ABSTRACT
A 66 year-old woman with no history of renal or liver disease presented with progressive asthenia and diffuse myalgia. She cited 5 months history of mild hyperlipidemia under treatment with rosuvastatin (10 mg/day). Clinical examination documented both an increase in liver size and proximal muscle weakness, with difficulty in raising arms above the head. Blood tests showed the presence of renal, liver and muscle failure, with no evidence of virological, immunological or haematological diseases. Rosuvastatin treatment was stopped and blood values normalised within five days; but because of an increase in cholesterol plasma levels, rosuvastatin (10 mg/day) was restarted. Two days later, the patient returned to our observation due to the development of asthenia and muscle weakness, with an increase in creatine phosphokinase, 12,165 U/l. Rosuvastatin was discontinued and replaced with pravastatin (40 mg/day) with a complete resolution of clinical and laboratory findings in about six days. Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.
Subject(s)
Aryl Hydrocarbon Hydroxylases/physiology , Fluorobenzenes/adverse effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Pyrimidines/adverse effects , Rhabdomyolysis/chemically induced , Sulfonamides/adverse effects , Aged , Cytochrome P-450 CYP2C9 , Female , Humans , Rhabdomyolysis/enzymology , Rosuvastatin CalciumABSTRACT
The Lp(a) is a low density lipoprotein produced by the liver and it seems to be related to vascular diseases. There is a large individual variability of Lp(a) in the blood levels in the different subjects. The mechanism of the Lp(a) in the pathogenesis of atherosclerosis is not completely clear. There are a lot of different hypotheses and, one of these, is based on the structural analogy of apo(a) with plasminogen. According to current knowledge, it seems that there is a strong relationship between Lp(a) levels and coronary artery disease. Instead, there are still doubts about the real relationship between Lp(a) and stroke. Furthermore, Lp(a) levels seems to be influenced by some other cardiovascular risk factors: fibrinogen, cigarette smoke, and other. Actually, the dosage of the protein is not very useful in clinical practice.
