Objective: Increased levels of fibrinogen and plasminogen activator inhibit
or 1 (PAI-1) are associated with an increased risk of ischemic coronary dis
ease and its complications. Since atherogenic dyslipidemias are well-known
risk factors for coronary heart disease, this study aimed to determine whet
her Type IIb dyslipidemia, one of the most atherogenic dyslipidemias, is ac
companied by increased PAI-1 and fibrinogen synthesis. The additional aim o
f this study was to evaluate the effect of micronized fibrates on the level
s of PAI-1 and fibrinogen in patients with Type IIb dyslipidemia. Subjects:
Thirty patients with Type IIb dyslipidemia and 12 age-matched control subj
ects were studied. Fourteen patients were treated with fenofibrate and 16 w
ere treated with ciprofibrate for 1 month. Methods: Plasma PAI-1 levels wer
e measured by the ELISA method with Diagnostica Stago kit. The level of fib
rinogen was measured by the Clauss method. Results: PAI-1 levels in dyslipi
demic patients before treatment differed significantly in both the fenofibr
ate 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), fi
brinogen 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 insig
nificant decrease in PAI-1 levels (76.28 +/- 21.60 ng/ml, NS) and in a sign
ificant 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 significa
ntly. Conclusion: Type IIb dyslipidemic patients have increased levels of P
AI-1 and fibrinogen. Micronized fibrates decreased not only lipid levels bu
t also the levels of fibrinogen and PAI-1 in these patients.