Secretory leukocyte proteinase inhibitor is preferentially increased in patients with acute respiratory distress syndrome

被引:26
作者
Sallenave, JM
Donnelly, SC
Grant, IS
Robertson, C
Gauldie, J
Haslett, C [1 ]
机构
[1] Univ Edinburgh, Sch Med, Dept Med, Rayne Lab, Edinburgh EH8 9AG, Midlothian, Scotland
[2] Western Gen Hosp, Intens Therapy Unit, Edinburgh EH4 2XU, Midlothian, Scotland
[3] Royal Infirm Hosp, Dept Accid & Emergency, Edinburgh, Midlothian, Scotland
[4] McMaster Univ, Dept Pathol, Hamilton, ON, Canada
关键词
acute respiratory distress syndrome; alpha-1-proteinase inhibitor; antiproteinase; elafin; inflammation; secretory leukocyte proteinase inhibitor;
D O I
10.1183/09031936.99.13510299
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Inappropriate release of proteases from inflammatory and stromal cells can lead to destruction of the lung parenchyma, Antiproteinases such as alpha-l-proteinase inhibitor (alpha(1)-Pi), secretory leukocyte proteinase inhibitor (SLPI) and elastase-specific inhibitor (elafin) control excess production of human neutrophil elastase, In the present study, the concentrations of alpha(1)-Pi, SLPI and elafin found in bronchoalveolar lavage (BAL) fluid from control subjects, patients at risk of developing acute respiratory distress syndrome (ARDS) and patients with established ARDS were determined, Levels of all three inhibitors were raised in patients compared with normal subjects. SLPI was increased in the group of patients who were at risk of ARDS and went on to develop the condition, compared with the "at-risk" group who did not progress to ARDS (p=0.0083), alpha(1)-Pi and elafin levels were similar in these two populations. In patients with established ARDS, both alpha(1)-Pi and SLPI levels were significantly increased, compared to patients at risk of ARDS who did (p=0.0089) or did not (p=0.0003) progress to ARDS, The finding of increased antiproteinases shortly before the development of acute respiratory distress syndrome provide further evidence for enhanced inflammation prior to clinical disease.
引用
收藏
页码:1029 / 1036
页数:8
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