脓毒症患者血小板功能障碍的机制研究进展

doi:10.3969/j.issn.1002-1949.2017.10.001

摘要
图/表
参考文献(36)
相关文章 (15)

全文: PDF (3882 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要脓毒症是由感染诱发的全身炎症反应，严重者可引起休克、多器官功能障碍甚至死亡。重症脓毒症常引起凝血功能障碍，尤其是血小板质和量的变化。血小板在脓毒症发病机制中的作用尚不清楚。血小板质和量的变化与脓毒症患者严重程度及病死率具有明显的相关性。血小板功能障碍机制的研究是目前研究的热点之一。本文综述血小板质和量的变化，对预测脓毒症的严重程度及预后有重要的意义。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	付鹤鹏
	张玉想

收稿日期: 2016-12-30

基金资助:首都卫生发展科研专项项目（首发2014-3-5072）

通讯作者: 张玉想（1965-），女，博士，主任医师，硕士生导师，E-mail：15810550308@163.com

作者简介: 付鹤鹏（1988-），男，硕士研究生，住院医师。

引用本文:

付鹤鹏，张玉想. 脓毒症患者血小板功能障碍的机制研究进展[J]. 中国急救医学, 2017, 37(10): 873-877.
Fu He-peng, Zhang Yu-xiang. Mechanism of platelet dysfunction in patients with sepsis. Chinese Journal of Critical Care Medicine, 2017, 37(10): 873-877.

链接本文:

http://www.cnemergency.org.cn/CN/10.3969/j.issn.1002-1949.2017.10.001 或 http://www.cnemergency.org.cn/CN/Y2017/V37/I10/873

［1］Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock(Sepsis-3)［J］.JAMA, 2016, 315(8):801-810. ［2］Shankar-Hari M, Phillips GS, Levy ML, et al. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock(Sepsis-3)［J］. JAMA, 2016, 315(8):775-787.  ［3］Seymour CW, Liu VX,Iwashyna TJ, et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions forSepsis and Septic Shock(Sepsis-3)［J］. JAMA, 2016, 315(8):762-774. ［4］Rhodes A, Evans LE,Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016 ［J］. Intensive Care Med, 2017, 43(3):304-377. ［5］Stoller J, Halpin L, Weis M, et al. Epidemiology of severe sepsis: 2008-2012［J］. J Crit Care, 2016, 31(1):58-62.  ［6］Liao XL, Xie ZC, Kang Y. New Concept for Surviving Sepsis: from Phenomenon to Essence［J］. Sichuan Da Xue Xue Bao Yi Xue Ban, 2016, 47(4):570-573. ［7］王洪霞,刘健. 血小板在脓毒症中的作用［J］. 医学综述, 2005, 11(5):455-456. ［8］Levi M. Platelets in Critical Illness［J］. Semin Thromb Hemost, 2016, 42(3):252-257.  ［9］Claushuis TA, van Vught LA, Scicluna BP, et al. Thrombocytopenia is associated with a dysregulated host response in critically ill sepsis patients［J］. Blood, 2016, 127(24):3062-3072 ［10］Katz JN, Kolappa KP, Becker RC. Beyond Thrombosis : The Versatile Platelet in Critical Illness［J］. Chest, 2011, 139(3):658-668. ［11］Rondina MT, Garraud O. Emerging evidence for platelets as immune and inflammatory effector cells［J］. Front Immunol, 2014, 5:653. ［12］Bockmeyer CL, Claus RA, Budde U, et al. Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor［J］. Haematologica, 2008, 93(1):137-140. ［13］Levi M, van der Poll T. Endothelial injury in sepsis［J］. Intensive Care Med, 2013, 39(10):1839-1842. ［14］Shannon O. Platelet interaction with bacterial toxins and secreted products［J］. Platelets, 2015, 26(4):302-308. ［15］Hurley SM, Kahn F, Nordenfelt P, et al. Platelet-Dependent Neutrophil Function Is Dysregulated by M Protein from Streptococcus pyogenes［J］. Infect Immunol, 2015, 83(9):3515-3525. ［16］Xu X, Sun B. Platelet granule secretion mechanisms: Are they modified in sepsis ［J］. Thromb Res, 2015, 136(5):845-850. ［17］Kral JB, Schrottmaier WC, Salzmann M, et al. Platelet Interaction with Innate Immune Cells［J］. Transfus Med Hemother, 2016, 43(2):78-88. ［18］Thomas MR, Storey RF. The role of platelets in inflammation［J］. Thromb Haemost, 2015, 114(3):449-458. ［19］Ishikura H, Nishida T, Murai A, et al. New diagnostic strategy for sepsis-induced disseminated intravascular coagulation: a prospective single-center observational study［J］. Crit Care, 2014, 18(1):R19. ［20］Simmons J, Pittet JF. The coagulopathy of acute sepsis［J］. Curr Opin Anaesthesiol, 2015, 28(2):227-236. ［21］de Stoppelaar SF, van′t Veer C, van der Poll T. The role of platelets in sepsis［J］. Thromb Haemost, 2014, 112(4):666-677. ［22］Lipinska-Gediga M. Platelets in sepsis - are there any new aspects ［J］. Anaesthesiol Intensive Ther, 2017, 49(2):167-172. ［23］Ali RA, Wuescher LM, Worth RG. Platelets: essential components of the immune system［J］. Curr Trends Immunol, 2015, 16:65-78. ［24］Kim SJ, Jenne CN. Role of platelets in neutrophil extracellular trap(NET)production and tissue injury［J］. Semin Immunol, 2016, 28(6):546-554. ［25］Duerschmied D, Bode C, Ahrens I. Immune functions of platelets［J］. Thromb Haemost, 2014, 112(4): 678-691. ［26］Semeraro N, Ammollo CT, Semeraro F, et al. Coagulopathy of Acute Sepsis［J］. Semin Thromb Hemost, 2015, 41(6):650-658. ［27］Koenen RR. The prowess of platelets in immunity and inflammation［J］. Thromb Haemost, 2016, 116(4):605-612.  ［28］Deppermann C, Kubes P. Platelets and infection［J］. Semin Immunol, 2016, 28(6):536-545. ［29］陈明发，吴珺，杨东亮，等. NOD1和NOD2介导的信号通路及其抗病毒免疫应答研究进展［J］. 国际免疫学杂志， 2013, 36(3):167-169. ［30］Kim YK, Shin JS, Nahm MH. NOD-Like Receptors in Infection, Immunity, and Diseases［J］. Yonsei Med J, 2016, 57(1):5-14. ［31］Zhang S, Zhang S, Hu L, et al. NOD2 Receptor is Expressed in Platelets and Enhances Platelet Activation and Thrombosis［J］. Circulation, 2015, 131(13):316-323. ［32］Tsao CM, Ho ST, Wu CC. Coagulation abnormalities in sepsis［J］. Acta Anaesthesiol Taiwan, 2015, 53(1):16-22. ［33］Lee K, Chang Y, Song K, et al. Associations between Single Nucleotide Polymorphisms of High Mobility Group Box 1 Protein and Clinical Outcomes in Korean Sepsis Patients［J］. Yonsei Med J, 2016, 57(1):111-117. ［34］Davis RP, Miller-Dorey S, Jenne CN. Platelets and coagulation in infection［J］. Clin Transl Immunology, 2016, 5(7):e89. ［35］Semeraro F, Ammollo CT, Morrissey JH, et al. Extracellular histones promote thrombin generation through platelet-dependent mechanisms: involvement of platelet TLR2 and TLR4［J］. Blood, 2011, 118(7):1952-1961. ［36］Semeraro N, Ammollo CT, Semeraro F, et al. Sepsis, thrombosis and organ dysfunction［J］. Thromb Res, 2012, 129(3):290-295.