Koch Christian, Ruhrmann Sophie, Pöhlmann Michael, Schneck Emmanuel, Arneth Borros, Zajonz Thomas, Sander Michael, Weigand Markus A, Uhle Florian
1 Department of Anesthesiology and Intensive Care Medicine, University Hospital of Giessen and Marburg , Giessen, Germany .
2 Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, University Hospital of Giessen and Marburg , Giessen, Germany .
Surg Infect (Larchmt). 2018 Jul;19(5):480-487. doi: 10.1089/sur.2017.266. Epub 2018 Apr 23.
The high mortality rate of patients suffering from severe trauma is based not only on the mechanism of injury, but also on the higher risk for development of subsequent infections. Therefore, the early recognition of infection after severe trauma is of particular importance for patient outcome. However, early diagnosis is often masked by the consequences of the sterile, damage-triggered immune response. Our study sought to analyze the course of soluble CD14-subtype (sCD14-ST, presepsin) compared with clinically established inflammatory and infectious biomarkers in a cohort of patients with severe trauma.
Between January 2015 and February 2016, 50 patients suffering from severe trauma (Injury Severity Score [ISS] > 16) were enrolled and followed up for seven consecutive days after intensive care unit (ICU) admission. Clinical routine data, signs of infection, and the inflammatory biomarkers presepsin, C-reactive protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6) were assessed.
Regarding the well-established biomarkers CRP, PCT, and IL-6, we observed trauma-associated alterations (day 1: CRP 13 mg/L, interquartile range [IQR] 0-129; PCT 1.1 μg/L, IQR 0-13; IL-6 108 pg/mL, IQR 29-795), which did not correlate with the clinical development of systemic inflammatory response syndrome (SIRS), whereas elevated plasma concentrations of presepsin in the clinical course were associated with the presence of SIRS (presepsin: no-SIRS vs. SIRS p = 0.03).
Our study investigates systematically the kinetic of presepsin compared with established inflammatory and infectious markers after severe trauma. Presepsin is neither affected by the early post-traumatic nor the delayed immune response over seven days after trauma, making it a possible option as a diagnostic biomarker of infection worth further evaluation.
严重创伤患者的高死亡率不仅基于损伤机制，还基于后续感染发生风险更高。因此，早期识别严重创伤后的感染对患者预后尤为重要。然而，早期诊断常被无菌性、损伤引发的免疫反应后果所掩盖。我们的研究旨在分析一组严重创伤患者中可溶性CD14亚型（sCD14-ST，可溶性髓系细胞触发受体-1）的变化过程，并与临床已确立的炎症和感染生物标志物进行比较。
2015年1月至2016年2月，纳入50例严重创伤患者（损伤严重程度评分[ISS]>16），在重症监护病房（ICU）入院后连续随访7天。评估临床常规数据、感染迹象以及炎症生物标志物可溶性髓系细胞触发受体-1、C反应蛋白（CRP）、降钙素原（PCT）和白细胞介素-6（IL-6）。
关于已确立的生物标志物CRP、PCT和IL-6，我们观察到与创伤相关的变化（第1天：CRP 13mg/L，四分位数间距[IQR]0-129；PCT 1.1μg/L，IQR 0-13；IL-6 108pg/mL，IQR 29-795），这些变化与全身炎症反应综合征（SIRS）的临床进展无关，而临床过程中可溶性髓系细胞触发受体-1血浆浓度升高与SIRS的存在相关（可溶性髓系细胞触发受体-1：无SIRS与SIRS相比，p=0.03）。
我们的研究系统地研究了严重创伤后可溶性髓系细胞触发受体-1与已确立的炎症和感染标志物相比的动力学变化。可溶性髓系细胞触发受体-1在创伤后早期及创伤后7天的延迟免疫反应中均未受影响，使其有可能作为一种值得进一步评估的感染诊断生物标志物。
