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The Treatment of Rheumatoid Arthritis Complicated by Chronic Hypercortisonism, and the Theoretical Causal Role of Certain Amine Oxidases

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Abstract

THE recognition by Hench, Kendall, Slocumb, and Polley1 in 1948 of the desirable effects exerted by cortisone and corticotropin on inflammation and swelling in patients with rheumatoid arthritis and associated diseases is considered one of the great medical discoveries of our time. However, it has since become apparent that the effect of these hormonal agents is not specific, that the desirable effect is only temporary, and that acute or chronic hypercortisonism may ensue from overdosage. The undesirable effects that may occur have been described by Slocumb, Polley, Ward, and Hench,2 and include alteration in electrolyte and water metabolism, decrease in carbohydrate tolerance, acneiform eruption, hirsutism, striae, deposition of fat, menstrual disorders, hyper-acidity, delay in wound healing, and hypertension. Chronic overdosage is variously evidenced by emotional instability, increased fatigability and muscle aching, inability to concentrate, and depressed psychomotor activity. When these signs and symptoms are present, withdrawal of the corticosteroids may be extremely difficult, and must be accomplished slowly and gradually over a period of months; during this period, the patient must co-operate fully with the physician and must get 12 to 14 hours of sleep nightly together with extra periods of rest during the day.2 Too rapid reduction in dosage may result in a flare-up of the rheumatoid arthritis, and in some patients, corticosteroid therapy may have to be continued indefinitely.2

Recently Scherbel, Schuchter, and Harrison3 reported a method of administering a combination of chemotherapeutic agents to patients with progressive and persistently active rheumatoid arthritis. Despite decrease of corticosteroid dosage, . . .


 

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