目前尚不清楚，哪些伴随出血性休克的重伤患者最可能从1:1:1和1:1:2（血浆：血小板：红细胞）复苏策略中受益。通过鉴定创伤分子内分型，可以揭示出对各种复苏策略有差异治疗反应的患者亚组。为了从分子数据中派生创伤内分型（TE），并确定这些内分型是否与死亡率以及1:1:1和1:1:2复苏策略的差异治疗反应相关，本研究是对实际的、随机分配的、最佳血小板和血浆比率（PROPPR）临床试验的二次分析，研究对象是来自12个北美创伤中心的重伤个体。研究数据分析是在2021年8月2日至2022年10月25日期间进行的。通过对抵达医院时采集的血浆生物标记物进行K均值聚类，找出的创伤内分型。利用多元相对风险（RR）回归调整年龄、性别、创伤中心、创伤机制和创伤严重度评分（ISS），检验TE与30天死亡率之间的关联性。采用RR回归模型评估输血策略的差异治疗反应，该模型包括内分型与治疗组乘积相互作用项，调整年龄、性别、创伤中心、创伤机制和ISS。本研究分析的对象是来自PROPPR试验参与者的478名患者（中位数[IQR]年龄，34.5 [25-51]岁；男性384名[80%]）。 发现了一个在K均值聚类中具有最佳性能的双类模型。TE-1（n = 270）的特点是炎性生物标志物（如白细胞介素8和肿瘤坏死因子α）浓度更高，与TE-2（n = 208）相比，30天死亡率显著增加。治疗组和TE之间存在显著的30天死亡率相互作用。1:1:2治疗的TE-1死亡率为28.6%，而1:1:1治疗的死亡率为32.6%；1:1:2治疗的TE-2死亡率为24.5%，而1:1:1治疗的死亡率为7.3%（交互作用P = 0.001）。本研究的二次分析结果表明，在医院抵达时从血浆生物标志物派生的内分型与创伤患者对1:1:1和1:1:2复苏策略的治疗反应有差异。这些发现支持了危重创伤人群分子异质性的概念，并为为高风险不良结果的患者量身定制治疗提供了启示。

It is not clear which severely injured patients with hemorrhagic shock may benefit most from a 1:1:1 vs 1:1:2 (plasma:platelets:red blood cells) resuscitation strategy. Identification of trauma molecular endotypes may reveal subgroups of patients with differential treatment response to various resuscitation strategies.To derive trauma endotypes (TEs) from molecular data and determine whether these endotypes are associated with mortality and differential treatment response to 1:1:1 vs 1:1:2 resuscitation strategies.This was a secondary analysis of the Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) randomized clinical trial. The study cohort included individuals with severe injury from 12 North American trauma centers. The cohort was taken from the participants in the PROPPR trial who had complete plasma biomarker data available. Study data were analyzed on August 2, 2021, to October 25, 2022.TEs identified by K-means clustering of plasma biomarkers collected at hospital arrival.An association between TEs and 30-day mortality was tested using multivariable relative risk (RR) regression adjusting for age, sex, trauma center, mechanism of injury, and injury severity score (ISS). Differential treatment response to transfusion strategy was assessed using an RR regression model for 30-day mortality by incorporating an interaction term for the product of endotype and treatment group adjusting for age, sex, trauma center, mechanism of injury, and ISS.A total of 478 participants (median [IQR] age, 34.5 [25-51] years; 384 male [80%]) of the 680 participants in the PROPPR trial were included in this study analysis. A 2-class model that had optimal performance in K-means clustering was found. TE-1 (n = 270) was characterized by higher plasma concentrations of inflammatory biomarkers (eg, interleukin 8 and tumor necrosis factor α) and significantly higher 30-day mortality compared with TE-2 (n = 208). There was a significant interaction between treatment arm and TE for 30-day mortality. Mortality in TE-1 was 28.6% with 1:1:2 treatment vs 32.6% with 1:1:1 treatment, whereas mortality in TE-2 was 24.5% with 1:1:2 treatment vs 7.3% with 1:1:1 treatment (P for interaction = .001).Results of this secondary analysis suggest that endotypes derived from plasma biomarkers in trauma patients at hospital arrival were associated with a differential response to 1:1:1 vs 1:1:2 resuscitation strategies in trauma patients with severe injury. These findings support the concept of molecular heterogeneity in critically ill trauma populations and have implications for tailoring therapy for patients at high risk for adverse outcomes.