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Coagulation abnormalities in dengue hemorrhagic Fever: serial investigations in 167 Vietnamese children with Dengue shock syndrome.

Abstract:
The pathophysiological basis of hemorrhage in dengue infections remains poorly understood, despite the increasing global importance of these infections. A large prospective study of 167 Vietnamese children with dengue shock syndrome documented only minor prolongations of prothrombin and partial thromboplastin times but moderate to severe depression of plasma fibrinogen concentrations. A detailed study of 48 children revealed low plasma concentrations of the anticoagulant proteins C, S, and antithrombin III, which decreased with increasing severity of shock, probably because of capillary leakage. Concurrent increases in the levels of thrombomodulin, tissue factor, and plasminogen activator inhibitor type 1 (PAI-1) indicated increased production of these proteins. Thrombomodulin levels suggestive of endothelial activation correlated with increasing shock severity, whereas PAI-1 levels correlated with bleeding severity. Dengue virus can directly activate plasminogen in vitro. Rather than causing true disseminated intravascular coagulation, dengue infection may activate fibrinolysis primarily, degrading fibrinogen directly and prompting secondary activation of procoagulant homeostatic mechanisms.
Publication status:
Published

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Publisher copy:
10.1086/341410

Authors

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Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Tropical Medicine
Role:
Author


Journal:
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America More from this journal
Volume:
35
Issue:
3
Pages:
277-285
Publication date:
2002-08-01
DOI:
EISSN:
1537-6591
ISSN:
1058-4838


Language:
English
Keywords:
Pubs id:
pubs:38274
UUID:
uuid:71672020-38e0-429b-9c6a-d575359e4294
Local pid:
pubs:38274
Source identifiers:
38274
Deposit date:
2012-12-19
ARK identifier:

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