Corticosteroid-Induced Myopathy Workup
- Author: Patrick M Foye, MD; Chief Editor: Stephen Kishner, MD, MHA more...
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. 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.
Muscle biopsy in chronic (classic) steroid myopathy 
Muscle biopsy shows preferential atrophy of type II fibers, particularly the fast-twitch glycolytic fibers (type IIB).[10, 15] Some atrophy of other type II fibers and, to a small degree, type I muscle fibers can occur. Increased variation in the diameter of muscle fibers occurs. A lack of evidence of muscle fiber inflammation is reported. There is a distinct lack of necrosis or regeneration of muscle. Less active muscles appear to be affected preferentially.
Muscle biopsy in acute steroid myopathy
Muscle biopsy shows focal and diffuse necrosis of all fiber types, without predilection for type II fibers.
Electromyography (EMG) and nerve conduction studies (NCSs) in chronic (classic) steroid myopathy 
Motor and sensory NCS results typically are normal. Repetitive stimulation studies do not reveal significant decrement or increment. EMG studies reveal normal insertional activity with little abnormal spontaneous activity (positive sharp waves and fibrillation potentials). EMG may reveal a mild decrease in motor unit action-potential amplitude during maximal recruitment. In moderate-to-severe cases, studies may show an early recruitment pattern.
EMG and NCS in acute steroid myopathy 
Some case reports have indicated abnormal EMG findings, including abnormal spontaneous activity (positive sharp waves and fibrillation potentials), early recruitment, and small, polyphasic motor units. There have also been findings suggestive of the development of associated neuropathy following high-dose corticosteroid treatment.
Muscle biopsy typically shows a preferential atrophy of type II fibers, particularly the fast-twitch glycolytic fibers (type IIB), with some atrophy of other fiber types.[10, 15] There is a distinct lack of necrosis or regeneration of muscle. Some studies, however, have reported focal and diffuse necrosis of all fiber types, without predilection for type II fibers.
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