Comparative Biochemical Response to Malaria Infection in Children with and Without Sickle Cell Trait in Ondo State

Sickle cell trait (HbAS genotype) confers partial protection against severe malaria, but the biochemical dimensions of this protective mechanism in Nigerian children during natural malaria infection episodes have been inadequately characterized analytically. This study comparatively investigates the biochemical response to malaria infection in children with sickle cell trait (HbAS) and those with normal haemoglobin (HbAA) in Ondo State. A case-control design enrolled eighty malaria-positive children aged two to ten years: forty with confirmed HbAS genotype and forty with HbAA genotype matched for age, sex, malaria parasitaemia density, and clinical severity score. Samples were collected at the febrile acute phase and fourteen days post-treatment. Biochemical parameters included haemoglobin, reticulocyte count, lactate dehydrogenase, serum haptoglobin, indirect bilirubin, MDA, ferritin, pro-inflammatory cytokines (TNF-alpha, IL-6, IL-10), and plasma lactate as a marker of metabolic acidosis risk. HbAS children showed significantly higher haemoglobin and haematocrit during infection and significantly lower reticulocyte responses, indicating less haemolytic destruction. LDH and indirect bilirubin were significantly lower in HbAS children, confirming reduced intravascular haemolysis. MDA was significantly lower in HbAS children, suggesting reduced parasite-driven oxidative injury. IL-10, an anti-inflammatory cytokine, was significantly higher in HbAS children, while TNF-alpha was lower, indicating a more regulated inflammatory response. Plasma lactate was significantly lower in HbAS children. These biochemical differences provide mechanistic insights into the HbAS protection mechanism during natural Plasmodium falciparum infection. Keywords: sickle cell trait, malaria, biochemical response, haemolysis, Ondo State.