinic of the Maternal Health Association, Cleveland.

Footnotes
Received for publication Sept 9, 1966; accepted Oct 24.

Read in part before the Annual Meeting of the American College of Physicians, April 18, 1966, New York.

Reprint requests to 3550 Warrensville Center Road, Shaker Heights, Ohio 44122.

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