Sepsis Pathophysiology, Chronic Critical Illness, and Persistent Inflammation-Immunosuppression and Catabolism Syndrome.
Sepsis Pathophysiology, Chronic Critical Illness, and Persistent Inflammation-Immunosuppression and Catabolism Syndrome.
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脓毒症病理生理学、慢性危重疾病、持续性炎症-免疫抑制和分解代谢综合征。
DOI：
10.1097/ccm.0000000000002074
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发表时间：
2017-02
影响因子：
8.8
通讯作者：
Moldawer LL
中科院分区：
文献类型：
--
作者：
Mira JC;Gentile LF;Mathias BJ;Efron PA;Brakenridge SC;Mohr AM;Moore FA;Moldawer LL
为评价脓毒症病理生理学的演变范式，提出一种新的危重病人表型的演变，其潜在的潜在机制，以及它对未来脓毒症治疗和研究的意义。使用PubMed、MEDLINE、EMBASE和Google Scholar进行文献搜索。败血症仍然是最令人虚弱和昂贵的疾病之一，其发病率并未下降。正在改变的是我们的定义(S)，它的临床病程，以及我们如何处理败血症患者。脓毒症曾经被认为是一种过度活跃的炎症综合征，现在被认为是一种异常的宿主保护性免疫综合征。幸运的是，更早地认识到并遵守了治疗捆绑包，导致了多器官衰竭和住院死亡率的下降。不幸的是，越来越多的脓毒症患者，特别是老年人，患有慢性危重疾病(CCI)，很少能完全康复，往往会经历惰性死亡。CCI患者经常表现出“持续性炎症-免疫抑制和分解代谢综合征”或PICS，这里提出PICS导致了许多这些不良的临床结果。PICS的潜在原因目前尚不清楚，但越来越多的证据表明，骨髓生成改变、效应T细胞功能降低和未成熟髓系来源的抑制细胞扩张都是导致PICS的原因之一。虽然新的治疗干预措施分别针对炎症反应、免疫抑制反应和蛋白质分解代谢反应，但CCI和PICS败血症患者的成功治疗可能需要更多的补充方法。
To provide an appraisal of the evolving paradigms in the pathophysiology of sepsis, propose the evolution of a new phenotype of critically ill patients, its potential underlying mechanism, and its implications for the future of sepsis management and research. Literature search using PubMed, MEDLINE, EMBASE, and Google Scholar. Sepsis remains one of the most debilitating and expensive illnesses, and its incidence is not declining. What is changing is our definition(s), its clinical course, and how we manage the septic patient. Once thought to be predominantly a syndrome of over exuberant inflammation, sepsis is now recognized as a syndrome of aberrant host protective immunity. Earlier recognition and compliance with treatment bundles has fortunately led to a decline in multiple organ failure and in-hospital mortality. Unfortunately, more and more sepsis patients, especially the aged, are suffering chronic critical illness (CCI), rarely fully recover and often experience an indolent death. Patients with CCI often exhibit ‘a persistent inflammatory-immunosuppressive and catabolic syndrome’ or PICS, and it is proposed here that PICS contributes to many of these adverse clinical outcomes. The underlying cause of PICS is currently unknown, but there is increasing evidence that altered myelopoiesis, reduced effector T-cell function and expansion of immature myeloid-derived suppressor cells are all contributory. Although newer therapeutic interventions are targeting the inflammatory, the immunosuppressive, and the protein catabolic responses individually, successful treatment of the septic patient with CCI and PICS may require a more complementary approach.