What is the role of lab studies in the diagnosis of corticosteroid-induced myopathy?

Updated: Sep 10, 2019
  • Author: Patrick M Foye, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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In chronic (classic) steroid myopathy, serum levels of creatine kinase typically are within the reference range. Creatinine excretion in the urine increases dramatically and can precede the clinical appearance of myopathy by several days. [1] Myoglobinuria and rhabdomyolysis are absent.

In acute steroid myopathy, most patients have high levels of serum creatine kinase, as well as associated myoglobinuria.

Although circulating muscle proteins such as creatine kinase and myoglobin are increased in acute steroid myopathy, glucocorticoid down-regulation of protein synthesis may lead to decreased levels of these proteins in chronic steroid myopathy.

A recent, randomized, placebo-controlled study aimed to determine the effects of dexamethasone on circulating levels of muscle protein. Following 1 week of dexamethasone 8 mg by mouth daily, the 10 subjects in the experimental group all had significantly decreased serum creatine kinase levels, 4 of which fell below the lower limit of normal. Serum myoglobin was also decreased in all 10 subjects; however, there was a trend of greater decrease in creatine kinase than myoglobin, which corresponds to the greater expression of creatine kinase in type II muscle fibers. As mentioned previously, corticosteroid-induced myopathy causes preferential atrophy of type II muscle fibers. [18]

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