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Open Access 01-12-2015 | Research
Glucose-6-phosphate dehydrogenase deficiency among malaria patients of Honduras: a descriptive study of archival blood samples
Published in: Malaria Journal | Issue 1/2015
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Background
The frequency of deficient variants of glucose-6-phosphate dehydrogenase (G6PDd) is particularly high in areas where malaria is endemic. The administration of antirelapse drugs, such as primaquine, has the potential to trigger an oxidative event in G6PD-deficient individuals. According to Honduras´ national scheme, malaria treatment requires the administration of chloroquine and primaquine for both Plasmodium vivax and Plasmodium falciparum infections. The present study aimed at investigating for the first time in Honduras the frequency of the two most common G6PDd variants.
Methods
This was a descriptive study utilizing 398 archival DNA samples of patients that had been diagnosed with malaria due to P. vivax, P. falciparum, or both. The most common allelic variants of G6PD: G6PD A+376G and G6PD A−376G/202A were assessed by two molecular methods (PCR–RFLP and a commercial kit).
Results
The overall frequency of G6PD deficient genotypes was 16.08%. The frequency of the “African” genotype A− (Class III) was 11.9% (4.1% A− hemizygous males; 1.5% homozygous A− females; and 6.3% heterozygous A− females). A high frequency of G6PDd alleles was observed in samples from malaria patients residing in endemic regions of Northern Honduras. One case of Santamaria mutation (376G/542T) was detected.
Conclusions
Compared to other studies in the Americas, as well as to data from predictive models, the present study identified a higher-than expected frequency of genotype A− in Honduras. Considering that the national standard of malaria treatment in the country includes primaquine, further research is necessary to ascertain the risk of PQ-triggered haemolytic reactions in sectors of the population more likely to carry G6PD mutations. Additionally, consideration should be given to utilizing point of care technologies to detect this genetic disorder prior administration of 8-aminoquinoline drugs, either primaquine or any new drug available in the near future.