Effect of Ciprofibrate on Lipoproteins,Fibrinogen,Renal Function,and Hepatic Enzymes

Aim: The action of ciprofibrate in hypertriglyceridemic patients is well established. Not only is ciprofibrate able to alter the lipid profile, but it can also change the values of fibrinogen, C-reactive protein, creatinine, transaminases, y-glutamyl transpeptidase and serum alkaline phosphatase. However, previous studies focused on the effect of ciprofibrate in hypertriglyceridemic patients, leaving unanswered the question of whether ciprofibrate exerts the same effect on hyperlipidemic patients with normal triglyceride values. The aim of this study is to answer this question.

Methods: In this randomized clinical trial, 64 men and women with elevated cholesterol or triglyceride levels were included. Two subgroups were formed according to triglyceride levels: one (36 patients) with elevated triglyceride levels (> 200 mg/dL [2.26 mmolIL]) and another (28 patients) with normal triglyceride levels (< 200 mg/dL [2.26 mmol/l]). After a 6-week period of step 1 diet according to the National Cholesterol Education Program, ciprofibrate (100 mg once daily) was administered for 16 weeks. Primary efficacy points were the changes of lipid parameters (total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, triglycerides, apoproteins Al, B, E and lipoprotein [a], high sensitivity C reactive protein, fibrinogen, glucose, insulin, aspartate transaminase, alanine transaminase, y-glutamyl transpeptidase, alkaline phosphatase, urea and creatinine levels in a fasting blood sample before and after treatment with ciprofibrate.

Results: The subgroup with triglyceride < 200 mg/dL (2.26 mmol/L): After the administration of ciprofibrate total cholesterol and low-density lipoprotein cholesterol were reduced by 15% (P < 0.001), and 19% (P < 0.001), respectively, while high-density lipoprotein cholesterol increased by 9% (P = 0.02). Apoproteins B and E levels were reduced by 21% (P < 0.001) and 11% (P = 0.002), respectively. Subgroup with triglyceride > 200 mg/dL (2.26 mmol/L): After the administration of ciprofibrate, no significant change in LDL cholesterol levels was observed. Total cholesterol levels were reduced by 15% (P < 0.001) and high-density lipoprotein cholesterol levels were increased by 13% (P = 0.004). Apoprotein B and apoprotein E levels were reduced by 16% (P < 0.001) and 30% (P < 0.001), respectively. Apoprotein-Al levels were increased by 5% (P = 0.024). In the whole group of patients, the fibrinogen levels fell by 7% (P = 0.043), and the serum creatinine level increased by 10% (P < 0.001). This rise in serum creatinine was more pronounced in patients with low triglyceride levels (15% vs 5%, P = 0.009). Ciprofibrate decreased C-reactive protein levels by 26% in 44 patients who had C-reactive protein measurements (P < 0.001). y-glutamyl transpeptidase activity was similarly decreased (by approximately 40%) in both groups of patients. Alkaline phosphatase activity decreased in both groups, a reduction which was greater in hypertriglyceridemics (20% vs 10%, P = 0.004).

Conclusions: Ciprofibrate improved some of the vascular risk factors, such as total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apoproteins Al, B, and E, and fibrinogen levels in both hypertriglyceridemics and normotriglyceridemics. In addition, ciprofibrate raised the serum creatinine and improved the activity of the hepatic enzymes in the plasma in both patient subgroups.