Ciprofibrate treatment decreases non-high density lipoprotein cholesterol and triglycerides and increases high density lipoprotein cholesterol in patients with Frederickson type IV dyslipidemia phenotype.

OBJECTIVE: The combination of hypertriglyceridemia and low high density lipoprotein (HDL) cholesterol is one of the most common lipid abnormalities. Thus, the aim of this study was to determine the effects of ciprofibrate on lipid profile in patients with Frederickson's type IV dyslipidemia phenotype. RESEARCH DESIGN AND METHODS: Seventy-five patients with type IV dyslipidemia were assigned at random to 1 of 2 therapeutic options: group A (control), American Heart Association (AHA) Step II diet and physical activity; and group B, AHA diet, physical activity, and ciprofibrate 100 mg daily for 8 weeks. The lipid profile of all patients was determined at baseline and after therapeutic intervention. RESULTS: Patients in group B (treated with ciprofibrate) compared with group A (control) had significantly higher reductions in total cholesterol (downward arrow 14.2% vs. downward arrow 4.8%; P < 0.02), triglycerides (downward arrow 38.0% vs. downward arrow 21.6%; P < 0.007), very low density lipoprotein cholesterol (downward arrow 38.0% vs. downward arrow 21.6%; P < 0.007), non-HDL cholesterol (downward arrow 20.5% vs. downward arrow 7.1%; P < 0.007), and total cholesterol/high density cholesterol ratio (downward arrow 25.6% vs. downward arrow 9.4%; P < 0.01). The ciprofibrate group had a significantly higher increase in HDL cholesterol levels compared with the other group (upward arrow 25.0% vs. upward arrow 9.6%, P < 0.02). CONCLUSIONS: Ciprofibrate treatment effectively reduced triglyceride-rich particles and non-HDL cholesterol, and significantly increased HDL cholesterol, proving its effectiveness in patients with low HDL cholesterol and type IV Frederickson's hyperlipidemia.

Increased serum malondialdehyde and decreased nitric oxide within 24 hours of thrombotic stroke onset.

BACKGROUND AND PURPOSE: Ischemia/reperfusion generates free oxygen radicals, which react with the unsaturated lipids of biomembranes resulting in the generation products such as malondialdehyde. Malondialdehyde could be a sensor for tissue damage and reperfusion. Nitric oxide, released due to the early arrival of leukocytes in the brain parenchyma, could be a sensor for nonflow phenomenon. Thereby, the purpose of this research was to evaluate the behavior of malondialdehyde and nitric oxide within the 24 hours after the stroke onset. METHODS: Fifteen patients up to an age of 49 years, admitted to the emergency of University Hospital and Chiquinquirá Hospital in Maracaibo, Venezuela, were examined by a neurologist and underwent 12-lead electrocardiograms and computed tomography for the diagnosis of thrombotic stroke. Serum malondialdehyde and nitric oxide were measured as thiobarbituric acid adducts and total nitrites. Data were collected within the 24 hours after the stroke onset. RESULTS: Malondialdehyde for patients with stroke had a significant increase (P<0.001) when compared with healthy controls (47.9 +/- 7.1 vs. 1.7 +/- 0.2 micromol/L). Conversely, serum nitric oxide for patients with stroke had a significant decrease (P<0.001) when compared with the control group (14.5 +/- 1.4 vs. 41.3 +/- 3.7 micromol/L). The lowest values of malondialdehyde and the highest values of nitric oxide were observed in two patients, who died. CONCLUSIONS: Serum levels of malondialdehyde increase, and serum levels of nitric oxide diminish within 24 hours after the onset of thrombotic stroke onset. This suggests that serum malondialdehyde level could be used as potentially reliable and sensitive marker for reperfusion, whereas nitric oxide levels could acts as potential biochemical sensor for nonreflow phenomenon.