Uso de inhibidores de tirosina quinasa en carcinoma medular de tiroides: Experiencia institucional

Romina Luca; Florencia Tsou; Florencia do Pico; Sergio Rivero; Agustín Falco; Juan Manuel O’Connor; Matías Chacón; Reinaldo Chacón

doi:10.56969/oc.v22i1.75

Autores/as

Romina Luca Instituto Alexander Flemming, Buenos Aires
Florencia Tsou Instituto Alexander Fleming, Buenos Aires https://orcid.org/0000-0002-0322-0434
Florencia do Pico Instituto Alexander Fleming, Buenos Aires
Sergio Rivero Instituto Alexander Fleming, Buenos Aires https://orcid.org/0000-0002-7832-4203
Agustín Falco Instituto Alexander Fleming, Buenos Aires https://orcid.org/0000-0003-4487-2444
Juan Manuel O’Connor Instituto Alexander Flemming, Buenos Aires
Matías Chacón Instituto Alexander Flemming, Buenos Aires https://orcid.org/0000-0002-4935-9773
Reinaldo Chacón Instituto Alexander Fleming, Buenos Aires

DOI:

https://doi.org/10.56969/oc.v22i1.75

Palabras clave:

cáncer medular de tiroides, inhibitores de tirosina quinasa, sorafenib, sunitinib, vandetanib, medullary thyroid cancer, tyrosine kinase inhibitors

Resumen

El cáncer medular de tiroides (CMT) corresponde al 5% de los tumores de la glándula tiroides. El único tratamiento curativo es la cirugía. En pacientes con compromiso locorregional o a distancia, la enfermedad puede evolucionar en forma indolente o bien con una rápida progresión de síntomas, requiriendo tratamiento sistémico. Si bien el CMT se caracteriza por tener escasa respuesta a la quimioterapia (QT), la evidencia actual en estudios aleatorizados demostró que los inhibidores de tirosina quinasa (ITQ) han demostrado beneficio en supervivencia libre de progresión (SLP).

Se analizaron 6 pacientes con un seguimiento mediano de 29 meses. Todos presentaron más de dos sitios metastásicos. Dos requirieron tratamientos locorregionales (quimioembolización y RT). Los ITQ más utilizados fueron: vandetanib (3), sorafenib (2) y sunitinib (1). Un 50% inició tratamiento con dosis plenas y 3 requirieron reducción de dosis debido a toxicidad G3-G4. El intervalo libre de progresión (ILP) mediano, luego del inicio con ITQ, fue de 4.1 meses.

Citas

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