Co-Morbidly of Malaria and Typhoid Perturbs Lipid Homeostasis in Humans

Introduction: Malaria and typhoid diseases have remained endemic in low-income countries, including Nigeria. Aims: This study investigated the impact of malaria concurrently occurring with typhoid on plasma, erythrocytes, and lipoproteins lipid profile. Materials and Methods: Cholesterol, triacylglycerol (TAG) phospholipids (PLs), and non-esterified fatty acids (NEFAs) were determined spectrophotometrically in controls and patients presenting at the Out-Patient Clinic of the State Hospital, Abeokuta, Nigeria. Results: The presence of either or both parasitic infections provoked dyslipidaemia when compared with the controls. Dyslipidaemia was characterised by significant (P < 0.05) decreased plasma, erythrocytes, high density lipoprotein (HDL), and low density lipoprotein (LDL) cholesterol; however very LDL (VLDL) cholesterol increased. While hypertriglyceridemia was observed in plasma, hypotriglyceridemia was observed in the erythrocytes of the patients. In HDL, hypertriglyceridemia was observed in malaria-infected patients whereas hypotriglyceridemia was observed in typhoid-infected and co-infection subjects. Malaria and/or typhoid induced phospholipidaemia in plasma and erythrocytes, but provoked decreased HDL-phospholipids (PLs) only in malaria-infected patients. Malaria and/or typhoid elicited decreased LDL+VLDL-PLs. While increased plasma NEFAs concentration was observed in malaria-infected patients; malaria and co-infection resulted in decreased erythrocytes NEFAs. Malaria and/or typhoid caused decreased cholesterol/phospholipids molar ratio in plasma, erythrocytes, and HDL. Conclusion: The findings of this study indicate that parasitic protozoa and bacterial infections produce a plethora of effects on lipid metabolism, ranging from up-/down-regulation of certain lipid metabolites. These may be early biochemical events in the induction of atherosclerosis by parasitic infections.