• Am. J. Med. Sci. · Apr 2018

    Monocyte Programmed Death Ligand-1, A Predicator for 28-Day Mortality in Septic Patients.

    • Huiyu Tai, Hailin Xing, Dong Xiang, Zhiyun Zhu, Haifeng Mei, Wenbin Sun, and Wei Zhang.
    • Department of Intensive Care Unit, Taizhou People's Hospital, Medical School of Nantong University, Taizhou, Jiangsu, China.
    • Am. J. Med. Sci. 2018 Apr 1; 355 (4): 362-367.

    BackgroundSepsis is a great health burden for millions of people worldwide and plays a critical role in the cause of death in intensive care units. Previous studies have revealed that programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) play critical roles in the immunosuppression phase induced by sepsis. The objective of this present study was to establish whether PD-1/PD-L1 expressions were associated with 28-day mortality of septic patients.MethodsConsecutive patients admitted to the intensive care units of Taizhou People's Hospital for the treatment of sepsis from June 2014 through June 2016 were included. The demographic and clinical characteristics, laboratory tests, PD-1 and PD-L1 expressions on monocytes/CD4+T/CD8+T cells were compared between survivors and nonsurvivors. Univariate and multivariate logistic regression analyses were plotted for prognostic factors associated with mortality at day-28 in septic patients.ResultsA total of 177 septic patients were finally admitted to this study protocol, including 131 survivors and 46 nonsurvivors with a mortality of 26.0%. High PD-L1/monocytes expressions showed an independently significant association with 28-day mortality in septic patients (odds ratio: 4.73, 95% CI: 1.78-15.32, P = 0.033). The receiver operating characteristic curve analysis also indicated PD-L1/monocytes as a predicator for 28-day mortality with a cutoff value of 45.68%.ConclusionsOur results suggested monocyte PD-L1 expression on admission was an independent risk factor for day-28 mortality in septic patients.Copyright © 2018 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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