Disseminated intravascular coagulation and its immune mechanisms.
Disseminated intravascular coagulation and its immune mechanisms.
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传播血管内凝血及其免疫机制。
DOI：
10.1182/blood.2020007208
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发表时间：
2022-03-31
期刊：
影响因子：
20.3
通讯作者：
Lupu F
中科院分区：
文献类型：
--
作者：
Popescu NI;Lupu C;Lupu F
这一系列关于免疫止血的综述强调了免疫和止血之间的交叉。在第一篇文章中，施密特、Schrezenmeier和Kavanagh讨论了补体终末途径激活在阵发性睡眠性血红蛋白尿症、非典型溶血性尿毒症综合征、自身免疫性溶血性贫血和其他补体激活综合征相关血栓形成中的作用。在第二部分中，Popescu、Lupu和Lupu讨论了免疫应答通过对病原体相关或宿主来源的损伤相关分子模式的应答在弥散性血管内凝血起始中的作用，以及通过其他免疫和炎症途径的持续存在。在该系列的最后一篇文章中，Kizhakkedathu和Conway讨论了免疫炎症途径在血液暴露于生物材料器械或植入组织中的异物表面的反应中的作用。弥散性血管内凝血（DIC）是由感染性和非感染性病理触发的综合征，其特征在于血管内凝血酶的过度生成和纤维蛋白原的广泛蛋白水解转化。尽管DIC的临床表现多种多样，从血栓闭塞性损伤到出血素质，但其病因通常涉及血液凝固的过度激活以及抗凝剂和纤维蛋白溶解的重叠失调。血液凝固的启动是在血管内组织因子表达或接触途径激活后，对病原体相关或宿主来源的损伤相关分子模式作出反应。该过程通过炎症和免疫血栓形成机制进一步放大。抗凝剂的消耗和内皮稳态的破坏降低了调节控制和微血管血栓形成的传播。患者临床DIC的发展与发病率恶化和死亡率增加相关，无论基础病理如何;因此，及时识别DIC对于减少病理负担至关重要。由于导致DIC的触发因素和致病机制的多样性，诊断基于量化止血失衡、血小板减少和纤维蛋白原转化的算法。由于目前的诊断主要评估明显的消耗性凝血病，因此迫切需要更好地识别非明显的DIC和/或DIC前状态。DIC患者的治疗策略包括消除诱发因素和支持性治疗止血失衡。尽管有医疗护理，DIC患者的死亡率仍然很高，需要针对潜在的病理机制制定新的策略。
This review series on immunohemostasis highlights the crosstalk between immunity and hemostasis. In the first article, Schmidt, Schrezenmeier, and Kavanagh discuss the role of activation of the terminal pathway of complement in thrombosis associated with paroxysmal nocturnal hemoglobinuria, atypical hemolytic-uremic syndrome, autoimmune hemolytic anemia, and other complement activating syndromes. In the second, Popescu, Lupu, and Lupu discuss the role of immune response in the initiation of disseminated intravascular coagulation through responses to pathogen-associated or host-derived damage-associated molecular pattern, and its perpetuation through other immune and inflammatory pathways. In the final article of the series, Kizhakkedathu and Conway discuss the role of immunoinflammatory pathways in the response of exposure of blood to foreign surfaces in biomaterial devices or implanted tissues. Disseminated intravascular coagulation (DIC) is a syndrome triggered by infectious and noninfectious pathologies characterized by excessive generation of thrombin within the vasculature and widespread proteolytic conversion of fibrinogen. Despite diverse clinical manifestations ranging from thrombo-occlusive damage to bleeding diathesis, DIC etiology commonly involves excessive activation of blood coagulation and overlapping dysregulation of anticoagulants and fibrinolysis. Initiation of blood coagulation follows intravascular expression of tissue factor or activation of the contact pathway in response to pathogen-associated or host-derived, damage-associated molecular patterns. The process is further amplified through inflammatory and immunothrombotic mechanisms. Consumption of anticoagulants and disruption of endothelial homeostasis lower the regulatory control and disseminate microvascular thrombosis. Clinical DIC development in patients is associated with worsening morbidities and increased mortality, regardless of the underlying pathology; therefore, timely recognition of DIC is critical for reducing the pathologic burden. Due to the diversity of triggers and pathogenic mechanisms leading to DIC, diagnosis is based on algorithms that quantify hemostatic imbalance, thrombocytopenia, and fibrinogen conversion. Because current diagnosis primarily assesses overt consumptive coagulopathies, there is a critical need for better recognition of nonovert DIC and/or pre-DIC states. Therapeutic strategies for patients with DIC involve resolution of the eliciting triggers and supportive care for the hemostatic imbalance. Despite medical care, mortality in patients with DIC remains high, and new strategies, tailored to the underlying pathologic mechanisms, are needed.
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DOI：
10.1073/pnas.91.19.8767
发表时间：
1994-09-13
影响因子：
11.1
作者：
CELI, A;PELLEGRINI, G;FURIE, B
通讯作者：
FURIE, B
影响因子：
10.8
作者：
Chappell, Daniel;Jacob, Matthias;Becker, Bernhard F.
通讯作者：
Becker, Bernhard F.
影响因子：
20.3
作者：
Dunzendorfer, S;Kaneider, N;Wiedermann, CJ
通讯作者：
Wiedermann, CJ
影响因子：
3.5
作者：
De Palma, Raffaele;Cirillo, Plinio;Cimmino, Giovanni
通讯作者：
Cimmino, Giovanni
影响因子：
158.5
作者：
Ackermann, Maximilian;Verleden, Stijn E.;Jonigk, Danny
通讯作者：
Jonigk, Danny