| ORIGINAL ARTICLE |
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| Year : 2013 | Volume
: 5
| Issue : 12 | Page : 703-706 |
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Oxidative low density lipoprotien prohibited plasmodium falciparum clearance in type 2 diabetes mellitus via cluster differentiation 36
Hassan Hijazi1, Hisham Waggiallah2, Atif Alagib3
1 AL-Ghad International Colleges for Applied Health Science, Qassim, Saudi Arabia
2 Department of Medical Laboratory, Faculty of Medical Applied Science, Taibah University, Almadenah Almonawarah, Saudi Arabia
3 Tropical Medicine Research Institute, National Centre for Research, Ministry of Science and Technology, Sudan
Correspondence Address:
Hisham Waggiallah
Department of medical laboratory, Faculty of medical applied science, Taibah University. P.O Box 3001, Almadenah Almonawarah
Saudi Arabia
 Source of Support: no confl icts of interest,
including specifi c fi nancial interests, relationships, and/ or affi liations
relevant to the subject matter or materials included., Conflict of Interest: None  | Check |
DOI: 10.4103/1947-2714.123255
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Background: Cluster of differentiation 36 (CD36) is reported to function as a receptor of erythrocytes infected with Plasmodium falciparum (PF) and as an oxidized low-density lipoprotein (oxLDL). Aim: The aim of this study was to investigate the impact of CD36 in PF parasitized red blood cells in high concentration of oxLDL of T2 diabetes mellitus patients. Material and Methods: This cross-sectional study was conducted among diabetic patients. A total of 45 samples were collected from diabetic patients with more than 8% of HbA1c and more than 170 mg/dL of oxLDL. Results: The mean difference between CD36 negative and positive controls was found to be statistically significant (P ≤ 0.001). The mean difference between CD36 positive control and CD36 in diabetic patients with oxLDL ≥ 170 mg/dL also was statistically significant. Conclusion: High concentration of oxidative low density of lipoprotein more than 170 mg/dL leads to block CD36 receptor on infected red blood. This process believed to contribute in parasite survival by avoiding phagocytic clearance in the spleen. |
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