Rhabdomyolysis secondary to lovastatin therapy

  • A A Manoukian
    Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822
  • N V Bhagavan
    Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822
  • T Hayashi
    Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822
  • T A Nestor
    Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822
  • C Rios
    Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822
  • A G Scottolini
    Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822

書誌事項

公開日
1990-12-01
権利情報
  • https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model
DOI
  • 10.1093/clinchem/36.12.2145
公開者
Oxford University Press (OUP)

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説明

<jats:title>Abstract</jats:title> <jats:p>We report a case of lovastatin-induced rhabdomyolysis and resulting life-threatening renal failure. Lovastatin, a hypocholesterolemic agent, decreases endogenous cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.88). This agent has been implicated in causing rare serious side effects in various clinical settings; however, the mechanism of these adverse reactions is not understood. The clinical course of our patient was characterized by profound muscle weakness with marked increases in serum creatine kinase and myoglobin. Light- and electron-microscopic studies of skeletal muscle of our patient demonstrated a noninflammatory myopathy suggestive of ongoing rhabdomyolysis with vacuolization and focal degeneration of myocytes. The patient's symptoms and the laboratory values referable to rhabdomyolysis resolved after discontinuation of the drug. We speculate that the rhabdomyolysis was due to mitochondrial damage secondary to inadequate synthesis of coenzyme Q and heme A, members of the electron-transport system of the inner mitochondrial membrane.</jats:p>

収録刊行物

  • Clinical Chemistry

    Clinical Chemistry 36 (12), 2145-2147, 1990-12-01

    Oxford University Press (OUP)

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