Información del artículo
Introducción
Se analizan las definiciones y las teorías fisiopatológicas que se han elaborado para explicar la evolución del síndrome inflamatorio hacia la disfunción multisistémica, analizando el valor predictivo de los diferentes mediadores y de los cambios metabólicos. Tras revisar las características del síndrome inflamatorio se recogen los diferentes intentos terapéuticos para modular el SIRS
MaterialSe ha revisado la bibliografía recogida en Medline, fundamentalmente estudios clínicos realizados en pacientes críticos
ResumenSe describen tres síndromes (SIRS, CARS y MARS) que pueden configurar la respuesta inflamatoria. La evolución hacia la disfunción multisistémica es explicada por diversas teorías, pero queda por estudiar los mecanismos que permiten la modulación y supresión de la respuesta inflamatoria. A pesar de su importancia fisiopatológica, las citocinas de inicio no son buenos marcadores pronósticos. Los marcadores de fase aguda, así como los cambios en el metabolismo lipídico y del hierro, muestran una mejor correlación con la evolución. Tras comentar que la respuesta inflamatoria no es proporcional, estructural ni universal, se revisan los diversos intentos terapéuticos que pretenden antagonizar dicha respuesta. Se comentan las tres líneas que deben regir para las investigaciones futuras
Palabras clave:
SIRS
CARS
síndrome de disfunción multisistémica
marcadores inflamatorios
reactantes de fase aguda
Introduction
The different syndrome definitions that have been developed to explain how the inflammatory syndrome may herald multisystemic dysfunction. Thus, the predictive value of the different mediators and metabolic changes have been analyzed. Once the inflammatory syndrome features were revised, those therapeutic approaches that will likely improve its prognosis are resumed
MethodsSystematic review of Medline’s bibliography, focusing on clinical trials performed in critically ill patients
SummaryThree syndromes (SIRS, CARS, MARS) which can comprise the inflammatory syndome are described. Several hypothesis illustrate its progression to multisystemic dysfunction, but further research is required to explain how inflammation can be regulated or even suppressed. Early relieved cytokines play a major role, but are devoid of prognostic value; on the other hand acute phase markers and changes in lipid and iron metabolism correlate better with final outcome. While the inflammatory reaction is by no means proportional, structural nor universal we turn to assay the different therapeutic approaches intended to antagonize it. The three principles which should underlie further research are reviewed
Key words:
SIRS
CARS
multysystemic dysfunction syndrome
inflammatory markers
acute phase reactants
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