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>Revistas >Revista de Hematología >Año 2013, No. 1


Geyer HL, Tibes R, Mesa RA
Inhibición de JAK-2: su empleo en mielofibrosis y lecciones iniciales de la experiencia mexicana
Rev Hematol Mex 2013; 14 (1)

Idioma: Inglés
Referencias bibliográficas: 64
Paginas: 26-36
Archivo PDF: 640.91 Kb.


Texto completo




RESUMEN

Las neoplasias mieloproliferativas BCR-ABL negativas incluyen a la trombocitosis esencial o primaria, a la policitemia vera y a la mielofibrosis primaria. Este último padecimiento destaca por ser el de mayor morbilidad y mortalidad entre las subclases. El complejo biogenético subyacente a estas hemopatías clonales ha tenido, históricamente, avances notables en terapias contra genes específicos e inhibición de las citocinas proinflamatorias fundamentales para el inicio de los síntomas.
El descubrimiento de la mutación JAK2V617F condujo a la integración de biomarcadores genéticos para estrategias diagnósticas y terapéuticas. La década pasada quedó marcada por el desarrollo rápido de terapias con inhibidores de JAK2 capaces de reducir la esplenomegalia, las citopenias y los síntomas constitucionales con mínima mielosupresión y toxicidad secundaria.
El ruxolitinib fue el primer inhibidor JAK2 aprobado por la FDA en 2011 para riesgo alto e intermedio de mielofibrosis. El año pasado se realizaron avances notables en el entendimiento de eficacia, tolerabilidad y repercusiones en la esperanza de vida, incluido el análisis post-hoc de los ensayos COMFORT-I y COMFORT-II, la repercusión del fármaco a pesar de las trombocitopenias de base y efectos del estado mutacional de JAK2V617F. Sin embargo, la integración de los avances científicos en la práctica clínica permanece como un reto para todo el personal de salud que participa en el tratamiento de pacientes con mielofibrosis primaria.
El desarrollo reciente de los programas de abastecimiento individual de pacientes (Individual Patient Supply Programs) y los programas de uso compasivo (Compassionate Use Programs) se han extendido significativamente y las terapias eficaces a pacientes, que de otro modo no serían accesibles fuera del entorno de ensayos clínicos. Mientras se examina el futuro de los tratamientos de las neoplasias mieloproliferativas, está claro que la integración de los avances científicos debe permanecer paralela al tiempo-sensibilidad de la aplicación del paciente, para ofrecerle mayor alivio a quienes padecen alguna clase de neoplasia mieloproliferativa.


Palabras clave: trombocitopenia esencial, policitemia vera, mielofibrosis, mielofibrosis primaria, neoplasias mieloproliferativas, inhibidor JAK2, leucemia aguda.


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