Abstract

HEMOGLOBIN A1C INDUCED DOWN-REGULATION OF CD36 OF PLASMODIUM FALCIPARUM PARASITIZED RED CELL

Objective: High values of glycosylated hemoglobin have been found to correlate with decreased deformability of erythrocyte. CD36 (Cluster of Differentiation 36) is an integral membrane protein found on the surface of many cell types of class B scavenger receptor family. Plasmodium falciparum and diabetes mellitus is associated many complications. Aim of this study to investigate the down-regulation of HbA1c to CD36 on P. falciparum parasitized red blood cells Diabetes mellitus patients. Methods: This is cross section study conducted among diabetic patients attending in Jabir Abo Eleiz diabetic center in Khartoum state. Venous blood samples were collected in heparin containers for Plasmodium falciparum culture, and random blood sugar. For HbA1c in 0.04 mg EDTA anticoagulant, 2-5 ml of blood was collected. Sample size was 45 samples and was collected from known diabetic patients with HbA1c more than 8%. All data were analyzed by using Statistical Package for Social Science (SPSS). Results: show the mean difference between CD36 negative control and CD36 positive control was found to be statistically significant increasing of CD36 presence at P. value =0.001 (P ≤0.001). The mean difference between CD36 positive control and diabetic patients with HbA1C more 8% was found to be statistically significant reduction of CD36 expression at p=0.001. Conclusion: Hyperglycemia (HbA1c) leads to decrease of CD36 expression and interfere with innate and active immunity. In this study HbA1c participates in increasing of P. falciparum malaria complications.

• PDF