Suppr超能文献

登革热和登革出血热中的血液学

Haematology in dengue and dengue haemorrhagic fever.

作者信息

Srichaikul T, Nimmannitya S

机构信息

Vichaiyuth Hospital, 114/4 Sretsiri Road, Bangkok, Thailand.

出版信息

Baillieres Best Pract Res Clin Haematol. 2000 Jun;13(2):261-76. doi: 10.1053/beha.2000.0073.

Abstract

Dengue fever (DF) and dengue haemorrhagic fever (DHF) are caused by the dengue virus. The major pathophysiological hallmark that distinguishes DHF from DF is plasma leakage as a result of increased vascular permeability. Following this leakage, hypovolaemic shock occurs as a consequence of a critical plasma volume loss. Constant haematological abnormalities occurring in DHF and frequently include bone marrow suppression, leucopenia and thrombocytopenia. An enhanced immune response of the host to a secondary DV infection is a feature of DHF and leads to many consequences. These are immune complex formation, complement activation, increased histamine release and a massive release of many cytokines into the circulation, leading to shock, vasculopathy, thrombopathy and disseminated intravascular coagulation (DIC). The mechanisms underlying the bleeding in DHF are multiple. These are vasculopathy, thrombopathy and DIC. Thrombopathy consists of thrombocytopenia and platelet dysfunction. DIC is prominent in patients with shock. The most severe DIC and massive bleeding are the result of prolonged shock and cause a fatal outcome. The mechanisms of thrombopathy and DIC and the proper management of DHF are reviewed and discussed.

摘要

登革热(DF)和登革出血热(DHF)由登革病毒引起。区分DHF与DF的主要病理生理特征是由于血管通透性增加导致的血浆渗漏。这种渗漏之后,由于关键的血浆量丢失会发生低血容量休克。DHF中持续出现血液学异常,常包括骨髓抑制、白细胞减少和血小板减少。宿主对二次登革病毒感染的免疫反应增强是DHF的一个特征,并会导致多种后果。这些后果包括免疫复合物形成、补体激活、组胺释放增加以及多种细胞因子大量释放到循环中,从而导致休克、血管病变、血栓形成异常和弥散性血管内凝血(DIC)。DHF出血的潜在机制是多方面的。这些机制包括血管病变、血栓形成异常和DIC。血栓形成异常包括血小板减少和血小板功能障碍。DIC在休克患者中较为突出。最严重的DIC和大量出血是长时间休克的结果,并会导致致命结局。本文对血栓形成异常和DIC的机制以及DHF的恰当管理进行了综述和讨论。

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