Effects of fibrates on plasma prothrombotic activity in patients with type IIb dyslipidemia.
OBJECTIVE
Increased levels of fibrinogen and plasminogen activator inhibitor 1 (PAI-1) are associated with an increased risk of ischemic coronary disease and its complications. Since atherogenic dyslipidemias are well-known risk factors for coronary heart disease, this study aimed to determine whether Type IIb dyslipidemia, one of the most atherogenic dyslipidemias, is accompanied by increased PAI-1 and fibrinogen synthesis. The additional aim of this study was to evaluate the effect of micronized fibrates on the levels of PAI-1 and fibrinogen in patients with Type IIb dyslipidemia.


METHODS
Thirty patients with Type IIb dyslipidemia and 12 age-matched control subjects were studied. Fourteen patients were treated with fenofibrate and 16 were treated with ciprofibrate for 1 month.


METHODS
Plasma PAI-1 levels were measured by the ELISA method with Diagnostica Stago kit. The level of fibrinogen was measured by the Clauss method.


RESULTS
PAI-1 levels in dyslipidemic patients before treatment differed significantly in both the fenofibrate and ciprofibrate treatment groups (101.18 +/- 36.47 ng/ml, 87.64 +/- 32.06 ng/ml, respectively) from those in the control group (32.32 +/- 7.39 ng/ml, p < 0.001). Compared with the control subjects (2.91 +/- 0.35 g/l), fibrinogen levels before treatment were higher in patients with dyslipidemia treated with ciprofibrate (3.42 +/- 0.59 g/l, NS) and fenofibrate (3.65 +/- 1.10 g/l, p < 0.05). One-month ciprofibrate treatment resulted in an insignificant decrease in PAI-1 levels (76.28 21.60 ng/ml, NS) and in a significant decrease in fibrinogen levels (2.73 +/- 0.40 g/l, p < 0.01). After one-month fenofibrate treatment PAI-1 levels (81.22 +/- 25.01 ng/ml, p < 0.01) and fibrinogen levels (2.95 0.72 g/l, p < 0.01) decreased significantly.


CONCLUSIONS
Type IIb dyslipidemic patients have increased levels of PAI-1 and fibrinogen. Micronized fibrates decreased not only lipid levels but also the levels of fibrinogen and PAI-1 in these patients.
Okopien
B
B
Department of Clinical Pharmacology, Medical University of Silesia, Katowice, Poland.
Cwalina
L
L
Lebek
M
M
Kowalski
J
J
Zielinski
M
M
Wisniewska-Wanat
M
M
Kalina
Z
Z
Herman
Z S
ZS
D000328:Adult; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002995:Clofibric Acid / Q000031:analogs & derivatives / Q000627:therapeutic use*; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use*; D058607:Fibric Acids; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D013927:Thrombosis / Q000097:blood / Q000209:etiology; D010959:Tissue Plasminogen Activator / Q000097:blood; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D058607:Fibric Acids; D000960:Hypolipidemic Agents; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D002995:Clofibric Acid; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator; C019304:ciprofibrate; D011345:Fenofibrate