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>Revistas >El Residente >Año 2016, No. 2


Martínez-Acosta G, Zermeño-González ML, Robles-Espinoza AI, Trujillo-Quiros J, Nava-Zavala AH, Rubio-Jurado B
Trombosis en mieloma múltiple hemostasia y citocinas implicadas
Residente 2016; 11 (2)

Idioma: Español
Referencias bibliográficas: 60
Paginas: 71-80
Archivo PDF: 315.80 Kb.


Texto completo




RESUMEN

El mieloma múltiple es una neoplasia que se origina por un desorden en la proliferación de células plasmáticas, se caracteriza por la producción de una proteína monoclonal en la sangre o en la orina y por la disfunción de algún órgano asociado. Sus manifestaciones clínicas se relacionan con el daño a órgano blanco, como son hipercalcemia, insuficiencia renal, anemia y lesiones óseas. La incidencia es de tres a cuatro casos por 100 mil/h, representa 1% de todas las neoplasias y 10% de las neoplasias hematológicas. La hemostasia es un mecanismo de defensa cuya finalidad es conservar la integridad vascular y evitar la pérdida de sangre mediante cambios fisiológicos que conducen a la formación de un trombo hemostático, reparar el daño y finalmente disolver el coágulo. De manera concomitante sucede la hemostasia primaria (interacción de plaquetas y endotelio) y la hemostasia secundaria (participación de los factores de coagulación), el modelo celular de la coagulación integra la fase celular. Existe un estado de hipercoagulabilidad en el cáncer en el que interactúan elementos del sistema de la hemostasia con células tumorales, endotelio, plaquetas, monocitos y neutrófilos. Las proteínas procoagulantes del cáncer, las proteínas fibrinolíticas, las citocinas y los factores de crecimiento endotelial son algunos elementos que participan. La enfermedad tromboembólica es más frecuente en el cáncer con un riesgo 4.3 veces mayor que en la población general y en mieloma múltiple, hasta 30% de los pacientes puede presentarla durante su historia natural, lo cual se relaciona con el tratamiento (inmunomoduladores, esteroides, alquilantes) y la interacción con factores trombóticos adquiridos.


Palabras clave: Cáncer, citocinas, hemostasia, tromboembolia pulmonar, trombosis venosa profunda.


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>Revistas >El Residente >Año2016, No. 2
 

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