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对间接急性肺损伤风险患者炎症标志物的前瞻性研究。

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

作者信息

Takala Annika, Jousela Irma, Takkunen Olli, Kautiainen Hannu, Jansson Sten-Erik, Orpana Arto, Karonen Sirkka-Liisa, Repo Heikki

机构信息

Department of Anesthesia and Intensive Care, Helsinki University Central Hospital, Finland.

出版信息

Shock. 2002 Apr;17(4):252-7. doi: 10.1097/00024382-200204000-00002.

DOI:10.1097/00024382-200204000-00002
PMID:11954822
Abstract

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.

摘要

由脓毒症和急性胰腺炎等损伤引发的全身炎症可能在间接急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)的发展过程中起作用。由于对ARDS诊断前数天全身炎症的进程了解甚少,我们前瞻性地监测了52例有风险患者的免疫炎症状态,并在其入住重症监护病房7天后评估了ALI和ARDS的存在情况。入院时,随后发生ALI的患者(n = 18)血清白细胞介素(IL)-8、IL-6和可溶性IL-2受体浓度显著高于未发生ALI的患者(n = 30)。在为期4天的随访中,ALI患者的IL-8和IL-6水平保持高位,而非ALI患者的相应水平下降。没有一个标志物能够区分ARDS患者(n = 9)和非ARDS的ALI患者(n = 9)。在11例急性胰腺炎患者中,ALI患者的IL-8、IL-6和吞噬细胞CD11b表达水平显著高于非ALI患者,而在14例大量输血患者中,ALI和非ALI患者的相应结果相当。结果支持了全身炎症在胰腺炎引发的ALI发展中起作用,但在大量输血引发的ALI中不起作用这一观点。这一发现如果在具有足够统计效力的研究中得到证实,表明大量输血患者不一定能从旨在改变全身炎症进程的新型生物疗法中获益。

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