Inflammation, coagulopathy, and the pathogenesis of multiple organ dysfunction syndrome
Inflammation, coagulopathy, and the pathogenesis of multiple organ dysfunction syndrome
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DOI：
10.1097/00003246-200107001-00032
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发表时间：
2001-07-01
影响因子：
8.8
通讯作者：
Marshall, JC
中科院分区：
文献类型：
--
作者：
Marshall, JC
目的：对感染病原体伤害宿主的机制的进一步了解正在导致脓毒症概念的新表述，我们回顾了炎症和凝血在多器官功能障碍综合征发病机制中的作用，并探索新疗法恢复促凝血和抗凝血机制之间良好生物平衡的潜力，这些机制在导致器官功能障碍的危及生命的过程中被破坏，数据来源：基础和临床文献中已发表的主要来源的叙述性回顾。数据摘要：宿主-病原体相互作用的传统模型将感染的发病率归因于微生物对宿主组织的直接细胞毒性作用。然而，大量的实验和临床证据表明，宿主的反应，而不是引发这种反应的触发因素，才是结果的更有效的决定因素。对宿主来源的炎症介质的复杂网络的阐明提出了单独针对这些介质可以改善患者预后的可能性，并且这种方法已经取得了一些小小的成功。最近，越来越明显的是，炎症反应反过来通过诱导组织缺氧和细胞损伤（通过组织坏死或通过诱导程序性细胞死亡或凋亡）来介导其有害作用。因此，针对炎症激活的下游后果（例如微血管凝血或急性肾上腺功能不全）的治疗策略代表了减弱脓毒症反应以提高生存率并最大限度地减少器官功能障碍的最新且最有前途的方法。全身炎症的适应不良后遗症体现在多器官功能障碍综合征的概念中，是当代重症监护病房患者生存的主要障碍。对这一极其复杂的过程的进一步了解不仅将提供有效的新治疗选择，而且有望将危重疾病从生物学僵局（在此期间临床医生仅支持衰竭的器官）转变为可以成功治疗的疾病。
Objective: An improved understanding of the mechanisms through which infecting pathogens harm the host is leading to new formulations of the concept of sepsis, We review the roles of inflammation and coagulation in the pathogenesis of the multiple organ dysfunction syndrome, and explore the potential of new therapies to restore the fine biological balance between procoagulant and anticoagulant mechanisms that are disrupted during the life-threatening processes that lead to organ dysfunction,Data Sources:Narrative review of published primary sources in the basic and clinical literature.Data Summary:Traditional models of host-pathogen interactions ascribe the morbidity of infection to the direct cytotoxic effects of micro-organisms on host tissues. However, abundant experimental and clinical evidence has revealed that it is the response of the host, rather than the trigger that elicited it, that is the more potent determinant of outcome. The elucidation of a complex network of host-derived inflammatory mediators raised the possibility that targeting these individually could improve patient outcomes, and some modest successes with this approach have been achieved. More recently, it is becoming evident that the inflammatory response, in turn, mediates its deleterious effects by inducing tissue hypoxia, and cellular injury, either through tissue necrosis or through the induction of programmed cell death or apoptosis, Thus, treatment strategies that target the downstream consequences of the activation of inflammation, for example, microvascular coagulation or acute adrenal insufficiency, represent the latest, and some of the most promising approaches to attenuation of the septic response to improve survival, and minimize organ dysfunction, The maladaptive sequelae of systemic inflammation, embodied in the concept of the multiple organ dysfunction syndrome, comprise the leading obstacle to survival for patients admitted to a contemporary intensive care unit Further insights into this intimidatingly complex process will not only provide potent new therapeutic options, but promise to transform critical illness from a biological standoff, during which the clinician merely supports failing organs, to a disease that can be successfully treated.