I Diretriz sobre o consumo de Gorduras e Saúde Cardiovascular Definição do grau dos níveis de evidência Recomendações Classe I: Condições para as quais há evidências conclusivas e, na sua falta, consenso geral de que o procedimento é seguro útil/eficaz. Classe II: Condições para as quais há evidências conflitantes e/ou divergência de opinião sobre segurança e utilidade/ eficácia do procedimento. Classe IIa: Peso ou evidência/opinião a favor do procedimento. A maioria aprova. Classe IIb: Segurança e utilidade/eficácia menos bem estabelecidas, não havendo predomínio de opniões a favor. Classe III: Condições para as quais há evidências e/ou consenso de que o procedimento não é útil/eficaz e, em alguns casos, pode ser prejudicial. Evidências Nível A: Dados obtidos a partir de múltiplos estudos randomizados de bom porte, concordantes e/ou de Metanálise robusta de estudos clínicos randomizados. Nível B: Dados obtidos a partir de Metanálise menos robusta, a partir de um único estudo randomizado ou de estudos não randomizados (observacionais). Nível C: Dados obtidos de opiniões consensuais de especialistas.
Objective: To verify the effects on the lipid pro®le of a product of fermented milk (Gaio 1 ) in patients with mild to moderate primary hypercholesterolemia. Design: The study was prospective, randomized, double-blinded and placebo controlled, with a crossover design. Subjects: Thirty-two patients (21 women and 11 men) with ages ranging between 36 and 65 years old were included in the study. All of them were on a controlled diet for at least 8 weeks. Intervention: Patients began, after clinical and laboratory analysis, in a randomized and double-blind manner to take 200 g daily of Gaio 1 or its placebo. After 8 weeks blood was collected again for lipid pro®le evaluation and the crossover was made. After an additional 8 weeks blood was collected for another lipid pro®le determination. Results: All patients included completed the study. Comparisons were made between means of lipid pro®le constituents after the placebo and active product periods. These showed signi®cant mean reduction of 5.3% (P 0.004) for total cholesterol, 6.15% (P 0.012) for LDL-cholesterol and no signi®cant variation for HDLcholesterol and triglycerides. The majority of patients presented no variation or had a decrease in their total cholesterol level. However, during the active product period, three patients showed an increase in cholesterol level by more than 5%. Conclusion: The fermented milk (Gaio 1 ) produced a small but statistically signi®cant decrease in total and LDL-cholesterol mean. However, not all subjects seem to respond to the product, and a few subjects showed a cholesterol increment. Further investigations are necessary to clarify this aspect.
ChOx are suitable biomarkers of oxidative stress and may be useful in clinical studies to follow drug effects on lipid oxidative modifications in diabetic patients.
AimsThe relationship between variants in SLCO1B1 and SLCO2B1 genes and lipid-lowering response to atorvastatin was investigated.Material and MethodsOne-hundred-thirty-six unrelated individuals with hypercholesterolemia were selected and treated with atorvastatin (10 mg/day/4 weeks). They were genotyped with a panel of ancestry informative markers for individual African component of ancestry (ACA) estimation by SNaPshot® and SLCO1B1 (c.388A>G, c.463C>A and c.521T>C) and SLCO2B1 (−71T>C) gene polymorphisms were identified by TaqMan® Real-time PCR.ResultsSubjects carrying SLCO1B1 c.388GG genotype exhibited significantly high low-density lipoprotein (LDL) cholesterol reduction relative to c.388AA+c.388AG carriers (41 vs. 37%, p = 0.034). Haplotype analysis revealed that homozygous of SLCO1B1*15 (c.521C and c.388G) variant had similar response to statin relative to heterozygous and non-carriers. A multivariate logistic regression analysis confirmed that c.388GG genotype was associated with higher LDL cholesterol reduction in the study population (OR: 3.2, CI95%:1.3–8.0, p < 0.05).ConclusionSLCO1B1 c.388A>G polymorphism causes significant increase in atorvastatin response and may be an important marker for predicting efficacy of lipid-lowering therapy.
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