Effects of statin treatment on uric acid homeostasis in patients with primary hyperlipidemia

Epidemiologic studies have shown that serum uric acid is a risk factor of coronary artery disease. In addition to fenofibrate, there is some evidence that atorvastatin may have a hypouricemic action, but the underlying mechanisms remain speculative. This randomized trial was conducted to investigate...

Full description

Saved in:
Bibliographic Details
Published in:The American heart journal 2004-10, Vol.148 (4), p.635-640
Main Authors: Milionis, Haralampos J., Kakafika, Anna I., Tsouli, Sofia G., Athyros, Vasilios G., Bairaktari, Eleni T., Seferiadis, Konstantinos I., Elisaf, Moses S.
Format: Article
Language:English
Subjects:
Acids
Atorvastatin Calcium
Biological and medical sciences
Cholesterol
Diabetes
Disorders of blood lipids. Hyperlipoproteinemia
Drug dosages
Enzymes
Family medical history
Female
Glucose
Heptanoic Acids - pharmacology
Heptanoic Acids - therapeutic use
Homeostasis
Homeostasis - drug effects
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Hyperlipidemias - blood
Hyperlipidemias - drug therapy
Hyperlipidemias - metabolism
Hypolipidemic Agents - pharmacology
Hypolipidemic Agents - therapeutic use
Immunoassay
Insulin
Insulin resistance
Kidney diseases
Laboratories
Lipids
Lipids - blood
Logistic Models
Low density lipoprotein
Male
Medical sciences
Metabolic diseases
Middle Aged
Mortality
Multivariate analysis
Pyrroles - pharmacology
Pyrroles - therapeutic use
Simvastatin - pharmacology
Simvastatin - therapeutic use
Triglycerides
Uric Acid - blood
Uric Acid - urine
Variables
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Epidemiologic studies have shown that serum uric acid is a risk factor of coronary artery disease. In addition to fenofibrate, there is some evidence that atorvastatin may have a hypouricemic action, but the underlying mechanisms remain speculative. This randomized trial was conducted to investigate the effects of atorvastatin and simvastatin on uric acid homeostasis in patients treated for primary hyperlipidemia. A total of 180 patients were enrolled; patients were randomly assigned to 40 mg/d of either atorvastatin or simvastatin. Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment; random urine samples were simultaneously obtained for creatinine, sodium, and uric acid determinations. Baseline serum uric acid levels correlated positively with the body mass index, serum insulin, creatinine, and triglyceride levels and inversely with serum HDL cholesterol levels. Both statins caused a favorable effect on lipids and a significant decrease in fibrinogen and high-sensitivity CRP levels. However, only atorvastatin reduced serum uric acid levels (from 5.6 ± 1.7 to 4.9 ± 1.5 mg/dL, P < .0001) by augmenting its urinary fractional excretion (from 10.4% ± 7.9% to 12.0% ± 7.4%, P < .01). In a multivariate logistic regression analysis, the reduction of uric acid levels was independently associated with baseline serum uric acid concentration but not to other variables, including lipid parameters (OR, 1.65; 95% CI, 1.14 to 2.40; P = .008). Atorvastatin (but not simvastatin) significantly lowered serum uric acid levels. This result may be in favor of a preferable choice of atorvastatin for the treatment of hyperlipidemic patients presenting with hyperuricemia.
ISSN:0002-8703
1097-6744
DOI:10.1016/j.ahj.2004.04.005