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
Jefferies WM. Low-Dosage Glucocorticoid Therapy: An Appraisal of Its Safety and Mode of Action in Clinical Disorders, Including Rheumatoid Arthritis. Arch Intern Med. 1967;119(3):265–278. doi:10.1001/archinte.1967.00290210097008
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