Related Experiment Video
Updated: Jan 6, 2026
Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
The Vascular Endothelium in Patients with Dengue Haemorrhagic Fever
Mutiara1, Stephen C L Koh2, Adang Bachtiar3
1Murni Teguh Memorial Hospital and Faculty of Medicine, University of North Sumatera, Medan, Indonesia.
Background:
Dengue fever is the most serious consequence of mosquito-borne infection worldwide. The pathophysiology of DHF in human is complex, which involve endothelial cell activation and impaired endothelial barrier leading to plasma leakage triggering the activation of the haemostatic system. The increased vascular permeability may lead to hypovolemia, hypotension and shock, which is life-threatening.
Aim:
The objective of the study was to determine the effects of dengue haemorrhagic fever on the vascular endothelium.
Methods:
Fifty patients (males 34, females 16), were recruited, Grade 1 (n = 41), Grade 2 (n = 6), Grade 3 (n = 2) and Grade 4 (n = 1) DHF. Blood sampling was performed at the febrile, defervescence and convalescent phases for the determination of haemoglobin, haematocrit, platelets, prothrombin fragment F1 + 2, Von Willebrand Factor (VWF), vascular endothelial growth factor (VEGF) and D-dimer levels. Fifteen normal subjects were recruited to serve as normal controls.
Results:
The patients aged between 4 and 54 years old. Grades 1 & 2 DHF showed no significant differences in the parameters studied. However, thrombocytopenia, elevated F1 + 2, VWF, VEGF and D-dimer levels were evident in febrile, defervescence and convalescent phases suggesting endothelial activation and plasma leakage. Pleural effusion was observed only in severe DHF. The three patients with Grades 3 and 4 DHF had similar study results. No mortality was recorded in the study.
Conclusion:
In dengue haemorrhagic fever, the vascular endothelium is activated, causing plasma leakage triggering the activation of the haemostatic system creating a hypercoagulable and enhanced fibrinolytic state evident by marked fibrinolysis.
