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脓毒症诱导的凝血病发病机制及抗凝治疗的最新进展

Recent Advances in Pathogenesis and Anticoagulation Treatment of Sepsis-Induced Coagulopathy.

作者信息

Man Chit, An Yuan, Wang Guo-Xin, Mao En-Qiang, Ma Li

机构信息

Department of Emergency, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.

出版信息

J Inflamm Res. 2025 Jan 18;18:737-750. doi: 10.2147/JIR.S495223. eCollection 2025.

Abstract

Coagulopathy in sepsis is common and is associated with high mortality. Although immunothrombosis is necessary for infection control, excessive thrombus formation can trigger a systemic thrombo-inflammatory response. Immunothrombosis plays a core role in sepsis-induced coagulopathy, and research has revealed a complex interplay between inflammation and coagulation. Different mechanisms underlying sepsis-related coagulopathy are discussed, including factors contributing to the imbalance of pro- and anticoagulation relevant to endothelial cells. The potential therapeutic implications of anticoagulants on these mechanisms are discussed. This review contributes to our understanding of the pathogenesis of coagulopathy in patients with sepsis. Recent studies suggest that endothelial cells play an important role in immunoregulation and hemostasis. Meanwhile, the non-anticoagulation effects of anticoagulants, especially heparin, which act in the pathogenesis of coagulopathy in septic patients, have been partially revealed. We believe that further insights into the pathogenesis of sepsis-induced coagulopathy will help physicians evaluate patient conditions effectively, leading to advanced early recognition and better decision-making in the treatment of sepsis.

摘要

脓毒症中的凝血病很常见,且与高死亡率相关。尽管免疫血栓形成对于控制感染是必要的,但过度的血栓形成会引发全身血栓炎症反应。免疫血栓形成在脓毒症诱导的凝血病中起核心作用,并且研究已经揭示了炎症与凝血之间复杂的相互作用。本文讨论了脓毒症相关凝血病的不同潜在机制,包括导致与内皮细胞相关的促凝和抗凝失衡的因素。还讨论了抗凝剂对这些机制的潜在治疗意义。这篇综述有助于我们理解脓毒症患者凝血病的发病机制。最近的研究表明,内皮细胞在免疫调节和止血中起重要作用。同时,抗凝剂尤其是肝素在脓毒症患者凝血病发病机制中的非抗凝作用已被部分揭示。我们相信,对脓毒症诱导的凝血病发病机制的进一步深入了解将有助于医生有效评估患者病情,从而在脓毒症治疗中实现更早期的识别和更好的决策。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ff/11752821/8a200d8ec578/JIR-18-737-g0001.jpg

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