<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yacoub S</submitter><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><funding>Wellcome Trust</funding><pagination>1453-1461</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5850435</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>65(9)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Dengue can cause increased vascular permeability that may lead to hypovolemic shock. Endothelial dysfunction may underlie this; however, the association of endothelial nitric oxide (NO) pathways with disease severity is unknown.&lt;h4>Methods&lt;/h4>We performed a prospective observational study in 2 Vietnamese hospitals, assessing patients presenting early (&lt;72 hours of fever) and patients hospitalized with warning signs or severe dengue. The reactive hyperemic index (RHI), which measures endothelium-dependent vasodilation and is a surrogate marker of endothelial function and NO bioavailability, was evaluated using peripheral artery tonometry (EndoPAT), and plasma levels of l-arginine, arginase-1, and asymmetric dimethylarginine were measured at serial time-points. The main o</pubmed_abstract><journal>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</journal><pubmed_title>Endothelial Nitric Oxide Pathways in the Pathophysiology of Dengue: A Prospective Observational Study.</pubmed_title><pmcid>PMC5850435</pmcid><funding_grant_id>G0801508</funding_grant_id><funding_grant_id>100562/Z/12/Z</funding_grant_id><funding_grant_id>G0600000</funding_grant_id><funding_grant_id>NF-SI-0507-10303</funding_grant_id><pubmed_authors>Yeo TW</pubmed_authors><pubmed_authors>Screaton G</pubmed_authors><pubmed_authors>Simmons C</pubmed_authors><pubmed_authors>Le DHT</pubmed_authors><pubmed_authors>Nguyen Ho HH</pubmed_authors><pubmed_authors>Van NT</pubmed_authors><pubmed_authors>Lien LT</pubmed_authors><pubmed_authors>Wills B</pubmed_authors><pubmed_authors>Yacoub S</pubmed_authors><pubmed_authors>Dong Thi HT</pubmed_authors><pubmed_authors>Ha QNT</pubmed_authors><pubmed_authors>Lam PK</pubmed_authors><pubmed_authors>Culshaw A</pubmed_authors><pubmed_authors>Huynh TT</pubmed_authors><pubmed_authors>Mongkolspaya J</pubmed_authors><pubmed_authors>Wertheim H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Endothelial Nitric Oxide Pathways in the Pathophysiology of Dengue: A Prospective Observational Study.</name><description>&lt;h4>Background&lt;/h4>Dengue can cause increased vascular permeability that may lead to hypovolemic shock. Endothelial dysfunction may underlie this; however, the association of endothelial nitric oxide (NO) pathways with disease severity is unknown.&lt;h4>Methods&lt;/h4>We performed a prospective observational study in 2 Vietnamese hospitals, assessing patients presenting early (&lt;72 hours of fever) and patients hospitalized with warning signs or severe dengue. The reactive hyperemic index (RHI), which measures endothelium-dependent vasodilation and is a surrogate marker of endothelial function and NO bioavailability, was evaluated using peripheral artery tonometry (EndoPAT), and plasma levels of l-arginine, arginase-1, and asymmetric dimethylarginine were measured at serial time-points. The main o</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Oct</publication><modification>2025-04-18T20:16:37.485Z</modification><creation>2019-03-26T23:22:56Z</creation></dates><accession>S-EPMC5850435</accession><cross_references><pubmed>28673038</pubmed><doi>10.1093/cid/cix567</doi></cross_references></HashMap>