[Effect of fluvastatin extended release on the protein-lipid structure of erythrocyte membrane and C-reactive protein in patients with hyperlipidemia]
- PMID: 17598653
[Effect of fluvastatin extended release on the protein-lipid structure of erythrocyte membrane and C-reactive protein in patients with hyperlipidemia]
Abstract
The aim of the study was to estimate the effects of 4-weeks therapy of fluvastatin extended release (XL) on lipids serum, C-reactive protein (CRP), erythrocyte structure membrane (thiobarbituric acid reactive substances--TBARS concentrations, membrane cholesterol and the activity of Na+K(+)-ATPase in erythrocytes) in patients with hyperlipidemia without any clinical signs of atherosclerosis.
Material and methods: The study comprised 37 persons, including 15 healthy volunteers and 22 patients with hyperlipidemia (TC > 200 mg/dl, LDL-C > 130 mg/dl, TG < 400 mg/dl) treated with fluvastatin XL 80 mg/d. Before and after 4 weeks of active treatment the following parameters were determined: lipids (by enzymatic method using BioMerieux tests), CRP (by immunoturbidimetric method), TBARS concentrations (by method of Stock and Dormandy), membrane cholesterol (method of Ilcy), Na+K(+)-ATPase activity (method of Bartosz et al.).
Results: It was noticed significantly higher concentrations of CRP, TBARS, membrane cholesterol and lower activity of Na+K(+)-ATPase in erythrocytes of patients with hyperlipidemia than in the control group. Fluvastatin XL caused a significant decrease in serum TC (by 18%), LDL-C (by 24%), TG (by 16%), CRP (by 23%) and TBARS (by 31%), membrane cholesterol (by 30%) in comparison to the initial values before active therapy. The activity of Na+K(+)-ATPase didn't significantly change. The mean values of CRP, TBARS, membrane cholesterol level after active treatment are still higher than in the control group.
Conclusion: The short-term treatment of fluvastatin extended release wasn't enough efficient to compensate disorders in erythrocyte membrane structure of patients with hyperlipidemia.
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