Study of metabolic changes-glycoprotein and phospholipids levels in patients of malaria

Rupal A. Tyagi, Amit G. Tyagi, Prema Ram Choudhary, Jaidev Singh Shekhawat


Background: In erythrocytic stage, malarial parasites meet their high glucose requirement only by modulating the host cell membrane by increasing transport of sugar across the host cell membrane. This leads to a transmembrane gradient of the substrate and finally leading to alterations of metabolic changes and permeability of RBC membrane. Therefore, the aim of present study was to determine the parameters which reflect the status of RBC membrane and their association with the severity of malaria in a large cohort of known patients of malaria, which was caused by the Plasmodium Species.

Methods: Blood sample were collected in EDTA bulb at the time of admission (day-1) and on third day (day-3). The samples were analyzed within 24 hours of collection. Erythrocytic total phospholipid is measured by modified connerty method, Total sialic acid (TSA) is measured by TBA/dimethyl sulphoxide method.

Results: The mean levels of erythrocytic phospholipid, plasma TSA and PBSA in the cases of malaria were significantly increase (P<0.001) as compared to those in the control group. In the follow up study the same parameters were studied in patients post anti-malarial treatment day-3. The level of erythrocyte phospholipid, plasma TSA and PBSA were reversed.

Conclusions: On the basis of the present study it is suggested that the anti-malarial drug regimen must be supported by antioxidants and trace elements supplementation to improve the status of deviated biochemical parameters towards normalcy.


Erythrocyte, Protein bound sialic acid, Phospholipids, Total sialic acid

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Epidemiology of Communicable Diseases. In: Park K. Park’s text book of Preventive and Social Medicine, 20th edition. Jabalpur (India): Banarsidas Bhanot; 2009:222-232.

Ramasamy R. Studies on glycoproteins in the human malaria parasite Plasmodium falciparum- lectin binding properties and the possible carbohydrate-protein linkage. Immunol Cell Biol.1987;65(2)147-52.

Mehlhorn H. Parasitology in Focus. Berlin Heidelberg Mehihorn, Edition 10th. Springer. 2002;1:18-45.

Vial HJ, Ancelin ML, Philippot JR, Thuet MJ. Biosynthesis and dynamics of lipid in Plasmodium-infected mature mammalian erythrocytes. Blood Cells. 1990;16(2-3):531-61.

Witola WH, Ben Mamoun C. Choline induces transcriptional repression and proteasomal degradation of the malarial phosphoethanolamine methyltransferase. Eukaryot Cell. 2007;6(9):1618-24.

Bhagvan NV. Medical Biochemistry; 4th edition: Elsevier publication: 2002:153-161.

Choudhary PR, Jani RD. Study of pulmonary function in patients with Metabolic syndrome. Physio Pharmacol. 2016;20:90-7.

Folch J, Lees M, Stanley GHS. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem. 1957;226:497-509.

Practical Clinical Biochemistry. In: Varley H. Vol. 1, 5th Ed., William Heinemann Medical Books Ltd, London: 1980;669-670.

Skoza L, Mohos S. Stable thiobarbitutic acid chromophore with dimethyl sulphoxide. Biochem J. 1976;159:457-62.

Leslie Collier, Albert Balows, Max Sussman. Microbiology and Microbial infections. Topley and Wilson’s; 9th edition; vol.5, Chapter-20; 1998:361-405.

Sumitha K, Ravichandiran K, Selvam R. Blood lipid changes in repeated infections of vivax malaria. Indian J Malariol. 1996;33(3):131-8.