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Neuropatía óptica hereditaria de Leber de aparición tardía y antiandrógenos para el cáncer de próstata: ¿existe un
Giulia Amore1,2, Michele Carbonelli3, Diego D'Angeli3
1Department of Medical and Surgical Sciences (DIMEC), Alma Mater Studiorum - University of Bologna, Bologna, Italy.
Frontiers in neurology
|September 2, 2025
Resumen
La terapia de privación de andrógenos (ADT) puede desencadenar la neuropatía óptica hereditaria de Leber (LHON) de aparición tardía en hombres con cáncer de próstata. Este desequilibrio hormonal, particularmente los niveles bajos de estrógeno, puede conducir a una reducción del número de copias de ADN mitocondrial y a la pérdida de la visión.
Área de la Ciencia:
- Oftalmología
- La genética
- Endocrinología
Sus antecedentes:
- La neuropatía óptica hereditaria de Leber (LHON) es una enfermedad de ADN mitocondrial hereditaria materna, que generalmente afecta a hombres jóvenes y muestra un efecto protector femenino, posiblemente debido a los estrógenos.
- La LHON de aparición tardía a menudo está relacionada con exposiciones tóxicas, pero los casos no relacionados con estos factores son menos conocidos.
Objetivo del estudio:
- Para reportar dos casos inusuales de LHON de aparición tardía en hombres mayores con cáncer de próstata.
- Investigar el papel potencial de la terapia de privación de andrógenos (TDA) en el desencadenamiento de la LHON en estos pacientes.
Principales métodos:
- Informes clínicos detallados de dos pacientes con LHON de aparición tardía.
- Análisis de perfiles hormonales (gonadotropina, estrógenos, andrógenos) y número de copias de ADN mitocondrial (ADNmt) en individuos afectados.
Principales resultados:
- Ambos pacientes desarrollaron LHON después de iniciar la terapia antirretroviral (enzalutamida y leuprolida) para el cáncer de próstata avanzado.
- Los pacientes presentaron niveles séricos muy bajos de gonadotropina, estrógenos y andrógenos, consistentes con la TDA.
- Se observó una reducción significativa del número de copias de ADNmt en ambos pacientes en comparación con los controles.
Conclusiones:
- ADT, al alterar el equilibrio hormonal (relación estrógeno-andrógeno) y potencialmente reducir el número de copias de ADNmt, puede desencadenar LHON de aparición tardía en individuos susceptibles.
- Esto sugiere una interacción compleja entre el estado hormonal y la función mitocondrial en la patogénesis de LHON.
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