Rhabdomyolysis induced by statins

This paper was published in Clinical Chemistry 1990 Dec;36(12):2145-7

Study title and authors:
Rhabdomyolysis secondary to lovastatin therapy.

Manoukian AA, Bhagavan NV, Hayashi T, Nestor TA, Rios C, Scottolini AG.
Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96822.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/2253372

This paper reports a case of lovastatin (Mevacor)-induced rhabdomyolysis (severe muscle breakdown which may lead to kidney damage).

(i) A 59 year old woman was admitted to hospital with a two day history of shortness of breath and difficulty walking. She had been discharged from hospital two weeks earlier for congestive heart failure and, since discharge, had experienced progressive weight gain and swelling of the feet and ankles such that walking had become difficult.
(ii) For 13 days before admission to hospital she had been taking lovastatin, 20 mg orally twice a day.
(iii) On the second hospital day she complained of profound muscle weakness in her lower extremities which progressed over several hours to include the upper extremities. In addition she could no longer walk because of severe pain.
(iv) Creatine kinase levels increased from 157 U/L two weeks before admission to 176,500 U/L on the twelfth hospital day. (High creatine kinase levels are a marker for rhabdomyolysis).
(v) The patient's symptoms and creatine kinase levels resolved after discontinuation of the statin drug.

As well as inhibiting the body from producing cholesterol, statins also repress the production of several other biologically essential compounds such as coenzyme Q10 and heme A which are important components in the system of mitochondrial energy production.

Mitochondria are known as the powerhouses of the cell. They are tiny cellular organelles that take in nutrients, break them down, and create energy for the cells.

Dr Manoukian speculates that the rhabdomyolysis was due to statin-induced mitochondrial damage secondary to inadequate synthesis of coenzyme Q10 and heme A.