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Modulación de la biosíntesis de eicosanoides insensibles a la aspirina por 6-metilprednisolona en la angina de pecho
Francesco Cipollone1, Antonina Ganci, Anita Greco
1Department of Medicine and Aging, University of Chieti G. D'Annunzio School of Medicine, Chieti, Italy. fcipollone@unich.it
Circulation
|January 8, 2003
Resumen
El tratamiento con glucocorticoides redujo la producción de leucotrieno C4 (LT C4) en pacientes con angina inestable, lo que sugiere inflamación.
Área de la Ciencia:
- Cardiología Cardiología.
- Investigación de la inflamación Investigación de la inflamación.
- Farmacología Farmacología.
Sus antecedentes:
- La inflamación está implicada en los síndromes coronarios agudos.
- Mediadores inflamatorios investigados en la angina inestable.
Objetivo del estudio:
- Para investigar los efectos de los glucocorticoides en la biosíntesis del leucotrieno C4 (LT C4) y el tromboxano A2 (TX A2) en la angina inestable.
- Para explorar el papel de la inflamación en la fisiopatología de la angina inestable.
Principales métodos:
- Comparación de LTE4 y 11-dehidro-TXB2 urinario en pacientes con angina inestable, angina estable y dolor torácico no isquémico.
- Se administra por vía intravenosa 6-metilprednisolona (6-MP) o placebo a pacientes con angina de pecho inestable.
- Se recogen muestras de orina antes y durante el tratamiento para medir la excreción de eicosanoides.
Principales resultados:
- El LTE4 urinario y el 11-dehidro-TXB2 se elevaron en pacientes con angina inestable.
- 6-MP disminuyó significativamente la excreción de LTE4 en pacientes con angina inestable.
- Los niveles de 11-dehidro-TXB2 no cambiaron significativamente con el tratamiento con 6-MP.
Conclusiones:
- Los leucotrienos vasoactivos (LT) y los tromboxanos (TX) pueden producirse en exceso en la angina inestable.
- Los glucocorticoides pueden suprimir la biosíntesis de LT C4 a corto plazo.
- Los glucocorticoides pueden ayudar a dilucidar el papel de la activación de las células inflamatorias en la angina inestable.
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