Methotrexate therapy in polymyositis.

Polymyositis, an inflammatory disorder of skeletal and occasionally cardiac muscle, may present as a myopathy alone, as one manifestation of a multisystem disorder, especially systemic sclerosis (Medsger, Rodnan, Moossy, and Vester, 1968; Thompson, Bluestone, Bywaters, Dorling, and Johnson, 1969; Brock, 1934), systemic lupus erythematosus (White, 1959; Dubois, 1966), and Sjogren's syndrome (Bunim, 1961), or in association with neoplastic lesions (Williams, 1959; Pearson, 1969). Weakness, particularly ofthe limb girdle musculature, is the dominant clinical manifestation, pain and tenderness being far less common (Pearson, 1962, 1966; Shulman, 1969). Irrespective of the clinical setting, histologically one finds infiltration of the affected muscle bundles with inflammatory cells, oedema separating myofibrils, and varying degrees of fibrillar fragmentation, degeneration, and regeneration. Loss of muscle mass is the eventual outcome unless effective suppression of the inflammatory process is achieved. Except for the response to surgery in those with resectable malignant lesions, corticosteroids are the drugs of choice (Pearson, 1966, 1969; Vignos, Bowling, and Watkins, 1964; Winkelmann, Mulder, Lambert, Howard, and Diessner, 1968). A significant number of patients, however, resist adequate control with these agents or are unable to tolerate the required dosage level. Improvement in steroid-refractory polymyositis has been reported after addition of the folic acid antagonist, Methotrexate (Malaviya, Many, and Schwartz, 1968; Sokoloff, Goldberg, and Pearson, 1971). It is our purpose to report five additional patients with steroid-refractory polymyositis treated with Methotrexate, emphasizing the drug toxicity as well as therapeutic response which characterized the majority. Diagnostic criteria