A prospective study of inflammation markers in patients at risk of indirect acute lung injury

被引:96
作者
Takala, A
Jousela, I
Takkunen, O
Kautiainen, H
Jansson, SE
Orpana, A
Karonen, SL
Repo, H
机构
[1] Univ Helsinki, Cent Hosp, Dept Anaesthesia & Intens Care, FIN-00029 Helsinki, Finland
[2] Univ Helsinki, Cent Hosp, Dept Clin Chem, FIN-00029 Helsinki, Finland
[3] Univ Helsinki, Cent Hosp, Dept Med, FIN-00029 Helsinki, Finland
[4] Rheumatism Fdn Hosp, SF-18120 Heinola, Finland
[5] Univ Helsinki, Haartman Inst, Dept Bacteriol & Immunol, FIN-00014 Helsinki, Finland
来源
SHOCK | 2002年 / 17卷 / 04期
关键词
ARDS; CD11b; IL-6; IL-8; pancreatitis; procalcitonin; sE-selectin; sIL-2R; transfusion;
D O I
10.1097/00024382-200204000-00002
中图分类号
R4 [临床医学];
学科分类号
1002 [临床医学]; 100602 [中西医结合临床];
摘要
Systemic inflammation triggered by insults like sepsis and acute pancreatitis may play a role in development of indirect acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Because little is known about the course of systemic inflammation on the days preceding diagnosis of ARDS, we prospectively monitored immune inflammatory status in 52 patients at risk and we assessed the presence of ALI and ARDS on day 7 after admission to the intensive care unit. On admission, serum interleukin (IL) 8, IL-6, and soluble IL-2 receptor concentrations were significantly higher in patients with subsequent ALI (n = 18) than in patients without ALI (n = 30). During a 4-day follow-up, IL-8 and IL-6 levels of ALI patients remained high and those of non-ALI patients decreased. None of the markers discriminated ARDS patients (n = 9) from non-ARDS ALI patients (n = 9). Among 11 patients with acute pancreatitis, ALI patients had significantly higher IL-8, IL-6, and phagocyte CD11b expression levels than did non-ALI patients, whereas among 14 patients with massive transfusion, respective findings in ALI and non-ALI patients were comparable. Results give credence to the view that systemic inflammation plays a role in development of ALI triggered by pancreatitis, but not in that by massive transfusion. This finding, if confirmed in studies with sufficient statistical power, suggests that the patients with massive transfusion do not necessarily benefit from novel biotherapies aimed at altering the course of systemic inflammation.
引用
收藏
页码:252 / 257
页数:6
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