title: 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.
abstract: OBJECTIVE
  Glucocorticoids are known to decrease protein synthesis and conduction velocity of muscle fibers. 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.
  
  
  METHODS
  A total of ten patients with Cushing's disease and 30 healthy controls matched for age, sex, and body mass index were compared.
  
  
  METHODS
  Blood sampling and electrophysiological tests on 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 (P<0.001 and P<0.05 respectively): the mean relative difference between patients and controls was 48.9% for CK and 21.4% for myoglobin. Muscle fiber conduction velocity (MFCV) and myoelectric manifestations of fatigue were significantly decreased in all muscles of the patients with respect to controls. The mean relative difference in MFCV 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 of myopathy that were obtained by needle electromyography in the patients.
  
  
  CONCLUSIONS
  Slowing of muscle fiber conduction and decreased levels of circulating muscle proteins are sensitive markers of impaired muscle function, which are suitable for use in combination with clinical assessment and standard electrodiagnostic tests for accurate identification and follow-up of myopathic patients.
authors.affiliation: Division of Endocrinology, Diabetology and Metabolism, Department of Internal Medicine, Molinette Hospital, University of Turin, C.so Dogliotti 14, 10126 Turin, Italy. marco.minetto@unito.it
authors.forename: Marco A
authors.initials: MA
authors.lastname: Minetto
authors.forename: Fabio
authors.initials: F
authors.lastname: Lanfranco
authors.forename: Alberto
authors.initials: A
authors.lastname: Botter
authors.forename: Giovanna
authors.initials: G
authors.lastname: Motta
authors.forename: Giulio
authors.initials: G
authors.lastname: Mengozzi
authors.forename: Roberta
authors.initials: R
authors.lastname: Giordano
authors.forename: Andreea
authors.initials: A
authors.lastname: Picu
authors.forename: Ezio
authors.initials: E
authors.lastname: Ghigo
authors.forename: Emanuela
authors.initials: E
authors.lastname: Arvat
mesh_terms: D000886:Anthropometry; D001284:Atrophy; D003402:Creatine Kinase / Q000378:metabolism; D003480:Cushing Syndrome / Q000503:physiopathology*; D004558:Electric Stimulation; D004568:Electrodiagnosis; D004576:Electromyography; D055724:Electrophysiological Phenomena; D005260:Female; D006801:Humans; D035002:Lower Extremity / Q000502:physiology; D008297:Male; D008875:Middle Aged; D018763:Muscle Fatigue / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000378:metabolism / Q000502:physiology*; D009124:Muscle Proteins / Q000096:biosynthesis*; D018908:Muscle Weakness / Q000209:etiology / Q000503:physiopathology; D009135:Muscular Diseases / Q000378:metabolism*; D009431:Neural Conduction / Q000502:physiology; D010865:Pilot Projects; D047748:Pituitary ACTH Hypersecretion / Q000378:metabolism*; D012132:Respiratory Muscles / Q000502:physiology
chemical_list: D009124:Muscle Proteins; D003402:Creatine Kinase