RESUMEN
The aims of this study were to determine Lipoprotein (a) [Lp(a)] concentrations in a sample of subjects from Maracaibo, Venezuela, and to determine the relationship of family risk factors for cardiovascular disease and their Lp(a) levels. Two hundred twenty-seven healthy individuals between 5 and 19 years of age of both genders and multiethnic origins were selected. A complete background clinical chart and laboratory test was conducted for each patient to discard cardiovascular diseases and confirm their healthy state. The Lp(a) concentration was determined using the double antibody enzyme-linked immunosorbent assay method. For inferential statistical analysis, one-factor analysis of variance tests and Student t test for independent observations were used according to each case, considered significant when P value was <0.05. No significant differences were observed when evaluating Lp(a) levels according to gender in all ages. Males showed no significant difference in Lp(a) levels between groups, but, in females, a significantly lower level (P < 0.03) in the group 5 to 9 years of age was found. When considering only age, significantly lower levels were observed (P < 0.03) in the 5- to 9-year-old group. When studying family risk factors of cardiovascular diseases, it was found that the group with family risk factors had a significantly higher Lp(a) concentration (P < 0.01) than those without family risk factors, observing that those who had four or more factors exhibited a significantly higher concentration than those with two to three risk factors (30.6 +/- 4.5 mg/dL versus 18.5 +/- 12.2 mg/dL, P < 0.009) and than those with one risk factor (30.6 +/- 4.5 mg/dL versus 21.6 +/- 1.4 mg/dL, P < 0.03). These results emphasize the clusters of family risk factors of cardiovascular disease with higher Lp(a) levels and also indicate that the evaluation of its concentration should be taken as an independent risk factor of atherosclerosis for the population in developmental ages.
Asunto(s)
Aterosclerosis/epidemiología , Enfermedades Cardiovasculares/sangre , Lipoproteína(a)/sangre , Adolescente , Adulto , Factores de Edad , Aterosclerosis/sangre , Enfermedades Cardiovasculares/epidemiología , Niño , Preescolar , Interpretación Estadística de Datos , Ensayo de Inmunoadsorción Enzimática , Femenino , Humanos , Masculino , Medición de Riesgo , Factores de Riesgo , Factores Sexuales , Venezuela/epidemiologíaRESUMEN
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.