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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/45940
Title: Intravascular haemolysis in severe Plasmodium knowlesi malaria: Association with endothelial activation, microvascular dysfunction, and acute kidney injury article
Authors: Bridget E. Barber
Matthew J. Grigg
Kim A. Piera
Timothy William
Daniel J. Cooper
Katherine Plewes
Arjen M. Dondorp
Tsin W. Yeo
Nicholas M. Anstey
Menzies School of Health Research
Mahidol University
The University of British Columbia
Nuffield Department of Clinical Medicine
Nanyang Technological University
Tan Tock Seng Hospital
Jesselton Medical Centre
Infectious Diseases Society Sabah
Queen Elizabeth Hospital
Keywords: Immunology and Microbiology;Medicine;Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Dec-2018
Citation: Emerging Microbes and Infections. Vol.7, No.1 (2018)
Abstract: © 2018 The Author(s). Plasmodium knowlesi occurs throughout Southeast Asia, and is the most common cause of human malaria in Malaysia. Severe disease in humans is characterised by high parasite biomass, reduced red blood cell deformability, endothelial activation and microvascular dysfunction. However, the roles of intravascular haemolysis and nitric oxide (NO)-dependent endothelial dysfunction, important features of severe falciparum malaria, have not been evaluated, nor their role in acute kidney injury (AKI). In hospitalised Malaysian adults with severe (n = 48) and non-severe (n = 154) knowlesi malaria, and in healthy controls (n = 50), we measured cell-free haemoglobin (CFHb) and assessed associations with the endothelial Weibel-Palade body (WPB) constituents, angiopoietin-2 and osteoprotegerin, endothelial and microvascular function, and other markers of disease severity. CFHb was increased in knowlesi malaria in proportion to disease severity, and to a greater extent than previously reported in severe falciparum malaria patients from the same study cohort. In knowlesi malaria, CFHb was associated with parasitaemia, and independently associated with angiopoietin-2 and osteoprotegerin. As with angiopoietin-2, osteoprotegerin was increased in proportion to disease severity, and independently associated with severity markers including creatinine, lactate, interleukin-6, endothelial cell adhesion molecules ICAM-1 and E-selectin, and impaired microvascular reactivity. Osteoprotegerin was also independently associated with NO-dependent endothelial dysfunction. AKI was found in 88% of those with severe knowlesi malaria. Angiopoietin-2 and osteoprotegerin were both independent risk factors for acute kidney injury. Our findings suggest that haemolysis-mediated endothelial activation and release of WPB constituents is likely a key contributor to end-organ dysfunction, including AKI, in severe knowlesi malaria.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85045897734&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/45940
ISSN: 22221751
Appears in Collections:Scopus 2018

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