[Erythrocyte fluidity in patients with hyperlipidemia during statins therapy].
The lipid composition of erythrocyte membrane is in a state of dynamic equilibrium with plasma lipoproteins and reflects the processes taking place in extracellular environment. The recent studies were devoted to the phenomenon of modification of atherosclerosis development by statins. The aim of the study was evaluation of three statins: simvastatin, atorvastatin and pravastatin on plasma lipidogram and fluidity of erythrocytes membranes in patients (pts) with hyperlipidemia (hlp) type II.


METHODS
the study comprised 114 pts, including 94 pts with hlp type II without concomitant chronic diseases and 20 healthy volunteers. Pts were qualified to treatment with statins if their LDL-cholesterol concentration (LDL-C) was above 170 mg/dL (4,1 mmol/L), total cholesterol (TC) > 250 mg/dL (6,5 mmol/L) and triglicerydes (TG) < 400 mg/dL (4,5 mmol/L). Pts were randomised to three groups: group I-n = 31 pts treated with atorvastatin (10 mg/d); group Il-n = 31 with simvastatin (20 mg/d), group III-n = 32 with pravastatin (20 mg/d).


METHODS
after 4 and 12 weeks of active treatment the following parameters were determined: TC, HDL-C, TG (by enzymatic method using BioMerieux tests); LDL-C was calculated from the Friedewald formula and erythrocyte membranes fluidity by electron paramagnetic resonance with two spin labels (5-DSA, 16-DSA).


RESULTS
During statin therapy significant decrease of TC, LDL-C, TG was observed, both after 4 and 12 weeks, as compared with initial values. All statins after 4 weeks of therapy caused a significant increase of membrane fluidity in its surface layer at carbon 5 depth. The values of parameter S after 12 weeks did not differ significantly from the values in the control group. The percent decrease of membrane microviscosity at carbon 5 depth did not correlate significantly with percent changes plasma TC and LDL-C. Atorvastatin appeared to be the strongest drug liquidizing erythrocytes membranes. There were no significant changes in fluidity of membrane in its deeper layers (at carbon 16 level).


CONCLUSIONS
Statins therapy was beneficial not only for modification of plasma lipids but caused the increase of erythrocytes membrane fluidity in the surface layer.
Broncel
Marlena
M
Klinika Chorób Wewnetrznych z Oddziałem Farmakologii Klinicznej i Terapii Monitorowanej UM w Lodzi.
Chojnowska-Jezierska
Julita
J
Koter-Michalak
Maria
M
Franiak
Ida
I
D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004910:Erythrocyte Membrane / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects*; D008563:Membrane Lipids / Q000378:metabolism; D008875:Middle Aged; D017035:Pravastatin / Q000008:administration & dosage; D011758:Pyrroles / Q000008:administration & dosage; D019821:Simvastatin / Q000008:administration & dosage; D018709:Statistics, Nonparametric; D014280:Triglycerides / Q000097:blood
D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D008563:Membrane Lipids; D011758:Pyrroles; D014280:Triglycerides; D002784:Cholesterol; D000069059:Atorvastatin; D019821:Simvastatin; D017035:Pravastatin