English

Abstract

Malaria continues to be one of the major public health problem of India. Almost all deaths are caused by Plasmodium falciparum infected malaria. 1 Under normal physiological conditions, liver ensures homeostasis of lipid and lipoprotein metabolism. 2 Hepatocellular damage often associated with severe and acute P falciparum infections impairs these processes, leading to alteration in plasma lipid profile and lipoprotein patterns. An observation on the nature of dyslipidaemia in malaria patients with reference to correlation if any that exists between malaria and lipid profile in these patients was performed. Results revealed that the total cholesterol, HDL and LDL decreased while triglyceride and VLDL were found to increase in malaria patients. It can be concluded that alteration in lipid profile can be an index of malaria infection but specificity of malaria infection with lipid changes is questionable and need further studies. INTRODUCTION: Malaria is a protozoan disease transmitted by the bite of infected Anopheles mosquitoes. The most important of the parasitic diseases of humans, it is transmitted in 108 countries containing 3 billion people and causes nearly 1 million deaths each year. Almost all deaths are caused by falciparum malaria.3 India is a vast country with multiethnic society of 1.2 billion living in diverse geo-ecological paradigms and ecotype of malaria. Malaria continues to be one of the major public health problem of India with around 1.5-2 million confirmed cases/year, of which approximately 1000 reported malarial death per year. 4 As per World Health Organization report 2011-2012, South-east Asia region bear the second largest burden of malaria (13%), only being next to African region (81%). Among South-east Asia region, India shares two thirds of the burden (66%) followed by Myanmar (18%) and Indonesia (10%).5 Contrary to the African scenario, where much of the malaria mortality burden is borne by the infants and children, in India, it is the middle productive ages in both genders that suffer the most. 6 Under normal physiological conditions, liver ensures homeostasis of lipid and lipoprotein metabolism. 7 Hepatocellular damage often associated with severe and acute P falciparum infections impairs these processes, leading to alteration in plasma lipid and lipoprotein patterns.¶⁻· Parasites forage nutrients from their host as well as possess limited enzyme pathway for de novo synthesis of certain nutrients. So far, studies suggest that there may be some factors or enzymes, which allow the parasite to breakup and consume lipid/cholesterol from their host and utilize them for internalization of eukaryotic protozoa or for reproduction in case of helminthes.¸ Plasmodium is incapable of de novo synthesis of fatty acids and cholesterol; but it can fabricate its glycerides and phosphoglycerides with host-supplied nutrients, and can produce the glyceryl moiety during glycolysis.¹