title: [Effect of ciprofibrate on the endothelial dysfunction of patients with combined dyslipidemia].
abstract: Endothelial dysfunction can be detected in the early phase of atherosclerosis. Two unresolved questions have been raised the wether, (1) the dyslipidemic state alone without any other risk factors can be harmful for the endothelial function measured by ultrasound, and (2) the use of the antilipidemic fibrate is sufficient to influence the endothelial functions. From 38 subjects with solitary combined dyslipidaemia 32 (84%) showed endothelial dysfunction measured by flow mediated vasodilatation (FMD) on the forearm and this group of patients was featured only by higher fibrinogen levels (no differences on BMI, serum lipid and glucose level). The patients with endothelial dysfunction were treated with 100 mg of ciprofibrate per day (12 women, 20 men, average age: 44.6 +/- 9 years, BMI 24.6 +/- 3.4 kg/m2). The pretreatment serum lipid levels were: total cholesterol 6.9 +/- 0.4, triglyceride 4.2 +/- 0.3, HDL cholesterol 1.13 +/- 0.21 mmol/l. After the 4 weeks treatment period the cholesterol and triglyceride level decreased, the concentration of HDL cholesterol increased significantly, which changes were in correspondence with significant improvement of FMD (3.9 +/- 0.7% vs. 7.0 +/- 1.6%). The level of fibrinogen also declined significantly. At the 8th week there were no significant further changes compared to the data received at the 4th week. Using the lineal regressive analysis the improved vasodilatator respond at both check points was correlated only with the fall of total cholesterol level. The ciprofibrate was suspended after the 8th week for a 4 weeks period and the triglyceride and the fibrinogen levels increased whereas the HDL cholesterol level decreased significantly. The FMD impaired significantly (to 5.8 +/- 1.2%). There were no correlations among the changes. The results demonstrated the lipid and probably non-lipid-factors are important in these early damages of endothelial functions.
authors.affiliation: Markusovszky Kórház, Szombathely, III. Belgyógyászat.
authors.forename: I
authors.initials: I
authors.lastname: Kovács
authors.forename: J
authors.initials: J
authors.lastname: Tarján
authors.forename: A
authors.initials: A
authors.lastname: Császár
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002995:Clofibric Acid / Q000031:analogs & derivatives / Q000494:pharmacology* / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D058607:Fibric Acids; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D016014:Linear Models; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014664:Vasodilation
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D058607:Fibric Acids; D000960:Hypolipidemic Agents; D008055:Lipids; D014280:Triglycerides; D002995:Clofibric Acid; C019304:ciprofibrate