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ASPECTOS ACTUALES DEL TRATAMIENTO ANTIBIOTICO Y LA LIBERACION DE ENDOTOXINAS

(especial para SIIC © Derechos reservados)
En el tratamiento de las infecciones graves la liberación de endotoxinas varía de acuerdo con el antibiótico empleado.
Autor:
René Gordon holzheimer
Columnista Experto de SIIC

Institución:
Martin Luther -University Halle

Artículos publicados por René Gordon holzheimer
Recepción del artículo
27 de Abril, 2005 		Aprobación
3 de Mayo, 2005
Primera edición
19 de Enero, 2006 		Segunda edición, ampliada y corregida
7 de Junio, 2021

ASPECTOS ACTUALES DEL TRATAMIENTO ANTIBIOTICO Y LA LIBERACION DE ENDOTOXINAS

Resumen
La endotoxina es una de las causas principales de sepsis e insuficiencia multiorgánica en los seres humanos. Los antibióticos que se administran para tratar estas infecciones graves pueden liberar endotoxina de la pared bacterial y afectar al paciente. Se consideraba que los antibióticos específicos de la proteína ligadora de penicilina (PLP) 2, por ejemplo, imipenem, liberaban menores cantidades de endotoxina libre que los antibióticos específicos de la PLP 3, como la ceftazidima. Este efecto contribuye al aumento de la actividad bactericida de los antibióticos específicos de la PLP 2, con los consiguientes cambios en la morfología de los patógenos, lo que posibilita la fagocitosis. Sin embargo, recientes estudios in vitro no pudieron repetir estos resultados. La liberación de endotoxina inducida por antibióticos puede cambiar con el tipo de patógeno y la dosificación del antibiótico. En estudios con animales, la liberación de endotoxina no se correlacionó con el efecto bactericida en todos los experimentos. La liberación de endotoxina inducida por antibióticos, así como los resultados, fue diferente según los modelos con animales, la localización de la infección, las cepas, la farmacodinamia y la dosificación del antibiótico. Los antibióticos bacteriostáticos, como lincomicina y clindamicina, indujeron la liberación de endotoxina. En algunos estudios la liberación de endotoxina inducida por imipenem fue similar a la causada por ceftazidima y mayor que la inducida por ciprofloxacina. Las tetraciclinas modificadas químicamente y la combinación de antibióticos evitaron el aumento en la liberación de endotoxinas. En pacientes con urosepsis se observaron resultados controvertidos al comparar imipenem con ceftazidima. En estudios clínicos de observación o en los análisis post hoc de ensayos clínicos aleatorizados se informaron diferencias en la liberación de endotoxina luego de la administración de imipenem y cefalosporinas. En conclusión, la liberación de endotoxina inducida por antibióticos podría ser clínicamente relevante. No obstante, en los estudios clínicos pueden interferir muchos factores que deben ser abordados debidamente cuando se analizan los estudios acerca de este tema.

Palabras clave
Liberación de endotoxina inducida por antibióticos, lipopolisacáridos


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CURRENT ASPECTS OF ANTIBIOTIC TREATMENT AND ENDOTOXIN RELEASE

Abstract
Endotoxin is a major cause of sepsis and organ failure in humans. Antibiotics, which are administrated to treat these severe infections, may release Endotoxin from the bacterial wall and may harm the patient. Penicillin-binding protein (PBP) 2-specific antibiotics, e.g., imipenem were considered to release less amounts of free Endotoxin than PBP 3-specific antibiotics, e.g., Ceftazidime. This effect has been contributed to an increased bactericidal activity of PBP 2-specific antibiotics and consecutive change in morphology of pathogens, enabling phagocytosis. Recent in vitro studies, however, were unable to repeat these results. The antibiotic-induced Endotoxin release may change with the type of pathogen and dosing of the antibiotic. In animal studies Endotoxin release did not show a correlation to the bactericidal effect in all experiments. Antibiotic-induced Endotoxin release and outcome was different with regard to animal models, location of infection, strains, pharmocodynamics and dosage of antibiotics. Bacteriostatic antibiotics, e.g., lincomycin and clindamycin, were able to induce Endotoxin release. In some studies imipenem caused either similar release of Endotoxin compared to ceftazidime or more compared to ciprofloxacin. Chemically modified tetracycline or combination of antibiotics prevented an increased Endotoxin release. In patients with urosepsis controversial results were observed when imipenem was compared to ceftazidime. In clinical observational studies or post-hoc analysis of a randomized clinical trial a differential release of Endotoxin after imipenem and cephalosporins has been reported. In conclusion, antibiotic-induced Endotoxin release may be clinically relevant. However, there are many interfering factors in clinical studies, which need to be addressed properly when analyzing studies on antibiotic-induced Endotoxin release.

Key words
Antibiotic-induced endotoxin release, LPS


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Especialidades
Principal: Infectología, Medicina Farmacéutica
Relacionadas: Cuidados Intensivos, Farmacología, Medicina Interna



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Bibliografía del artículo
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