STEROID MYOPATHY

Abstract

Weakness developing during the administration of a variety of steroids has been reported both experimentally and clinically. The condition remains sufficiently unfamiliar to warrant an additional report of the clinical manifestations and pathologic findings as demonstrated on biopsy. Ellis1 was regularly able to produce wide-spread necrosis in skeletal muscle of rabbits by the administration of 10 mg/kg/day of cortisone acetate, for 7 to 21 days. Though severe lesions were evident pathologically at the height of the reaction, complete restitution of function was reported 6 days after the omission of cortisone. In contrast to skeletal muscle, cardiac and smooth muscle remained unaffected both functionally and histologically. Mor phologically, cortisone-induced skeletal myopathy resembled that seen in potassium deficiency, but in the latter condition necrosis occurred in cardiac muscle as well. Oral administration of potassium did not protect the animals treated with cortisone, nor did generous doses of alpha-tocopherol. No evidence of virus infection could be discovered in the animals treated with cortisone, though pathologically similar lesions have been observed in a variety of infections. Weakness incident to the treatment of various diseases by triamcinolone (9-alpha-fluoro-16 alpha-hydroxyprednisolone) has been reported.2-5 Recovery from weakness occurred in a relatively short time following the omission of the drug, or following the substitution of non-halogenated steroid, particularly methylprednisolone or prednisone in dosages thought to be pharmacologically comparable. Weakness with eletromyographic evidence of myopathy following 11 weeks of treatment of asthma with dexamethasone (9 alpha-fluoro-16 alpha methylprednisolone) in doses of 2.25 mg/day in an adult male has been reported.6