Do muscle fiber conduction slowing and decreased levels of circulating muscle proteins represent sensitive markers of steroid myopathy? A pilot study in Cushing’s disease

Objective: Glucocorticoids are known to decrease protein synthesis and conduction velocity of muscle fibres. However, the degree of impairment of muscle protein synthesis and conduction slowing in patients with Cushing’s disease remains poorly characterized. Our objective was to investigate whether and to what extent chronic endogenous hypercortisolism could decrease the circulating levels of muscle proteins and modify myoelectric indexes of sarcolemmal excitability and fatigability. Design: Ten patients with Cushing’s disease and thirty healthy controls matched for age, sex, and body mass index were compared. Methods: Blood sampling and electrophysiological tests for vastus lateralis, vastus medialis, and tibialis anterior muscles were performed. Results: Serum creatine kinase (CK) and plasma myoglobin were significantly lower in patients with respect to controls (respectively, p<0.001 and p<0.05): the mean relative difference between patients and controls was 48.9% for CK and 21.4% for myoglobin. Muscle fiber conduction velocity and myoelectric manifestations of fatigue were significantly decreased in all muscles of the patients with respect to controls. The mean relative difference in muscle fiber conduction velocity between patients and controls was 26.0% for vastus lateralis, 22.9% for vastus medialis, and 11.6% for tibialis anterior. These differences contrasted with the paucity of signs suggestive for myopathy that were obtained by needle EMG in the patients. Conclusions: Muscle fiber conduction slowing and decreased levels of circulating muscle proteins are sensitive markers of impaired muscle function which are suitable to be used in combination with clinical assessment and standard electrodiagnostic tests for accurate identification and follow-up of myopathic patients.