It would be useful to be able to define a specific early marker of ARDS, particularly if such a molecule belonged to one of the classes of mediators discussed above. This would allow early pharmacological treatment of the syndrome before or simultaneously with the appearance of the first symptoms. Such a role has been assigned to several mediators, often following the chronology of their discovery. Complement fragments, such as C5a, were initially believed to be the required marker. Subsequently, prostanoids and leukotrienes, coagulation proteins, etc. were thought to be the long-sought molecules. It is currently accepted that there is no marker specific for ARDS. Early studies of bronchoalveolar lavage fluid may provide a technique for the early rapid detection of the onset of ARDS, allowing early treatment.
Apart from specific causal therapy for ARDS and symptomatic supportive treatment of the respiratory failure and of the patient in general, the numerous attempts at pharmacological antimediator therapy have not been particularly successful ( Fig 1). This failure can be explained by the large number of mediators, their cascading interactions, the early generalization of the inflammatory reaction, and the development of multiple organ failure. The use of substances capable of inducing endogenous defenses, such as granulocyte colony-stimulating factor, granulocyte-monocyte colony-stimulating factor, and certain 'anti-inflammatory' cytokines, such as IL-4, IL-10, and IL-13, appears promising. Genetic therapy (by stimulation or repression of genes coding for molecules implicated in the pathogenesis of ARDS) is a possible future development.
Fig. 1 Main pathways for pharmacological therapy in ARDS (® indicates an inhibitory activity): LPS, lipopolysaccharides (endotoxins); PAF, platelet activating factor.
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