In severe dengue, plasma is lost after fever and viremia have resolved. Dengue-infected blood cells, mainly macrophages, release pro-inflammatory cytokines that disrupt occluded areas of vascular endothelial cells (occludin, claudin, EV-cadherin), resulting in decreased permeability and barrier reorganization, promoting plasma release. Loss of extravascular plasma leads to hypotension leading to dengue shock syndrome (DSS) 10-13 There are no effective antiviral drugs against dengue virus (DV). The possible pathophysiological mechanism of plasma loss in obese and dengue patients may be related to endothelial dysfunction caused by chronic release of proinflammatory cytokines caused by elevated leptin levels and reactive oxygen species (ROS) production.
Studies using chest x-ray or serial ultrasound scans to directly detect plasma loss have shown that progressive and significant fluid accumulation occurs only in a subset of dengue cases. Studies show that small pleural effusions seen on chest x-ray in the lateral position are relatively common findings in febrile non-dengue patients and in patients with DF, confirming the previous association. This indicates that a small pleural effusion alone is not a reliable marker of plasma leakage as a criterion for the clinical classification of dengue cases.
A limitation of this article is that the control population did not include patients with other serious infections such as septic shock. The increase in PBR hf observed in patients with severe plasma loss may also be nonspecific. Although the control population did not include patients with other severe febrile illnesses, SDC1 levels in patients with severe plasma loss in this study were several-fold higher than in most other published shock studies; this may be the case for dengue shock patients A plausible explanation is provided by the greater cause of plasma loss in patients with hemorrhagic and septic shock. We hypothesized that glycocalyx degradation would be (1) increased in dengue patients compared to OFI and (2) in dengue patients with or without plasma loss. However, there were no significant differences in comparing glycocalyx breakdown among dengue outpatients, most of whom had mild plasma losses and other non-severe febrile illnesses.
In another study, the plasma levels of VEGF and its soluble receptors were compared during illness in patients with DHF with those in patients with dengue fever (DF), a milder form of dengue viral infection without plasma loss. Dengue virus (DV) infections pose a serious health threat to populations living in tropical and subtropical regions.1 Infection with any of the 4 DV serotypes can cause a wide range of illnesses, from asymptomatic infection to severe life-threatening illness.2 Symptoms Dengue is commonly classified as dengue fever (DF), a self-limited febrile illness or a more severe form, dengue hemorrhagic fever (DHF), characterized by plasma loss in the chest and abdominal cavities and hemorrhagic diathesis. Infection with any of the four serotypes of dengue virus can lead to DHF, a syndrome characterized by a sudden and transient period of localized plasma loss that manifests as accumulation of fluid in the pleural and/or abdominal cavity during a decrease in body temperature.
However, most previous studies on predictors of plasma loss have yielded mixed results due to differences in study design, participant composition, and severe dengue case definitions. The definition and definition of diagnostic criteria for plasma leakage has long been overlooked, as highlighted here, even after the use of stringent inclusion criteria (a prospective cohort of patients with confirmed dengue), the estimated proportion of patients with plasma leakage was observed Values also vary widely between studies and lead to unreliable cumulative assessment of the surrogate DHF score (it is reported more frequently since it was part of the clinical classification in the 1997 WHO guidelines). This is consistent with clinical observations that the effects of plasma leakage on circulation are typically observed within 48 hours of temperature reduction. DF and OFI. In contrast, MMP-2 activity was upregulated by DENV-infected primary human large vascular endothelial cells and showed improved endothelial permeability, the only one with significant plasma loss during convalescence Elevated MMP.
MMP-9, which has previously been shown to be activated by DENV-infected immature dendritic cells and contribute to the molecular pathogenesis of DSS by improving endothelial permeability, was found to be significantly elevated during recovery in all patients. But it was not related to the severity of the plasma leak. A recent study demonstrated that the most potent permeability-enhancing cytokine, vascular endothelial growth factor A (VEGF-A), was elevated in DHF (44). Plasma levels of sVEGFR-2 in DHF patients progressively decreased over the course of disease and were inversely correlated with plasma viral load, providing in vivo correlations for in vitro results. The correlation between plasma viral load and subsequent reduction in sVEGFR2 levels supports this in vitro finding.
This decrease was associated with a concomitant increase in plasma free VEGF. Elevated liver enzymes and thrombocytopenia are commonly seen in both DF and DHF cases, but are more severe in DHF cases.
Leukotrienes are formed through the action of lipoxygenases on arachidonic acid substrates, including LTB4, LTC4, LTD4 and LTE4.67 In addition to being pro-inflammatory mediators and potent chemoattractants, some of them are also known to Increases vascular permeability and leads to leakage. Increased LTB4 activity has been observed in patients with acute dengue virus infection, and exposure of neutrophils to DENV induces LTB4 production. in dengue-infected mice 39 suggesting that leukotrienes may play an important role in dengue fluid loss. A study in 3 animal models (i.e., Gram-negative bacterial pneumonia, intra-abdominal sepsis, and H5N1 influenza virus infection) demonstrated that intravenous injection of the fissure prior to disease induction significantly reduced plasma leakage into the lung and other organ and reduce mortality. Does not affect pathogen-induced cytokine storm in animals. In another animal model of dengue shock syndrome, at day 3 post-infection with FX06, plasma loss through lung and intestinal capillaries was significantly reduced, hemoconcentration and fibrinogen consumption were reduced, and survival was improved, but serum , viral load in the liver and the brain were not affected.