In a follow-up study of 20 patients with zidovudine myopathy, four to six weeks after zidovudine was discontinued, myalgia resolved, strength improved or normalized, and spontaneous activity on the EMG decreased or disappeared. The unique histologic features of zidovudine myopathy are ragged red fibers, suggestive of mitochondrial abnormalities, and many cytochrome c oxidase-negative fibers. Although the newly introduced protease inhibitors have not been associated with myotoxicity, careful observation is warranted to determine whether it occurs after long-term use. Because cholesterol is the major sterol constituent of muscle membranes, reduction of the normal cholesterol pool available for membrane synthesis can increase membrane fluidity, leading to an unstable sarcolemma, myotonic discharges, and, in advanced cases, rhabdomyolysis. The EMG correlates include fibrillation potentials and myotonic or complex repetitive discharges.
Gradual recovery can occur after withdrawal of the offending drug.
Although a transient increase in the serum CK level and myalgia is common after treatment with lovastatin, the drug has been associated with clinically overt myopathic symptoms in fewer than five percent of treated patients. Combined drug use increases the risk of myopathy. Coadministration of cyclosporine and lovastatin to patients with heart or kidney transplants and hyperlipidemia appears to increase the incidence of myopathy with rhabdomyolysis. Patients with prolonged paralysis induced by such nondepolarizing blocking agents as pancuronium may manifest an acute myopathy after discontinuance of mechanical ventilation. Most of these patients received high doses of corticosteroids for status asthmaticus or another systemic illness for which artificial paralysis was induced to secure an aggressive pulmonary toilet.