Influence of sickle heterozygous status and glucose-6-phosphate dehydrogenase deficiency on the clinico-haematolgoical profile of Plasmodium falciparum-infected children

Abstract

Sickle haemoglobin (HbS) and glucose–6–phosphate dehydrogenase (G6PD) enzyme deficiency genes are known to offer reliable protection against falciparum malaria in malaria endemic areas of the world. However, the mechanism of protection is not yet completely understood. In this study, we investigated the contribution of HbS and G6PD enzyme deficiency status in ameliorating the severity of malaria attack by comparing the clinical symptoms, parasitaemia and
haematological profiles of Plasmodium falciparum–infected volunteer children. The selected group of children, G6PD deficient sickle heterozygotes (HbAS) (n = 5), G6PD non–deficient HbAS (n = 30), G6PD deficient dominant homozygotes (HbAA) (n = 10) and G6PD non–deficient HbAA (n = 30) were monitored for a period of one year with a view to elucidating further the involvement of HbS and G6PD enzyme deficiency in the protection of children against plasmodial infection. Results revealed greater severity (indicated by malarial anaemia), higher incidence of atypical thrombocytopenia, high white blood cell (WBC) counts and significantly higher (P < 0.05) parasite density and percentage parasitaemia in G6PD non–deficient HbAA subjects compared to G6PD non–deficient HbAS, G6PD deficient HbAS subject and G6PD deficient HbAA. Less severe clinical malarial symptoms were also observed more in G6PD deficient HbAS when compared to G6PD non-deficient HbAA subjects during malaria
attack. These results seem to indicate that inheriting both genetic defects reduces the profligacy of malaria parasite and hence, ameliorate the severity of acute falciparum malaria. Consequently, selective advantage against fatal falciparum malaria seems to be conferred since malarial anaemia, parasitaemia and severe malarial symptoms were significantly reduced.