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Ácido tranexámico en bolo más infusión aumenta paradójicamente la activación del complemento: un estudio secundario

Nicolle Barmettler1, Elizabeth R Maginot, Ernest E Moore

  • 1From the Division of Acute Care Surgery, Department of Surgery (N.B., E.R.M., F.I.G., C.M.W., T.B.M., A.C., K.S.S., D.H., G.E.V., R.H., C.D.B.), University of Nebraska Medical Center, Omaha, Nebraska; Department of Surgery (E.E.M., J.G.C.), Ernest E Moore Shock Trauma Center, Denver Health; Department of Surgery (H.B.M.), AdventHealth Porter, Denver, Colorado; Department of Cardiology (D.F.D.), Bern Center for Precision Medicine, University Hospital of Bern, Bern, Switzerland; School of Medicine and Psychology (R.G.), Australian National University, Canberra, Australia; Department of Biological Sciences, Hunter College (I.M.B.), New York, New York; The Australian Centre for Blood Diseases (R.L.M.), Monash University; Emergency and Trauma Centre (B.M.), Alfred Health, Melbourne, Australia; Department of Surgery (M.A.S.), Uniformed Services University of Health Sciences, Bethesda, Maryland; Section of Trauma and Acute Care Surgery, Department of Surgery (S.E.R.), University of Chicago Pritzker School of Medicine, Chicago, Illinois; Sauaia Statistical Solutions, L.L.C. (A.S.), Denver, Colorado; and Department of Cellular and Integrative Physiology (C.D.B.), University of Nebraska Medical Center, Omaha, Nebraska.

The journal of trauma and acute care surgery
|February 3, 2026
PubMed
Resumen
Este resumen es generado por máquina.

El ácido tranexámico (TXA) no redujo la activación temprana del complemento en pacientes con traumatismos. Paradójicamente, el TXA aumentó la activación del complemento a las 24 horas, lo que sugiere un papel complejo en la respuesta inflamatoria y cuestiona las estrategias de dosificación óptima.

Palabras clave:
ácido tranexámicoactivación del complementofibrinólisis

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Área de la Ciencia:

  • Traumatología y Medicina de Urgencias
  • Inmunología
  • Farmacología

Sus antecedentes:

  • El ácido tranexámico (TXA) muestra beneficios modestos de supervivencia en politraumatismos, pero sus efectos pueden extenderse más allá de la hemostasia.
  • La plasmina activa las proteínas del complemento y el TXA inhibe la generación de plasmina.
  • Este estudio investigó el impacto del TXA en la activación del complemento en pacientes con traumatismos.

Objetivo del estudio:

  • Determinar si la administración de TXA reduce la activación del complemento en pacientes con politraumatismos.
  • Explorar la relación entre el TXA, la plasmina y las vías del complemento después de un traumatismo.

Principales métodos:

  • Se analizaron muestras de plasma de 53 pacientes con politraumatismos del ensayo PATCH (TXA frente a placebo).
  • Se midieron marcadores de activación del complemento (C3a, C5a, sC5b-9) y niveles de plasmina-antiplasmina en Urgencias, a las 8 y 24 horas.
  • Se realizaron comparaciones estadísticas entre los grupos de TXA y placebo.

Principales resultados:

  • No hubo diferencias significativas en la activación del complemento o en los niveles de plasmina-antiplasmina entre los grupos de TXA y placebo en los primeros momentos (Urgencias, 8 horas).
  • Se observó un aumento significativo de los niveles de C3a y C5a en el grupo de TXA a las 24 horas posteriores al ingreso.
  • Estos hallazgos sugieren que el TXA puede potenciar paradójicamente la activación del complemento más tarde después de un traumatismo.

Conclusiones:

  • La administración de TXA aumentó paradójicamente la activación del complemento a las 24 horas en pacientes con politraumatismos.
  • Estos resultados indican la participación del TXA en la vía inflamatoria después de un traumatismo.
  • Las estrategias óptimas de dosificación de TXA en traumatismos requieren una mayor investigación debido a los efectos inflamatorios retardados.