Biomarcadores en la Hiperplasia Prostática Benigna (HPB)
Palabras clave:
hiperplasia prostática benigna (HPB), antígeno prostático específico (PSA), procalcitonina (PCT), antígeno carcinoembrionario (CEA), hormona gonadotropina coriónica (HCG) subunidad betaResumen
La Hiperplasia Prostática Benigna (HPB) es una de las condiciones más comunes en hombres mayores de 50 años. Esta enfermedad implica un agrandamiento no maligno de la próstata, lo que provoca síntomas obstructivos en el tracto urinario inferior, tales como dificultad para orinar, mayor frecuencia urinaria, y una micción intermitente o débil, lo que afecta significativamente la calidad de vida del paciente. Aunque el antígeno prostático específico (PSA) es el biomarcador estándar para evaluar diversas enfermedades prostáticas, su baja especificidad ha limitado su utilidad en el diagnóstico diferencial entre HPB y cáncer de próstata (CaP). Esta falta de especificidad ha llevado a la búsqueda de biomarcadores alternativos que puedan mejorar la precisión diagnóstica, reducir los diagnósticos erróneos, y ofrecer una evaluación más precisa de la progresión de la enfermedad. Los biomarcadores como la procalcitonina (PCT), el antígeno carcinoembrionario (CEA) y la gonadotropina coriónica humana (HCG), particularmente su subunidad beta, han sido propuestos como herramientas diagnósticas prometedoras. Estos biomarcadores no solo pueden mejorar la capacidad de diagnóstico, sino también ofrecer un monitoreo no invasivo de la inflamación prostática y la progresión de la HPB, lo que ayudaría a personalizar el tratamiento para cada paciente. Este artículo revisa la literatura científica relevante que examina la relación entre estos biomarcadores y la HPB, explorando su utilidad clínica en el diagnóstico y seguimiento de la enfermedad, así como los mecanismos fisiopatológicos subyacentes que los vinculan con la progresión de la enfermedad prostática.
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