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单纯性菌血症或细菌性休克中Hageman因子依赖性途径和补体系统的激活与抑制

Activation and inhibition of Hageman factor-dependent pathways and the complement system in uncomplicated bacteremia or bacterial shock.

作者信息

Kalter E S, Daha M R, ten Cate J W, Verhoef J, Bouma B N

出版信息

J Infect Dis. 1985 Jun;151(6):1019-27. doi: 10.1093/infdis/151.6.1019.

DOI:10.1093/infdis/151.6.1019
PMID:2582065
Abstract

Levels of components of the contact activation, coagulation, and complement systems and their main inhibitors were measured in 45 critically ill patients during 61 episodes of uncomplicated bacteremia or bacterial shock. Levels of Hageman factor (factor XII), prekallikrein, high-molecular-weight kininogen, factor XI, factor VII, total hemolytic complement, alternative pathway activity, and C3 were within the normal range during uncomplicated bacteremia (n = 29), but during fatal bacterial shock (n = 13) a significant decrease by 40%-50% was observed in all measurements. During nonfatal bacterial shock (n = 19) a moderate decrease was observed in most of these measurements. The capacity of plasma to inactivate kallikrein was significantly higher during bacteremia than during bacterial shock because of a significant increase in the level of C1 esterase inhibitor. Levels of antithrombin III and alpha 2-macroglobulin were below normal in all groups. Thus increased inhibition of the contact activation and complement systems is beneficial during bacteremia.

摘要

在45例危重症患者的61次无并发症菌血症或感染性休克发作期间,检测了接触激活系统、凝血系统和补体系统的成分及其主要抑制剂的水平。在无并发症菌血症(n = 29)期间,哈格曼因子(因子XII)、前激肽释放酶、高分子量激肽原、因子XI、因子VII、总溶血补体、替代途径活性和C3水平均在正常范围内,但在致命性感染性休克(n = 13)期间,所有测量值均显著下降40%-50%。在非致命性感染性休克(n = 19)期间,大多数测量值出现中度下降。由于C1酯酶抑制剂水平显著升高,菌血症期间血浆灭活激肽释放酶的能力显著高于感染性休克期间。所有组的抗凝血酶III和α2-巨球蛋白水平均低于正常。因此,在菌血症期间增加对接触激活系统和补体系统的抑制是有益的。

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