Hypolipidemic agents drug interactions: approach to establish and assess its clinical significance. Structured review. Franco 1,4 , Y. Henao 1 , M. Monsalve 1,4 , F.
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The relationship between hypercholesterolemia and the development of cardiovascular disease, especially coronary heart disease, is well established. In addition, cardiovascular disease risk is elevated in genetically inherited forms of hyperlipemia. Currently available evidence indicates that long-term lipid-lowering therapy reduces the risk of cardiovascular morbidity and mortality.
Risk stratification is important for defining target LDL cholesterol levels and for selecting appropriate therapy. Statins are regarded as first-line treatment for hypercholesterolemia, and fibrates as first-line treatment for hypertriglyceridemia. Both groups of compounds are safe and well-tolerated and have been shown to reduce risk in clinical trials. In patients who do not attain the target LDL cholesterol level, combination therapy is an option. The most useful combinations are a statin plus ezetimibe for severe hypercholesterolemia, and a statin plus a fibrate for mixed hyperlipemia.
Careful selection and follow-up of therapy can help to prevent the development of adverse events in liver or muscle.. Tratamiento de las hiperlipemias en pacientes con riesgo cardiovascular elevado. Management of Hyperlipemia in Clinical Practice. Descargar PDF. Rodrigo A. Autor para correspondencia. Departamento de Medicina Interna. Palabras clave:. Careful selection and follow-up of therapy can help to prevent the development of adverse events in liver or muscle.
Key words:. Goldstein, H. Hobbs, M. The metabolic and molecular basis of inherited disease, pp. Civeira, S. Castillo, R. Alonso, E. Merino-Ibarra, A. Cenarro, M. Artied, et al. Tendon xanthomas in familial hypercholesterolemia are associated with cardiovascular risk independently of the low-density lipoprotein receptor gene mutation.
Arterioscler Thromb Vasc Biol, 25 , pp. Alonso, S. Castillo, F. Civeira, J. Puzo, J. De la Cruz, M. Pocovi, et al.
Med Clin Barc , , pp. Hill, M. Hayden, J. Frohlich, P. Genetic and environmental factors affecting the influence of coronary artery disease in heterozygous familial hypercholesterolemia. Arterioscler Thromb, 11 , pp. Brown, J. Molecular genetics of the LDL receptor gene in familial hypercholesterolemia.
Hum Mutat, 1 , pp. Guidelines for the diagnosis and management of heterozygous familial hypercholesterolemia. Atherosclerosis, , pp. Tejedor, S. Castillo, P.
Mozas, E. Tejedor, et al. Reliable low-density DNA array based on allele-specific probes for detection of mutations causing familial hypercholesterolemia. Clin Chem, 51 , pp. Genest, S. Martin Munley, J. McNamara, J. Ordovas, J. Jenner, R. Myers, et al. Familial lipoprotein disorders in patients with premature coronary artery disease.
Circulation, 85 , pp. Veerkamp, J. De Graaf, S. Bredie, J. Hendriks, P. Demacker, A. Diagnosis of familial combined hyperlipidemia based on lipid phenotype expression in 32 families. Arterioscler Thromb Vasc Biol, 22 , pp. Pajukanta, I. Nuotio, J. Terwilliger, K. Porkka, K. Ylialo, J. Linkage of familial combined hyperlipidemia to chromosome 1qq Nat Genet, 18 , pp. Cortner, P. Coates, P. Prevalence and expression of familial combined hyperlipidemia in childhood.
J Pediatrics, , pp. Mahley, Y. Huang, S. Pathogenesis of type III hyperlipoproteinemia dysbetalipoproteinemia : questions, quandaries, and paradoxes.
J Lipid Res, 40 , pp. Dobmeyer, J. Lohrmann, G. Prevalence and association of atherosclerosis at three different arterial sites in patients with type III hyperlipoproteinemia. Rev Esp Cardiol, 53 , pp. De Backer, E. Ambrosioni, K. Borch-Johnsen, C. Brotons, R. Cifkova, J. Dallongeville, et al. Executive summary. Eur Heart J, 24 , pp. Grundy, J. Cleeman, C. Merz, H. Brewer, L. Clark, D.
2009, Número 1
Los pacientes deben consultar con su profesional de la salud si tienen cualquier pregunta o inquietud sobre estatinas. Los casos aparentemente no estaban vinculados con demencia fija o progresiva, como la enfermedad de Alzheimer. Un estudio reciente por Culver et al. Statin-associated memory loss: analysis of 60 case reports and review of the literature. Statin-associated adverse cognitive effects: survey results from patients.
U.S. Food and Drug Administration
Statins are lipid lowering agents that promote their effects on plasma lipids through the inhibition of HMG-CoA reductase, a crucial enzyme in the cascade of cholesterol synthesis, leading to reduction of tissue cholesterol pool and consequently, to an upregulation of the LDL receptor expression. There are considerable differences among statins regarding some pharmacokinetic properties, such as the coefficient of hydrophilicity, via liver metabolism especially regarding P cytochrome and isoenzymes , plasma half-life and efficacy of serum lipid changes. They may also differ regarding interactions with other drugs that share the same pathway of metabolism. Recently, many pleiotropic effects have been reported with these drugs, such as anti-inflammatory properties, improvement in endothelial function and benefits on hemostasis. Key words: Statins, pharmacokinetics, drug interactions. Figura 5.
Multicenter, open-label, randomized study comparing the efficacy of atorvastatin versus usual care in reducing refractory hypercholesterolemia in high-risk patients to target levels. Curr Therap Res. Status of statins, utilization and unanswered questions. Lipoprotein changes and reduction in the incidence of major coronary heart disease events in the Scandinavian simvastatin survival study.