CORTICOSTEROID-INDUCED MYOPATHY OF THE RESPIRATORY MUSCLES

Corticosteroids may cause myopathy of both skeletal and respiratory mu scles. This is of specific clinical importance in patients with chroni c obstructive pulmonary disease (COPD), who already have impaired resp iratory muscle function. After treatment with fluorinated steroids, si de-effects occur more frequently and are worse compared to treatment w ith non-fluorinated steroids. Acute myopathy and atrophy are caused by short-term high-dose corticosteroid administration, resulting in rhab domyolysis, diffuse muscle weakness and severe dyspnoea. In contrast, chronic myopathy occurs after prolonged treatment with corticosteroids , and results in proximal muscle weakness and type IIb fibre atrophy. The pathophysiology of steroid myopathy is unknown, but reduction in p rotein synthesis and increased glycogen accumulation may play a major role. Animal models have demonstrated weakening of the diaphragm and a decrease in body and diaphragm mass after corticosteroid administrati on. In humans, a reduction in respiratory and peripheral muscle streng th, an elevation of urinary creatine excretion and selective type IIb fibre atrophy may be observed. Treatment of corticosteroid-induced myo pathy consists of tapering the dose of steroids or switching to non-fl uorinated steroids.