Frequency of glucose-6-phosphate dehydrogenase deficiency in malaria patients from six African countries enrolled in two randomized anti-malarial clinical trialsReport as inadecuate




Frequency of glucose-6-phosphate dehydrogenase deficiency in malaria patients from six African countries enrolled in two randomized anti-malarial clinical trials - Download this document for free, or read online. Document in PDF available to download.

Malaria Journal

, 10:241

First Online: 17 August 2011Received: 19 May 2011Accepted: 17 August 2011

Abstract

BackgroundGlucose-6-phosphate dehydrogenase G6PD deficiency is common in populations living in malaria endemic areas. G6PD genotype and phenotype were determined for malaria patients enrolled in the chlorproguanil-dapsone-artesunate CDA phase III clinical trial programme.

MethodsStudy participants, aged > 1 year, with microscopically confirmed uncomplicated Plasmodium falciparum malaria, and haemoglobin ≥ 70 g-L or haematocrit ≥ 25%, were recruited into two clinical trials conducted in six African countries Burkina Faso, Ghana, Kenya, Nigeria, Tanzania, Mali. G6PD genotype of the three most common African forms, G6PD*B, G6PD*A A376G, and G6PD*A- G202A, A542T, G680T and T968C, were determined and used for frequency estimation. G6PD phenotype was assessed qualitatively using the NADPH fluorescence test. Exploratory analyses investigated the effect of G6PD status on baseline haemoglobin concentration, temperature, asexual parasitaemia and anti-malarial efficacy after treatment with CDA 2-2.5-4 mg-kg or chlorproguanil-dapsone 2-2.5 mg-kg both given once daily for three days or six-dose artemether-lumefantrine.

ResultsOf 2264 malaria patients enrolled, 2045 had G6PD genotype available and comprised the primary analysis population 1018 males, 1027 females. G6PD deficiency prevalence was 9.0% 184-2045; 7.2% N = 147 male hemizygous plus 1.8% N = 37 female homozygous, 13.3% 273-2045 of patients were heterozygous females, 77.7% 1588-2045 were G6PD normal. All deficient G6PD*A- genotypes were A376G-G202A. G6PD phenotype was available for 64.5% 1319-2045 of patients: 10.2% 134-1319 were G6PD deficient, 9.6% 127-1319 intermediate, and 80.2% 1058-1319 normal. Phenotype test specificity in detecting hemizygous males was 70.7% 70-99 and 48.0% 12-25 for homozygous females. Logistic regression found no significant effect of G6PD genotype on adjusted mean baseline haemoglobin p = 0.154, adjusted mean baseline temperature p = 0.9617, or adjusted log mean baseline parasitaemia p = 0.365. There was no effect of G6PD genotype p = 0.490 or phenotype p = 0.391 on the rate of malaria recrudescence, or reinfection p = 0.134 and p = 0.354, respectively.

ConclusionsG6PD deficiency is common in African patients with malaria and until a reliable and simple G6PD test is available, the use of 8-aminoquinolines will remain problematic. G6PD status did not impact baseline haemoglobin, parasitaemia or temperature or the outcomes of anti-malarial therapy.

Trial registrationClinicaltrials.gov: NCT00344006 and NCT00371735.

Electronic supplementary materialThe online version of this article doi:10.1186-1475-2875-10-241 contains supplementary material, which is available to authorized users.

Download fulltext PDF



Author: Nick Carter - Allan Pamba - Stephan Duparc - John N Waitumbi

Source: https://link.springer.com/







Related documents