Association of lipid profile alterations with severe forms of dengue in humans

Abstract

Previous studies have shown a relationship between circulating lipids and dengue virus infection; however, the association of altered lipid profiles with severe dengue remains little studied. The aim of this study was to determine the association between circulating lipid content and severe dengue and/or platelet counts. Ninety-eight patients (2-66 years old) classified as having dengue without warning signs (DNWS), dengue with warning signs (DWWS), or severe dengue (SD) and 62 healthy individuals were studied. Blood samples were tested for NS1, anti-dengue IgM, platelet content, total cholesterol (TC), triglycerides (T), high-density lipoproteins (HDL), low-density lipoproteins (LDL) and very-low-density lipoproteins (VLDL). Lipid alterations were observed mainly in patients with SD. Increased T and VLDL was observed in SD, and increased HDL was observed in DWWS and SD. Decreased TC was found in all forms of dengue, and the lowest LDL values were found in SD. Platelet counts were significantly decreased in DWWS and SD when compare to DNWS. A positive correlation (p = 0.019) between LDL values and platelet counts and a negative correlation (p = 0.0162) between VLDL values and platelet counts were found. Lipid profile alterations were associated with severe dengue.

High Triglycerides Are Associated with Low Thrombocyte Counts and High VEGF in Nephropathia Epidemica

“…Thrombocyte counts below 50,000 cells/ μ L are considered to be a risk factor for bleeding [25–27]. Recently, a correlation was demonstrated between thrombocyte counts and low density lipids in patients with the severe form of dengue infection [28], suggesting a role for lipid metabolism in the pathogenesis of thrombocytopenia. Therefore, we sought to determine whether low thrombocyte counts were associated with changes in lipid and cytokine profiles of NE cases.…”

The correlation of TNF alpha levels with the lipid profile of dengue patients

“…In the same line of evidence, Survana and Rane confirmed later that low levels of cholesterol, HDL, and LDL are associated with severe forms of dengue infection, supporting the hypothesis of van Gorp et al They also observed that VLDL values were different between DF, DHF, and Dengue shock syndrome (DSS) patients, but triglycerides, HDL, and LDL showed no differences (both studies were performed on a pediatric population and they used 1997 WHO dengue guideline for the patient classification in their studies). In contrast Duran's study, which included both adult and pediatric patients (based on 2009 WHO classification for dengue disease), observed a significant decrease in total cholesterol, HDL, and LDL levels, as well as an increase in triglyceride, and VLDL levels, in patients with severe forms of dengue infection.…”

“…The last two decades have seen an increasing interest in the study of the possible relationships between the development of severe dengue and changes in circulating lipids . Lipid metabolism is extensively regulated by cytokines during the host response to infection .…”

“…Lipids play an important role in bacterial, parasitic, and viral infections . Changes in the serum lipid profile have been observed during dengue virus (DENV) infections . Furthermore, it has been reported that the lipid profile status may contribute to the pathogenesis of different manifestations of DENV infections in humans .…”

OSBPL10, RXRA and lipid metabolism confer African-ancestry protection against dengue haemorrhagic fever in admixed Cubans

“…A direct link between dengue infection progression and lipid profile changes has been made, so that lipids may be used as predictors of clinical outcome [29]: increased T and HDL and decreased LDL were observed in severe dengue. Recent metabolic and lipid profiling in serum samples from dengue cohorts [30, 31] have reinforced these earlier findings, showing that DENV infection causes temporary changes in metabolites involved in acute inflammatory responses, with major perturbed metabolic pathways including fatty acid biosynthesis, fatty acid beta-oxidation, phospholipid catabolism and steroid hormone pathway, and that progression into DSS is associated with certain metabolites (phosphatidylcholines, diacylglycerol, phosphatidic acid, phosphatidylserine, triglycerides, and diacylglycerophosphoglycerol) that may act in endothelial cell homeostasis and vascular barrier function.…”