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Genotipo de fibrinógeno y riesgo de aterosclerosis periférica

F G Fowkes¹, J M Connor, F B Smith

¹Wolfson Unit for Prevention of Peripheral Vascular Diseases, Department of Public Health Sciences, University of Edinburgh, UK.

Lancet (London, England)

|March 21, 1992

Resumen

Las variaciones genéticas en el beta fibrinógeno influyen en el riesgo de aterosclerosis periférica. Esta asociación es independiente de los niveles plasmáticos de fibrinógeno, lo que sugiere que los cambios estructurales o los genes vinculados juegan un papel.

Área de la Ciencia:

Genética cardiovascular Genética cardiovascular Genética cardiovascular Genética cardiovascular Genética cardiovascular
Biología Molecular Biología Molecular
Epidemiología La epidemiología.

Sus antecedentes:

Existen pruebas contradictorias con respecto al impacto del genotipo de fibrinógeno en los niveles plasmáticos de fibrinógeno.
La relación entre el genotipo de fibrinógeno y el riesgo de enfermedad aterosclerótica sigue siendo poco estudiada.

Objetivo del estudio:

Investigar si los genotipos específicos de fibrinógeno están asociados con un mayor riesgo de aterosclerosis periférica.
Explorar el vínculo entre el genotipo de fibrinógeno y la enfermedad arterial periférica (EAP).

Principales métodos:

Se llevó a cabo un estudio de caso-control basado en la población utilizando datos del Estudio de la Arteria de Edimburgo.
Se analizaron 121 sujetos con enfermedad arterial periférica (casos) y 126 controles sanos de edad y sexo coincidentes.
Se evaluó el genotipo del fibrinógeno, específicamente el alelo de 4.2 kb en el locus beta del fibrinógeno (digestión Bcl I), y las concentraciones plasmáticas de fibrinógeno.

Principales resultados:

Las concentraciones plasmáticas medias de fibrinógeno fueron significativamente más altas en los casos en comparación con los controles (p < 0,001).
Una mayor proporción de casos fueron homocigotos o heterocigotos para el alelo de 4,2 kb en el locus beta fibrinógeno en comparación con los controles (frecuencia alelo 0,197 vs 0,097, p < 0,005).
Los haplotipos extendidos para 4,2 kb de heterocigotos se asociaron con un mayor riesgo de enfermedad arterial periférica, independientemente de varios factores de riesgo.

Conclusiones:

La variación en el locus beta fibrinógeno se asocia con un mayor riesgo de aterosclerosis periférica.
La asociación observada no está mediada únicamente por elevadas concentraciones plasmáticas de fibrinógeno.
El riesgo puede deberse a una variante estructural del fibrinógeno o a un desequilibrio de enlace con un gen vecino.

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