Research Article, Int J Cardiovasc Res Vol: 7 Issue: 4
Macrophage Migration Inhibitory Factor Gene Polymorphisms (MIF-173CC) Genotyping in Patients with Cardiac Dysfunction: Relationship to Diabetes Mellitus
Abdelsabour M1*, Idriss NK2, Mohamed NA2, Osama AM2 Gaber MA2, Alfarash A3, Saad K4, Elgamal DA5
1Department of Cardiology, Assiut University, Assiut, Egypt
2Department of Medical Biochemistry, Faculty of Medicine, Assiut University, Assiut, Egypt
3Faculty of Agriculture, Assiut University, Assiut, Egypt
4Department of Pediatrics, Faculty of Medicine, Assiut University, Assiut, Egypt
5Department of Histology and Cell Biology, Faculty of Medicine, Assiut University, Assiut, Egypt
*Corresponding Author : Naglaa Kamal Idriss
Assoicate professor of Medical Biochemistry, Faculty of Medicine, Assiut University, Egypt
E-mail: [email protected]
Received: May 01, 2018 Accepted: June 18, 2018 Published: June 26, 2018
Citation: Abdelsabour M, Idriss NK, Mohamed NA, Osama AM, Gaber MA, et al. (2018) Macrophage Migration Inhibitory Factor Gene Polymorphisms (MIF- 173CC) Genotyping in Patients with Cardiac Dysfunction: Relationship to Diabetes Mellitus. Int J Cardiovasc Res 7:4. doi: 10.4172/2324-8602.1000356
Introduction: Macrophage migration inhibitory factor (MIF) is an important mediator in inflammation and pathogenesis of cardiomyopathy (CMP). We aim to explore any possible association between polymorphisms of MIF genes and CMP in a cohort of Egyptian patients with cardiac dysfunction with or without diabetes mellitus and to investigate the alliance between the identified genotype and their medical features.
Patients and methods: This is a case-control study where 57 patients with CMP were consecutively admitted to CCU compared with 98 matched healthy controls. Patients were subjected to careful clinical history and physical examination, ECG, routine investigations, and echocardiography. All participants were analyzed for codon -173 G/C polymorphism in MIF genes by using PCR-RFLP methods.
Results: We found higher Frequency of MIF-173 GG genotype in both diabetic and nondiabetic CMP patients compared to controls (p<0.05). However, we did not find any significant difference in the MIF genotyping between the CMP with or without DM.
Conclusion: Our results advocate that MIF may have implications for our understanding of the pathophysiology and perturbation in CMP process. We suggested that GG genotype of MIF (-173) gene may be a risk factor for patients with CMP.