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Carol Lee Koski, MD; David H. Rifenberick, PhD; Stephen R. Max, PhD

Arch Neurol. 1974;31(6):407-410.

Abstract
Corticosteroids cause severe atrophy of skeletal muscle. We have assessed the oxidative capacity of rat skeletal muscles following prolonged steroid administration. Dexamethasone caused severe atrophy and loss of oxidative capacity. Hydrocortisone also caused severe atrophy and loss of oxidative capacity, but to a lesser extent. These effects were reversible. White muscles were more severely affected than red. Palmitate oxidation was less severely affected than that of other substrates. Diphenylhydantoin failed to reverse the effects of steroid treatment on muscle. Administration of dexamethasone to hypophysectomized rats caused them to lose weight and undergo muscular wasting, but did not result in oxidative deficits. Thus, mitochondrial defects do not represent the primary lesion in steroid atrophy. Additional hormonal actions are probably involved in the pathogenesis of steroid atrophy.

Author Affiliations
From the departments of neurology (Drs. Koski, Rifenberick, and Max) and pediatrics (Dr. Max), University of Maryland School of Medicine, Baltimore.

Footnotes
Accepted for publication May 13, 1974.

Reprint requests to Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201 (Dr. Max).

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