2005, Número 4
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Rev Invest Clin 2005; 57 (4)
Resistencia a la proteína C activada y actividad de anticoagulante lúpicoinducidas por plasma y por anticuerpos purificadoshumanos del IgG anti Β2-glicoproteína I
Viveros ME, Cabiedes J, Reyes E, Cabral AR
Idioma: Ingles.
Referencias bibliográficas: 54
Paginas: 563-571
Archivo PDF: 104.52 Kb.
RESUMEN
Introducción. Investigamos la resistencia a la proteína C activada (RPCA) y la actividad de anticoagulante lúpico (AL), inducidas por anticuerpos anti-Β
2-glicoproteína-I (anti-Β
2GP-I).
Pacientes y métodos. Estudiamos los plasmas y sueros persistentemente positivos para anti-Β
2GP-I de 29 pacientes: 22 tuvieron trombosis (12 con síndrome de antifosfolípidos [SAF] primario y 10 con SAF secundario a lupus eritematoso generalizado [LEG]) y siete sin trombosis (todos con LEG). Como controles estudiamos 25 sueros de personas clínicamente sanas. Detectamos anticuerpos anticardiolipina, anti-Β
2GP-I IgG (y sus subclases) e IgM por ELISA en placas irradiadas y no irradiadas. Evaluamos la RPCA por medio del tiempo parcial de tromboplastina activada y por la prueba modificada. Estudiamos la mutación FV de Leiden por PCR y el anticoagulante lúpico con el método de dRVVT screening y confirmatorio. Después de purificar los anti-Β
2GP-I séricos con una columna de antígeno unido a sefarosa, analizamos por ELISA sus isotipos, subclases y reactividad contra Β
2GP-I y algunos fosfolípidos.
Resultados. Los títulos de anti-Β
2GP-I IgG fueron más altos en placas irradiadas que en no irradiadas (p = 0.002), predominó la subclase IgG2. Quince plasmas (13 de pacientes con trombosis) tuvieron AL y 15 (13 también de pacientes con trombosis) indujeron el fenotipo de RPCA. Once plasmas (todos de pacientes con trombosis) indujeron ambas actividades. Dos pacientes fueron heterocigotos para la mutación de Leiden. Dos anticuerpos purificados monoespecíficos para Β
2GP-I indujeron el fenotipo de la RPCA y la actividad de AL in vitro.
Conclusiones. Nuestros resultados sugieren que la RPCA, inducida por los anti-Β
2GP-I que concomitantemente tienen actividad de AL, puede tener implicaciones patogénicas en la trombofilia del SAF.
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