Bezafibrate-lnduced myopathy no evidence for defects in muscle metabolism

G. Vita, A. Toscano, G. Mileto, F. Pilrone, M. T. Ferro, E. Gagliardi, N. Bresolin, F. Fortunalo, C. Messina

Research output: Contribution to journalArticlepeer-review


A 58-year-old man with chronic renal failure developed severe muscle pain and tenderness I week after starting bezafibrate 400 mg daily. Serum creatine kinase was 32,280 U/l. Muscle biopsy revealed scattered necrotic fibers and mild type 2b atrophy. Muscle total and free carnitine were at the upper limits of the normal range. Biochemical investigations of muscle homogenate showed normal carnitine pelmityl transferase (CPT) as well as normal individual glycolytic and mitochondrial enzyme activities. Withdrawal of the drug was followed by rapid clinical improvement. Our study casts doubt on the hypothesis that bezafibrate is able to affect muscle metabolic pathways. It is likely that the drug acts on cholesterol constituents of the muscle membrane. producing discontinuities of the sarcolemma and initiating cell necrosis.

Original languageEnglish
Pages (from-to)168-172
Number of pages5
JournalEuropean Neurology
Issue number2
Publication statusPublished - 1993


  • Bezafibrate
  • Myopathy
  • Renal failure
  • Rhabdomyolysis

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology


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