Thesis (M.Sc.)--Chulalongkorn University, 2004

Background: In dengue hemorrhagic fever (DHF), the major cause of hypovolemic shock and circulatory failure is increase in vascular permeability. Although many cytokines were reported to play a role, the pathogenesis of vascular leakage remains unclear. In this study, we investigated the role of VEGF in the pathogenesis of DHF and dengue shock syndrome (DSS). Methods: 41 serologically confirmed dengue infected children were assigned to be dengue fever (DF), DHF without shock and DSS. Serum samples for vascular endothelial growth factor (VEGF), complete blood count and liver enzymes (ALT and AST) were collected at first day of fever, defervescence, discharge and follow-up time. All patients underwent ultrasonographic studies for pleural effusion index and cardiac index at each stage of disease. Results: During the illness, serum VEGF levels were lower in patients of more severe illness. At follow-up period, significant increment of serum VEGF was foundin all patients, except 1 with DF. There was no relationship between serum VEGF level and cardiac index, pleural effusion index or liver enzymes. Conclusion: We hypothesized that VEGF could have a role in repairing process of endothelial damage in recovery phase of dengue infection, similar to many other diseases that had been previously studied.