title: [The clinical and muscular pathological features of statin-induced myopathy].
abstract: OBJECTIVE
  To explore clinical and muscular pathological features of statin-induced myopathy.
  
  
  METHODS
  Nine patients were enrolled in this study, who were diagnosed as statin-induced myopathy by muscle biopsy in Peking University First Hospital from April, 2012 to October, 2014. The clinical data and pathological findings were analyzed.
  
  
  RESULTS
  The exposure time to statins varied from 4 days to 4 years in the total of 9 patients, 6 males and 3 females, with the average age of 63 ± 6 (55 to 74) years old. Three patients suffered from myalgia and 6 patients complained of weakness mainly at the proximal limbs, while no symptoms occured in 3 patients. Serum creatine kinase (CK) increased in all patients with the maximum value varied from 468 to 8 000 U/L. Serum myositis antibodies were tested in 7 patients and all were negative. Electromyogram was performed in six patients with myogenic damage found in 2 patients. MRI of bilateral thigh muscle was carried out in six patients with muscle edema and mild fatty infiltration found in 2 patients. All patients underwent skeletal muscle biopsy with histochemical and immunohistochemical staining. The main muscular pathological features were muscle fiber atrophy, necrosis, regeneration and increased lipid droplets. Ragged blue fiber, cytochrome C oxidase-negative muscle fibers and decreased NADH activity were observed in some patients. MHC-I expressed in the sarcolemma of muscle fibers at various levels. Mild C5b-9 staining was found in the endomysium, capillary and cytoplasm. Symptoms and the level of CK were improved in 7 patients after discontinuing statins or changing to another statin, while the immunosuppressive therapy were used in 2 patients and shown to be effective.
  
  
  CONCLUSIONS
  Statin induced myopathy is self-limiting in most patients, with improvement after discontinuation of statins. Few patients with autoimmune necrotic myopathy need immunosuppressive therapy.
authors.affiliation: Department of Neurology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Lingchao
authors.initials: L
authors.lastname: Meng
authors.affiliation: Department of Neurology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Department of Neurology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Neurology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Zhaoxia
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Neurology, Peking University First Hospital, Beijing 100034, China.
authors.forename: He
authors.initials: H
authors.lastname: Lyu
authors.affiliation: Department of Neurology, Peking University First Hospital, Beijing 100034, China; Email: yuanyun2002@sohu.com.
authors.forename: Yun
authors.initials: Y
authors.lastname: Yuan
mesh_terms: D000068476:Beijing; D001706:Biopsy; D003402:Creatine Kinase / Q000097:blood*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008279:Magnetic Resonance Imaging; D008297:Male; D018482:Muscle, Skeletal / Q000473:pathology; D009135:Muscular Diseases / Q000139:chemically induced* / Q000473:pathology; D009220:Myositis / Q000097:blood*; D009336:Necrosis
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D003402:Creatine Kinase