脓毒症性凝血病发病机制的研究进展  

Research Progress on the Pathogenesis of Sepsis-Induced Coagulopathy

作　　者：柯书豪 刘秀娟[2] 

机构地区：[1]承德医学院研究生学院,河北 承德 [2]秦皇岛市第一医院重症医学科,河北 秦皇岛

出　　处：《临床医学进展》2025年第2期1138-1143,共6页Advances in Clinical Medicine

摘　　要：脓毒症(sepsis)是危重症患者常见的死亡原因。在脓毒症中,促凝血途径和抗凝途径之间的平衡被打破,导致全身凝血酶生成、抗凝活性受损和纤维蛋白溶解抑制,称为脓毒症性凝血病(sepsis-induced coagulopathy, SIC)。SIC是脓毒症的一种常见的并发症,见于24%的脓毒症患者和66%的脓毒性休克患者,并且通常与不良临床结局和高死亡率有关。SIC发病机制复杂,目前尚未完全阐明,最近的临床研究对SIC的分子发病机制产生了新的见解,本文就脓毒症性凝血病的发病机制进行综述。Sepsis is a common cause of death in critically ill patients. In sepsis, the balance between procoagulant and anticoagulant pathways is disrupted, leading to systemic thrombin generation, impaired anticoagulant activity, and inhibition of fibrinolysis, a condition known as sepsis-induced coagulopathy (SIC). SIC is a common complication of sepsis, affecting 24% of sepsis patients and 66% of those with septic shock, and is usually associated with poor clinical outcomes and high mortality rates. The pathogenesis of SIC is complex and not yet fully understood. Recent clinical studies have provided new insights into the molecular mechanisms of SIC. This review aims to summarize the pathogenesis of sepsis-induced coagulopathy.

关 键 词：脓毒症 凝血病 发病机制 

分 类 号：TB3[一般工业技术—材料科学与工程]