From the Department of Surgery (S.L., H.M., B.H., M.K., N.K., J.W., S.A., J. Scioscia, E.S., A.R., J.B., M.N., U.K., J. Sperry, T.R.B.) and Pittsburgh Transfusion and Trauma Research Center (S.L., H.M., B.H., M.K., N.K., J.W., S.A., J. Scioscia, E.S., A.R., J.B., M.N., U.K., J. Sperry, T.R.B.), University of Pittsburgh, Pittsburgh; Lake Erie College of Osteopathic Medicine (B.H.), Erie, Pennsylvania; Department of Cardiology (J.W.), The Third Xiangya Hospital, Central South University, Changsha, China; Section for Transfusion Medicine (P.I.J., J. Stensballe), Capital Region Blood Bank, Rigshospitalet and Department of Anesthesia and Trauma Center (J. Stensballe), Centre of Head and Orthopaedics, Rigshospitalet, Copenhagen University Hospital, Copenhagen; Emergency Medical Services (J. Stensballe), The Capital Region of Denmark, Hillerød, Denmark; and Center for Systems Immunology, Departments of Immunology (J.D.) and Computational and Systems Biology (J.D.), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
J Trauma Acute Care Surg. 2023 Jun 1;94(6):803-813. doi: 10.1097/TA.0000000000003880. Epub 2023 Feb 13.
Severe traumatic injury with shock can lead to direct and indirect organ injury; however, tissue-specific biomarkers are limited in clinical panels. We used proteomic and metabolomic databases to identify organ injury patterns after severe injury in humans.
Plasma samples (times 0, 24, and 72 hours after arrival to trauma center) from injured patients enrolled in two randomized prehospital trials were subjected to multiplexed proteomics (SomaLogic Inc., Boulder, CO). Patients were categorized by outcome: nonresolvers (died >72 hours or required ≥7 days of critical care), resolvers (survived to 30 days and required <7 days of critical care), and low Injury Severity Score (ISS) controls. Established tissue-specific biomarkers were identified through a literature review and cross-referenced with tissue specificity from the Human Protein Atlas. Untargeted plasma metabolomics (Metabolon Inc., Durham, NC), inflammatory mediators, and endothelial damage markers were correlated with injury biomarkers. Kruskal-Wallis/Mann-Whitney U tests with false discovery rate correction assessed differences in biomarker expression across outcome groups (significance; p < 0.1).
Of 142 patients, 78 were nonresolvers (median ISS, 30), 34 were resolvers (median ISS, 22), and 30 were low ISS controls (median ISS, 1). A broad release of tissue-specific damage markers was observed at admission; this was greater in nonresolvers. By 72 hours, nine cardiac, three liver, eight neurologic, and three pulmonary proteins remained significantly elevated in nonresolvers compared with resolvers. Cardiac damage biomarkers showed the greatest elevations at 72 hours in nonresolvers and had significant positive correlations with proinflammatory mediators and endothelial damage markers. Nonresolvers had lower concentrations of fatty acid metabolites compared with resolvers, particularly acyl carnitines and cholines.
We identified an immediate release of tissue-specific biomarkers with sustained elevation in the liver, pulmonary, neurologic, and especially cardiac injury biomarkers in patients with complex clinical courses after severe injury. The persistent myocardial injury in nonresolvers may be due to a combination of factors including metabolic stress, inflammation, and endotheliopathy.
严重创伤伴休克可导致直接和间接的器官损伤;然而,在临床检测中,组织特异性生物标志物十分有限。我们使用蛋白质组学和代谢组学数据库来鉴定人类严重创伤后的器官损伤模式。
纳入两项院前随机试验的创伤患者入院后(到达创伤中心后 0、24 和 72 小时)的血浆样本,进行多重蛋白质组学分析(博尔德科罗拉多的 SomaLogic 公司)。患者根据结局进行分类:未解决组(72 小时后死亡或需要≥7 天的重症监护)、解决组(30 天存活且需要<7 天的重症监护)和低损伤严重程度评分(ISS)对照组。通过文献回顾确定了已建立的组织特异性生物标志物,并与人类蛋白质图谱中的组织特异性进行交叉参考。非靶向血浆代谢组学(达勒姆北卡罗来纳州的 Metabolon 公司)、炎症介质和内皮损伤标志物与损伤生物标志物相关。采用 Kruskal-Wallis/Mann-Whitney U 检验(假发现率校正)评估不同结局组间生物标志物表达的差异(显著性;p<0.1)。
在 142 名患者中,78 名是非解决者(中位数 ISS,30),34 名是解决者(中位数 ISS,22),30 名是低 ISS 对照组(中位数 ISS,1)。入院时观察到广泛的组织特异性损伤标志物释放;非解决者的释放量更大。72 小时时,与解决者相比,非解决者中仍有 9 种心脏、3 种肝脏、8 种神经和 3 种肺部蛋白显著升高。心脏损伤标志物在非解决者中的升高幅度最大,在 72 小时时与促炎介质和内皮损伤标志物呈显著正相关。非解决者的脂肪酸代谢物浓度低于解决者,尤其是酰基辅酶 A 和胆碱。
我们发现,在严重创伤后临床情况复杂的患者中,即刻释放组织特异性生物标志物,并持续升高肝脏、肺部、神经和特别是心脏损伤生物标志物。非解决者中持续存在的心肌损伤可能是多种因素共同作用的结果,包括代谢应激、炎症和内皮病变。