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Plasma levels of granulocyte elastase‐α 1 ‐proteinase inhibitor complex in patients with disseminated intravascular coagulation: Pathophysiologic implications
Author(s) -
Okajima Kenji,
Fujise Ryuji,
Motosato Yuichi,
Ushijima Masato,
Okabe Hiroaki,
Takatsuki Kiyoshi
Publication year - 1994
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830470204
Subject(s) - disseminated intravascular coagulation , medicine , pathophysiology , gastroenterology , elastase , respiratory failure , neutrophil elastase , inflammation , chemistry , enzyme , biochemistry
To Investigate the role of neutrophil activation in the pathophysiology and sequelae of disseminated intravascular coagulation (DIC), we measured plasma levels of granulocyte elastase‐α 1 ‐proteinase inhibitor complex (GEPIC) in 41 patients with DIC and 27 patients with similar underlying conditions but without DIC. Mean GEPIC levels were significantly higher in patients with DIC (421.0 ± 45.6 ng/ml) than in patients without DIC (246.1 ± 41.9 ng/ml, P < 0.01). Significant differences were also noted in DIC patients with or without infection (474.7 ± 61.2 ng/ml vs. 302.4 ± 48.9 ng/ml, P < 0.04), with or without organ dysfunction (546.6 ± 72.7 ng/ml vs. 305.6 ± 42 ng/ml, P < 0.01), and with or without respiratory failure (640.0 ± 91.2 ng/ml vs. 328.1 ± 55.1 ng/ml, P < 0.01). No significant difference was found in mean GEPIC levels in DIC patients with or without renal failure, heart failure, hepatic failure, or gastrointestinal bleeding. The frequency of respiratory failure correlated with rising plasma levels of GEPIC. Mortality was higher in patients with GEPIC levels >500 ng/ml (53.8%) than in patients with GEPIC levels <500 ng/ml (28.6%). This correlation was particularly strong in patients with DIC, infection, and respiratory failure. Based on these data, we suggest that neutrophil activation, triggered by the coagulation cascade and perhaps augmented by endotoxin or cytokine release with infection, significantly contributes to respiratory failure and mortality in patients with DIC. © 1994 Wiley‐Liss, Inc.