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Factores inflamatorios y rinusinusitis crónica: una revisión paraguas
Stergios T Lialiaris1, Konstantinos Chaidas1, George Fyrmpas1
1Εar, Nose, and Throat Department, University Hospital of Alexandroupolis, School of Medicine, Democritus University of Thrace, Alexandroupolis, GRC.
Cureus
|February 19, 2026
Resumen
La rinusinusitis crónica (RSC) implica distintas vías inmunológicas, incluida la inflamación de Tipo 1, 2 y 3. Comprender estos endotipos es clave para tratamientos dirigidos y para controlar la RSC de manera eficaz.
Área de la Ciencia:
- Inmunología
- Otorrinolaringología
- Medicina Respiratoria
Sus antecedentes:
- La rinusinusitis crónica (RSC) es una afección inflamatoria prevalente que afecta las fosas nasales y los senos paranasales.
- La RSC se presenta con características clínicas y mecanismos subyacentes heterogéneos, lo que complica la clasificación y el tratamiento.
- Existen dos fenotipos principales: RSC sin pólipos nasales (CRSsNP) y RSC con pólipos nasales (CRSwNP).
Objetivo del estudio:
- Revisar y sintetizar la evidencia sobre las distintas vías inflamatorias y patrones inmunológicos en la RSC.
- Explorar la heterogeneidad de los endotipos de la RSC y sus implicaciones clínicas.
- Evaluar el potencial del manejo impulsado por endotipos y las terapias biológicas.
Principales métodos:
- Se realizó una revisión paraguas siguiendo las directrices PRISMA.
- Se realizaron búsquedas sistemáticas de literatura en Scopus y PubMed.
- Se incluyeron 64 estudios publicados entre mayo de 1968 y agosto de 2025 y se sintetizaron los hallazgos de forma cualitativa.
Principales resultados:
- La inflamación de la RSC implica distintos patrones de células T helper (Th1, Th2, Th17, Th22) y células T reguladoras (Treg).
- La inflamación de Tipo 1 (a menudo en CRSsNP) presenta interferón-gamma, IL-12 e infiltración neutrófila.
- La inflamación de Tipo 2 (común en CRSwNP) involucra TSLP, IL-25, IL-33, citoquinas Th2 y eosinófilos, afectando la producción de moco y el transporte epitelial.
- La inflamación de Tipo 3 (Th17) está relacionada con IL-17, IL-22 y la defensa del huésped contra microbios.
Conclusiones:
- Las vías inflamatorias en la RSC son diversas y pueden superponerse, influyendo en los fenotipos de la enfermedad.
- Las comorbilidades como la enfermedad respiratoria exacerbada por aspirina y la fibrosis quística impactan los endotipos de la RSC.
- El manejo impulsado por endotipos, incluidas las terapias biológicas como dupilumab, muestra promesa pero requiere una mayor refinación para una estratificación y selección de tratamiento óptimas del paciente.
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