ABSTRACT
Familial hypercholesterolemia is associated with premature coronary heart disease. In patients with familial hypercholesterolemia, monotherapy with hydroxymethylglutaril coenzyme. A reductase inhibitors rarely achieves the goal of desirable low-density lipoprotein levels. Epidemiological studies suggest that populations with a high dietary intake of marine n3 fatty acids are protected against coronary heart disease. Hepatic synthesis and secretion of very low density lipoproteins are reduced during fish oil supplementation while other effects on lipid and lipoprotein metabolism are controversial. Fourteen patients affected by familial heterozygous hypercholesterolemia on chronic treatment with simvastatin were enrolled in a double blind, placebo controlled, randomized crossover trial that evaluated the effect of fish oil ethyl ester (Esapent, 5.1 g/day) on lipid and lipoprotein serum concentrations. Total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglycerides, apoprotein B, apoprotein AI, lipoprotein (a) did not show any significant variation during the four week treatment period with fish oil ethyl ester. The present data suggest that the possible favourable influence of fish oil on the progression of atherosclerosis in these high-risk patients might involve mechanisms which are different from lipid metabolism.
Subject(s)
Dietary Fats, Unsaturated/administration & dosage , Docosahexaenoic Acids/administration & dosage , Eicosapentaenoic Acid/administration & dosage , Hyperlipoproteinemia Type II/drug therapy , Plant Oils/administration & dosage , Adult , Aged , Anticholesteremic Agents/therapeutic use , Cross-Over Studies , Double-Blind Method , Drug Combinations , Female , Heterozygote , Humans , Hyperlipoproteinemia Type II/genetics , Lovastatin/analogs & derivatives , Lovastatin/therapeutic use , Male , Middle Aged , Olive Oil , Simvastatin , Time FactorsABSTRACT
BACKGROUND AND PURPOSE: Protein C and protein S have been found reduced in some patients with ischemic cerebrovascular diseases, but the relevance of this finding for prognosis is unsettled. METHODS: In 43 consecutive patients admitted over 6 months for acute ischemic stroke, protein C and free protein S were evaluated on admission, and at 2 and 6 months after stroke. Excluded were all patients with known causes liable to reduce the levels of protein C, free protein S, or both. RESULTS: In 14% of patients, abnormally low levels of protein C were found at entry. In comparison to the remaining sample, this group had a significantly lower initial score on the Barthel and Canadian neurological scales, a higher prevalence of emboligenic cardiac diseases, and had a higher mortality at 6 months. No statistical difference was found for the other vascular risk factors. Eight patients (18.4%) had abnormally low levels of free protein S at entry. In comparison to the remaining sample, there was no statistical difference in the severity scores, prevalence of emboligenic cardiac diseases, mortality, or vascular risk factors. CONCLUSIONS: These findings suggest that low levels of protein C in the acute stroke reflect the massive activation of coagulation factors and are predictive of adverse outcome, whereas the significance of low levels of free protein S remains to be clarified.
