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dc.contributor.authorYeo TWen
dc.contributor.authorLampah DAen
dc.contributor.authorTjitra Een
dc.contributor.authorGitawati Ren
dc.contributor.authorKenangalem Een
dc.contributor.authorPiera Ken
dc.contributor.authorGranger DLen
dc.contributor.authorLopansri BKen
dc.contributor.authorWeinberg JBen
dc.contributor.authorPrice RNen
dc.contributor.authorDuffull SBen
dc.contributor.authorCelermajer DSen
dc.contributor.authorAnstey NMen
dc.identifier.citationThe Journal of infectious diseases 2009-11-15; 200(10): 1522-9en
dc.description.abstractHemolysis causes anemia in falciparum malaria, but its contribution to microvascular pathology in severe malaria (SM) is not well characterized. In other hemolytic diseases, release of cell-free hemoglobin causes nitric oxide (NO) quenching, endothelial activation, and vascular complications. We examined the relationship of plasma hemoglobin and myoglobin to endothelial dysfunction and disease severity in malaria. Cell-free hemoglobin (a potent NO quencher), reactive hyperemia peripheral arterial tonometry (RH-PAT) (a measure of endothelial NO bioavailability), and measures of perfusion and endothelial activation were quantified in adults with moderately severe (n = 78) or severe (n = 49) malaria and control subjects (n = 16) from Papua, Indonesia. Cell-free hemoglobin concentrations in patients with SM (median, 5.4 micromol/L; interquartile range [IQR], 3.2-7.4 micromol/L) were significantly higher than in those with moderately severe malaria (2.6 micromol/L; IQR, 1.3-4.5 micromol/L) or controls (1.2 micromol/L; IQR, 0.9-2.4 micromol/L; P < .001). Multivariable regression analysis revealed that cell-free hemoglobin remained inversely associated with RH-PAT, and in patients with SM, there was a significant longitudinal association between improvement in RH-PAT index and decreasing levels of cell-free hemoglobin (P = .047). Cell-free hemoglobin levels were also independently associated with lactate, endothelial activation, and proinflammatory cytokinemia. Hemolysis in falciparum malaria results in NO quenching by cell-free hemoglobin, and may exacerbate endothelial dysfunction, adhesion receptor expression and impaired tissue perfusion. Treatments that increase NO bioavailability may have potential as adjunctive therapies in SM.en
dc.titleRelationship of cell-free hemoglobin to impaired endothelial nitric oxide bioavailability and perfusion in severe falciparum malaria.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Journal of infectious diseasesen
dc.subject.meshAnemia, Hemolyticen
dc.subject.meshEndothelium, Vascularen
dc.subject.meshMalaria, Falciparumen
dc.subject.meshMalaria, Vivaxen
dc.subject.meshMiddle Ageden
dc.subject.meshNitric Oxideen
dc.subject.meshSeverity of Illness Indexen
dc.subject.meshYoung Adulten
dc.identifier.affiliationInternational Health Division, Menzies School of Health Research and Charles Darwin University, Royal Darwin Hospital, Darwin, NT 0811, Australia..en
Appears in Collections:(a) NT Health Research Collection

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