• Seitaro Fujishima, Hiroshi Morisaki, Akitoshi Ishizaka, Yoshifumi Kotake, Masaru Miyaki, Kikuo Yoh, Kazuhiko Sekine, Junichi Sasaki, Sadatomo Tasaka, Naoki Hasegawa, Yohko Kawai, Junzo Takeda, and Naoki Aikawa.
• Department of Emergency and Critical Care Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. fujishim@sc.itc.keio.ac.jp
• Biomed. Pharmacother. 2008 Jun 1;62(5):333-8.

AbstractCritically ill patients are commonly associated with systemic inflammatory response syndrome (SIRS) and are at a greater risk of developing acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Under these conditions, large amounts of various cytokines are produced, which either directly or indirectly induce tissue injury and finally organ dysfunctions, through the activation of neutrophils and as a result of release of cytotoxic molecules, especially neutrophil elastase (NE). In the present study, we determined plasma neutrophil elastase-alpha-1 antitrypsin complex (NE-AT) and elastase digests of cross-linked fibrin (e-XDP) in critically ill patients to elucidate the significance of NE in the initiation and progression of ALI and ARDS in the presence or absence of SIRS. We found significantly increased levels of plasma NE-AT in the patients with ARDS, especially when the definition of SIRS was met. Among ALI/ARDS groups, plasma NE-AT, but not e-XDP, correlated significantly with the decrease in PaO(2)/FIO(2) ratio and the duration of ALI/ARDS. Furthermore, NE-AT, but not e-XDP, significantly increased in subgroups whose PaO(2)/FIO(2) ratio decreased by more than 20%. Such correlations and differences between the subgroups were not observed in the non-ALI patients. From these results, we speculate that NE-AT, but not e-XDP, may be predictive of progressive lung injury in the early stage of ALI and ARDS.

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