• P E Parsons.
• Department of Medicine, University of Colorado Health Sciences Center, Denver, USA.
• Clin. Chest Med. 2000 Sep 1; 21 (3): 467-76.

AbstractSince last reviewed in this forum, there have been remarkable advances in our understanding of the acute inflammatory process and how it contributes to the development of ALI. As stated in the beginning of this article, it is not possible to even begin to review all the specific advances that have been made. Instead, the author has focused on concepts that have emerged and improved our ability to study the pathogenesis of ARDS. These include the recognition that patients at risk for and with ARDS represent a heterogeneous population, that mediators or markers of inflammation cannot be considered in isolation, that a balance between proinflammatory mediators and inflammatory modulators may be important, and that there are several genetic factors that could contribute to the susceptibility for the development of ARDS. Hopefully these concepts can be expanded and clarified so that the next review of this topic can report on successful therapeutic interventions for the prevention and the treatment of ARDS.

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