Suppr超能文献

糖尿病酮症酸中毒会引发一种促血栓形成状态。

Diabetic ketoacidosis promotes a prothrombotic state.

作者信息

Carl G F, Hoffman William H, Passmore Gregory G, Truemper Edward J, Lightsey Alton L, Cornwell Philip E, Jonah Mary H

机构信息

Department of Neurology, Veteran's Administration Medical Center, Augusta, Georgia, USA.

出版信息

Endocr Res. 2003 Feb;29(1):73-82. doi: 10.1081/erc-120018678.

Abstract

Cerebrovascular accidents are one of the life-threatening complications of diabetic ketoacidosis (DKA) in children and adolescents. Our objective was to evaluate the effect of DKA and its treatment on factors known to affect thrombotic activity (protein C; protein S; von Willebrand factor, fibrinogen; homocysteine; and folate) by comparing seven adolescents with DKA prior to treatment and at 6, 24, and 120 hours after initiation of treatment. We found that protein C activity was significantly decreased by DKA, but normalized slowly following treatment. Free protein S was low throughout the study. Protein C antigen and protein S antigen showed varying degrees ofchange within the first 24 hours, but remained in the normal range, with the exception of the initial value of protein C antigen, which was elevated. von Willebrand factor (vWF) antigen and vWF activity were both significantly increased prior to treatment, but decreased with treatment. However, vWF activity remained elevated at 120 hours. Fibrinogen concentrations showed no significant changes throughout the study. Homocysteine was significantly decreased prior to treatment and increased with the initiation of treatment Folate was significantly increased prior to treatment, and decreased to high normal levels. The increased vWF and the decreased levels of protein C activity and of free protein S support the hypothesis that DKA and its treatment results in a prothrombotic state and activation of the vascular endothelium, which, in turn, predispose to cerebrovascular accidents.

摘要

脑血管意外是儿童和青少年糖尿病酮症酸中毒(DKA)的危及生命的并发症之一。我们的目的是通过比较7名DKA青少年治疗前以及开始治疗后6小时、24小时和120小时,评估DKA及其治疗对已知影响血栓形成活性的因素(蛋白C、蛋白S、血管性血友病因子、纤维蛋白原、同型半胱氨酸和叶酸)的影响。我们发现,DKA使蛋白C活性显著降低,但治疗后缓慢恢复正常。在整个研究过程中,游离蛋白S水平较低。蛋白C抗原和蛋白S抗原在最初24小时内呈现不同程度的变化,但除蛋白C抗原初始值升高外,其余均保持在正常范围内。血管性血友病因子(vWF)抗原和vWF活性在治疗前均显著升高,但随治疗降低。然而,vWF活性在120小时时仍升高。在整个研究过程中,纤维蛋白原浓度无显著变化。同型半胱氨酸在治疗前显著降低,治疗开始后升高。叶酸在治疗前显著升高,随后降至略高于正常水平。vWF升高以及蛋白C活性和游离蛋白S水平降低支持以下假设:DKA及其治疗导致血栓前状态和血管内皮激活,进而易引发脑血管意外。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验