Variants of resistin gene and the risk of idiopathic dilated cardiomyopathy in Pakistan.
BACKGROUND
In cardiovascular disease phenotypes, a genetic factor is an important determinant of both familial and non-familial dilated cardiomyopathies. Resistin is a novel adipocyte derived peptide, associated with inflammation and suggested to be involved in contractile abnormalities of cardiomyocytes.


METHODS
In this study, we examined the association of the RETN SNPs in - 420 and + 299 in patients with idiopathic dilated cardiomyopathy (IDCM). Patients with IDCM (n = 250) and healthy controls (n = 250) were enrolled in this study. RETN genotyping was performed by using PCR-RFLP method.


RESULTS
RETN - 420C > G and + 299G > A polymorphisms were significantly more prevalent in patient group vs. controls (P < 0.0001 and P = 0.0007, respectively). GG genotype at - 420 and AA genotype at + 299 were higher in the patient group compared with healthy controls (OR = 11.4, P < 0.0001, and OR = 2.3, P = 0.030, respectively). We found that the - 420G allele increased the risk of developing IDCM in patients (P < 0.0001). Moreover, there was a significant difference between G and A alleles at RETN + 299 from IDCM cases and controls (P = 0.0032). The RETN - 420G and + 299A haplotypes were more prevalent in the patient vs. control group (P < 0.0001).


CONCLUSIONS
The results suggest that the RETN - 420C > G and + 299G > A polymorphisms may have a role in the pathogenesis of IDCM.
Department of Biosciences, COMSATS Institute of Information Technology, Islamabad 45550, Pakistan.
Sabir
S
Hussain
Department of Biochemistry, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad 45320, Pakistan.
Javeria
J
Haroon
Department of Cardiology, Federal Government Polyclinic Hospital, G-5, Islamabad, Pakistan.
Shagufta
S
Ejaz
Department of Biochemistry, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad 45320, Pakistan.
Qamar
Q
Javed
Association; Idiopathic dilated cardiomyopathy; Pakistan; RETN gene; Single nucleotide polymorphism