Please use this identifier to cite or link to this item: https://hdl.handle.net/10137/5729
Email LibraryRMU.DOH@nt.gov.au to ask for this document in a different format
Title: Relationship of cell-free hemoglobin to impaired endothelial nitric oxide bioavailability and perfusion in severe falciparum malaria.
Authors: Yeo, Tsin W
Lampah, Daniel A
Tjitra, Emiliana
Gitawati, Retno
Kenangalem, Enny
Piera, Kim
Granger, Donald L
Lopansri, Bert K
Weinberg, J Brice
Price, Ric N
Duffull, Stephen B
Celermajer, David S
Anstey, Nicholas M
Citation: The Journal of infectious diseases 2009-11-15; 200(10): 1522-9
Abstract: Hemolysis 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.
Click to open PubMed article: https://www.ezpdhcs.nt.gov.au/login?url=https://www.ncbi.nlm.nih.gov/pubmed/19803726
Click to open Pubmed Article: https://www.ezpdhcs.nt.gov.au/login?url=https://www.ncbi.nlm.nih.gov/pubmed/19803726
Journal title: The Journal of infectious diseases
Publication Date: 2009-11-15
Type: Journal Article
URI: https://hdl.handle.net/10137/5729
DOI: 10.1086/644641
Appears in Collections:(a) NT Health Research Collection

Files in This Item:
There are no files associated with this item.


Items in ePublications are protected by copyright, with all rights reserved, unless otherwise indicated.