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dc.contributor.authorCaterina I. Fanelloen_US
dc.contributor.authorCorine Karemaen_US
dc.contributor.authorPamela Avellinoen_US
dc.contributor.authorGermana Banconeen_US
dc.contributor.authorAline Uwimanaen_US
dc.contributor.authorSue J. Leeen_US
dc.contributor.authorUmberto d'Alessandroen_US
dc.contributor.authorDavid Modianoen_US
dc.contributor.otherNuffield Department of Clinical Medicineen_US
dc.contributor.otherNational Malaria Control Programmeen_US
dc.contributor.otherUniversita degli Studi di Roma La Sapienzaen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherPrins Leopold Instituut voor Tropische Geneeskundeen_US
dc.date.accessioned2018-07-12T02:13:24Z-
dc.date.available2018-07-12T02:13:24Z-
dc.date.issued2008-12-29en_US
dc.identifier.citationPLoS ONE. Vol.3, No.12 (2008)en_US
dc.identifier.issn19326203en_US
dc.identifier.other2-s2.0-58149187879en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=58149187879&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/18655-
dc.description.abstractBackground: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common inherited human enzyme defect. This deficiency provides some protection from clinical malaria, but it can also cause haemolysis after administration of drugs with oxidant properties. Methods: The safety of chlorproguanil-dapsone+artesunate (CD+A) and amodiaquine+sulphadoxine-pyrimethamine (AQ+SP) for the treatment of uncomplicated P. falciparum malaria was evaluated according to G6PD deficiency in a secondary analysis of an open-label, randomized clinical trial [1]. 702 children, treated with CD+A or AQ+SP and followed for 28 days after treatment were genotyped for G6PD A- deficiency. Findings: In the first 4 days following CD+A treatment, mean haematocrit declined on average 1.94% (95% CI 1.54 to 2.33) and 1.05% per day (95% CI 0.95 to 1.15) respectively in patients with G6PD deficiency and normal patients; a mean reduction of 1.3% per day was observed among patients who received AQ+SP regardless of G6PD status (95% CI 1.25 to 1.45). Patients with G6PD deficiency recipients of CD+A had significantly lower haematocrit than the other groups until day 7 (p = 0.04). In total, 10 patients had severe post-treatment haemolysis requiring blood transfusion. Patients with G6PD deficiency showed a higher risk of severe anaemia following treatment with CD+A (RR = 10.2; 95% CI 1.8 to 59.3) or AQ+SP (RR = 5.6; 95% CI 1.0 to 32.7). Conclusions: CD+A showed a poor safety profile in individuals with G6PD deficiency most likely as a result of dapsone induced haemolysis. Screening for G6PD deficiency before drug administration of potentially pro-oxidants drugs, like dapsone-containing combinations, although seldom available, is necessary. © 2008 Fanello et al.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=58149187879&origin=inwarden_US
dc.subjectAgricultural and Biological Sciencesen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleHigh risk of severe anaemia after chlorproguanil-dapsone+artesunate antimalarial treatment in patients with G6PD (A-) deficiencyen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1371/journal.pone.0004031en_US
Appears in Collections:Scopus 2006-2010

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