Liu Jingjing, Zhou Gaosheng, Tong Zewen, Wang Xiaoting, Liu Dawei
Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, People's Republic of China.
J Inflamm Res. 2024 Sep 30;17:6815-6826. doi: 10.2147/JIR.S477495. eCollection 2024.
Metabolic changing is the significant host stress response during sepsis, but there is increasing evidence that uncontrolled metabolic reprogramming is a contributing factor to sepsis. Nevertheless, its association with outcome in patients with sepsis has been poorly investigated. As the key enzyme of metabolic reprogramming, the clinical value of PDK1 and LDH in patients with sepsis will be investigated in this study.
We collected serum from 167 ICU patients within 24 hours of admission for a single-center prospective observational study. The levels of PDK1 and LDH were detected by enzyme-linked adsorption method. Pearson or Spearman coefficient for correlation analysis between PDK1, LDH and clinical indicators. Areas under the ROC curves for evaluation of mortality prediction. Kaplan-Meier survival curve analysis was performed, and Cox proportional hazards model was performed to determine the risk factors for 28-day mortality.
The PDK1/LDH in the septic shock group was statistically different between both the sepsis group and ICU control group, and had good correlation with ScvO and lactate. In predicting 28-day mortality in patients with sepsis, the best AUC was observed for PDK1/LDH, and was higher than the AUC for PDK1, lactate, and SOFA. Additionally, patients with lower PDK1/LDH had markerablely higher 28-day mortality. The multivariate Cox proportional hazards model revealed that PDK1/LDH < 0.1808 were the independent risk factors for 28-day mortality in sepsis.
The level of PDK1/LDH at admission was markedly decreased in patients with septic shock, which can serve as a novel independent prognostic biomarker for predicting mortality.
代谢变化是脓毒症期间重要的宿主应激反应，但越来越多的证据表明，不受控制的代谢重编程是脓毒症的一个促成因素。然而，其与脓毒症患者预后的关系尚未得到充分研究。作为代谢重编程的关键酶，本研究将探讨丙酮酸脱氢酶激酶1（PDK1）和乳酸脱氢酶（LDH）在脓毒症患者中的临床价值。
我们收集了167例入住重症监护病房（ICU）患者入院后24小时内的血清，进行单中心前瞻性观察研究。采用酶联吸附法检测PDK1和LDH水平。采用Pearson或Spearman系数对PDK1、LDH与临床指标进行相关性分析。绘制受试者工作特征（ROC）曲线下面积以评估死亡预测能力。进行Kaplan-Meier生存曲线分析，并采用Cox比例风险模型确定28天死亡率的危险因素。
脓毒性休克组的PDK1/LDH与脓毒症组和ICU对照组相比差异有统计学意义，且与中心静脉血氧饱和度（ScvO）和乳酸有良好的相关性。在预测脓毒症患者28天死亡率方面，PDK1/LDH的曲线下面积（AUC）最佳，高于PDK1、乳酸和序贯器官衰竭评估（SOFA）评分的AUC。此外，PDK1/LDH较低的患者28天死亡率显著较高。多因素Cox比例风险模型显示，PDK1/LDH<0.1808是脓毒症患者28天死亡率的独立危险因素。
脓毒性休克患者入院时PDK1/LDH水平显著降低，可作为预测死亡率的新型独立预后生物标志物。
