Drug-induced myopathy and rhabdomyolysis are rare adverse drug reactions (ADR). 
They have been seen after the introduction of modern lipid-lowering drugs more 
regularly. The first description after medication with clofibrate dates back to 
1968. Apparently, all fibrates can induce myopathy. It usually starts after a 
few days of medication, or after prolonged use, showing muscle weakness and/or 
pain. Concomitantly, the enzyme creatininephosphokinase (CPK) is raised 
dramatically. Muscular necrosis can follow leading secondarily to kidney 
failure, and eventually to death. For the class of statins, myopathy was more 
often seen after their introduction, and it became their most feared adverse 
effect, especially in combination of statins with other drugs (mibefradil, 
gemfibrozil, cyclosporin). In animal models the evolution of the disease and the 
mechanism of action may be elucidated. Though strong epidemiological data are 
lacking, the incidence of myopathy is probably similar for all lipid-lowering 
drugs and is in the range of 0.1-0.5% with monotherapy, increasing to 0.5-2.5% 
with combination therapy. Severe cases of rhabdomyolysis are rarer, but may have 
a significant mortality. The market success of cerivastatin within a short 
period has led to 100s of myopathies and some dozens of deaths. Though 
interactions on metabolism and ensuing high plasma levels can partially explain 
myopathy as intoxication, there are strong indications that other (endocrine, 
metabolic, genetic) factors might play a role in the pathophysiology. The 
patient population at risk should better be defined and withheld from 
myopathy-inducing drugs.