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Inicio Clínica e Investigación en Arteriosclerosis Efecto del etofibrato de liberación sostenida en pacientes con concentraciones ...
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Vol. 15. Núm. 1.
Páginas 8-15 (enero 2003)
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Vol. 15. Núm. 1.
Páginas 8-15 (enero 2003)
Acceso a texto completo
Efecto del etofibrato de liberación sostenida en pacientes con concentraciones plasmáticas de lipoproteína(a) > 300 mg/l
Extended-Release Etofibrate: Effect in Patients with Plasma Lp(A) Concentrations > 300 Mg/L
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3440
A. Nasiff-Hadada,
Autor para correspondencia
nasiff@infomed.sld.cu

Correspondencia: Hospital Hermanos Ameijeiras. San Lázaro, 701. 10300 La Habana. Cuba.
, P. Ramos-Marína, R. Simón-Carballob, N. Cordero-Rojasa, J. Sotoa, E. Meriño-Ibarraa
a Grupo de dislipidemias y aterosclerosis. Hospital Hermanos Ameijeiras. La Habana
b Instituto Nacional de Angiología y Cirugía Vascular. La Habana. Cuba
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Objetivos

Evaluar el efecto del etofibrato de liberación sostenida en las concentraciones de lipoproteína(a) [Lp(a)] plasmática en pacientes con concentraciones superiores a 300 mg/l después de 3 meses de dieta tipo etapa I del National Colesterol Education Program (NCEP)

Método

De un total de 112 pacientes examinados en la consulta externa de dislipidemias del Hospital Hermanos Ameijeiras, La Habana, se seleccionó a 20 pacientes (10 varones y 10 mujeres) que presentaron concentraciones séricas de Lp(a) superiores a 300 mg/l después de 3 meses de dieta hipolipemiante etapa I del NCEP. Se administró a los pacientes seleccionados etofibrato, 500 mg/día, durante 24 semanas. Se determinaron las concentraciones de colesterol y triglicéridos totales, de colesterol asociado a las lipoproteínas de baja (cLDL) y alta (cHDL) densidad y las de Lp(a) antes y a las 4, 12 y 24 semanas del tratamiento

Resultados

Se observaron reducciones significativas de colesterol, triglicéridos y cLDL y aumentos de cHDL en cada tiempo analizado en relación con el valor basal. Las concentraciones séricas de Lp(a) se redujeron significativamente (p < 0,01) con la administración de etofibrato: 856 mg/l en situación basal, 617 mg/dl a la cuarta semana después del tratamiento, 594 mg/l a la 12.a semana y 604 mg/l a la 24.a semana. La reducción ya fue significativa desde la cuarta semana de tratamiento y se mantuvo así hasta la 24.a semana. En 4 de los 20 pacientes, cuyas concentraciones basales de Lp(a) fueron las más bajas de todo el grupo, se observó un aumento significativo (p < 0,001) de la Lp(a) en la semana 24 de tratamiento (desde 559 a 636 mg/l)

Conclusiones

El etofibrato de liberación retardada, a dosis de 500 mg/día, redujo las concentraciones de Lp(a) en más del 30%, en relación a su valor basal, después de 4 semanas de su administración y mantuvo esta tendencia durante las 24 semanas de control en los pacientes con las concentraciones más elevadas; en los pacientes con concentraciones más bajas (aunque superiores a 300 mg/l) se incrementó ligera, pero significativamente la Lp(a). Estos efectos del etofibrato en la concentración de Lp(a) no han sido descritos con anterioridad

Palabras clave:
Lipoproteína(a)
Etofibrato
Objectives

To evaluate the effect of a sustainedrelease form of etofibrate on the lipoprotein(a) [Lp(a)] concentration in patients showing Lp(a) concentrations higher than 300 mg/l after a 3- month period of NCEP National Cholesterol Education Program (NCEP) step-I diet

Methods

Among 112-screened patients, 20 (10 female and 10 male) were selected when their Lp(a) concentrations were higher than 300 mg/l after 3-month period on NCEP step type-I diet. All selected patients received etofibrate retard (500 mg/day) during 24 weeks. Total cholesterol and triglycerides and cholesterol associated to low (LDLc) and high density (HDLc) lipoproteins, as well as Lp(a) concentrations were measured before and after 4, 12 and 24 weeks of etofibrate therapy

Results

Significant decrease respect to pretreatment values was observed for total cholesterol and triglyceride and for low (LDLc) and high (HDLc) cholesterol concentrations after etofibrate therapy. Lp(a) concentrations decreased significantly (p < 0.01) from 856 to 617 mg/l (after 4 weeks of etofibrate), 594 (after 12 weeks) and 604 (after 24 weeks). Significant reductions of Lp(a) occurred since week 4 of therapy. Four of the 20 treated patients, showed small, but significant (p < 0.001) increases (from 559 to 636 mg/l) of Lp(a) concentrations after etofibrate therapy; Lp(a) concentrations of these patients were the smallest among all the analyzed patients

Conclusions

Extended-release etofibrate at a dose of 500 mg/day reduced Lp(a) concentrations in a 30% after 4-weeks of therapy; the effect of etofibrate on Lp(a) concentrations extended until the end of therapy (at 24th week of treatment). Etofibrate reduced Lp(a) concentrations in patients showing higher Lp(a) concentrations; however, in patients showing smallest increases of Lp(a) a light, but significant, increase of Lp(a) was observed. These effects of etofibrate on Lp(a) concentrations are described for the first time

Key words:
Lipoprotein(a)
Etofibrate
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