Thrombocytopenia in Dengue: Interrelationship between
Virus and the Imbalance between Coagulation and Fibrinolysis
and Inflammatory Mediators
Summary:
Dengue causes serious infection in humans, resulting in morbidity and mortality in most tropical and subtropical areas of the world. Dengue viruses (DENVs) are the most important human arbo viruses worldwide and are transmitted by mosquitoes of the genus Aedes in the form of four distinct serotypes (DENV- 1, DENV-2, DENV-3, and DENV-4). And Thrombocytopenia has always been one of the criteria used by WHO guidelines as a potential indicator of clinical severity [20, 31]. In the most recent 2009 WHO guidelines, the definitions generally describe a rapid decline in platelet count or a platelet count less than 150,000 per microliter of blood
Thrombocytopenia may also be due to (1) platelet consumption during ongoing coagulopathy process, (2) activation of the complement system [113], or (3) increased peripheral sequestration [32, 114]. It has been shown in vitro that platelets undergo increased phagocytosis by macrophages in patients with secondary DENV infections by an uncharacterized mechanism. The detection of DENV antigens on the surface and in platelet-containing immune complexes from skin biopsy specimens has been well documented Dengue viral RNAwas detected in the platelets and plasma by conventional RT-PCR and EM, which confirmed the presence of dengue viral-like particles inside platelets isolated from patients. These data suggested that the presence of DENV in platelets might be associated with platelet dysfunction.
So in conclusion, Thrombocytopenia, coagulopathy, and vasculopathy are hematological abnormalities related to platelet and endothelial dysfunction generally observed in severe dengue. Among the causes and consequences, previous data have suggested an imbalance between clotting versus fibrinolysis systems as DIC. In a minority of patients with severe or prolonged shock, the abnormalities may be profound and, in combination with severe thrombocytopenia and the secondary effects of hypoxia and acidosis, may result in true DIC and major hemorrhage. To date, no scientific studies have suggested that platelet granule constituents can amplify inflammation and vascular permeability alteration during dengue. Several mechanisms are involved in thrombocytopenia and platelet dysfunction in dengue, indicating the complexity of dengue immune pathogenesis.
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