Comparative effects of atorvastatin, simvastatin, and fenofibrate on serum homocysteine levels in patients with primary hyperlipidemia

Autor: John C. Papakostas, Moses Elisaf, Haralampos J. Milionis, Konstantine Seferiadis, Anna I. Kakafika, George Chasiotis
Jazyk: angličtina
Rok vydání: 2003
Předmět:
Blood Glucose
Male
Simvastatin
Hyperhomocysteinemia
medicine.medical_specialty
Homocysteine
Fenofibrate/pharmacology/*therapeutic use
Atorvastatin
Hyperlipidemias
Hyperlipidemias/diet therapy/*drug therapy/metabolism
Heptanoic Acids/pharmacology/*therapeutic use
Uric Acid/blood
chemistry.chemical_compound
Blood Glucose/drug effects
Simvastatin/pharmacology/*therapeutic use
Fenofibrate
Internal medicine
Hyperlipidemia
medicine
Humans
Pyrroles
Pharmacology (medical)
Hypolipidemic Agents
Pharmacology
Analysis of Variance
business.industry
Cholesterol
Pyrroles/pharmacology/*therapeutic use
nutritional and metabolic diseases
Middle Aged
medicine.disease
Hypolipidemic Agents/pharmacology/*therapeutic use
Uric Acid
Endocrinology
chemistry
Homocysteine/*blood
Heptanoic Acids
Uric acid
lipids (amino acids
peptides
and proteins)

Female
business
medicine.drug
Popis: Hyperhomocysteinemia is regarded as an independent risk factor for cardiovascular disease. Lipid-lowering agents, such as fibrates, can modify homocysteine levels. However, less is known about the effect of statin therapy on homocysteine. The authors compared the effects of atorvastatin (40 mg/day), simvastatin (40 mg/day), and micronized fenofibrate (200 mg/day) on the serum concentrations of total homocysteine, vitamin B12, and folic acid in patients with primary hyperlipidemia. A total of 128 patients with primary hyperlipidemia (total cholesterol > 240 mg/dL and triglycerides < 350 mg/dL) were assigned to atorvastatin, simvastatin, or fenofibrate. Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment. Homocysteine correlated positively with serum creatinine and uric acid levels and inversely with serum folic acid levels. All treatment modalities reduced total, low-density lipoprotein (LDL) cholesterol, and triglyceride concentrations. High-density lipoprotein (HDL) cholesterol levels significantly increased only in the fenofibrate-treated patients (47.9 +/- 12.5 vs. 50.7 +/- 12.6 vs. 51.2 +/- 12.8 mg/dL, p < 0.01). Atorvastatin and fenofibrate treatment resulted in a significant reduction of serum uric acid levels (5.3 +/- 1.6 vs. 4.9 +/- 1.4 vs. 4.8 +/- 1.4 mg/dL, p < 0.0001 for atorvastatin; 5.6 +/- 1.6 vs. 4.3 +/- 1.4 vs. 4.4 +/- 1.4 mg/dL, p < 0.0001 for fenofibrate). Homocysteine levels were significantly increased only by fenofibrate (10.3 +/- 3.3 vs. 14.1 +/- 3.8 vs. 14.2 +/- 3.6 microU/L, p < 0.001) but did not change from baseline following statin treatment. Neither statins nor fenofibrate had any effect on serum vitamin B12 and folic acid levels. In contrast to fenofibrate, therapeutic dosages of atorvastatin and simvastatin have a neutral effect on serum homocysteine levels, which is in favor of their "cardioprotective" properties. J Clin Pharmacol
Databáze: OpenAIRE