پديد آورندگان :
Salimi، Saeedeh نويسنده Department of Clinical Biochemistry, Cellular and Molecular Research Center, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Salimi, Saeedeh , Naghavi، Anoosh نويسنده Department of Clinical Biochemistry, Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan, Iran Naghavi, Anoosh , Zakeri، Zahra نويسنده Department of Internal Medicine, Clinical Research Development Center, Faculty of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran Zakeri, Zahra , Nabizadeh، Sima نويسنده Department of English, Faculty of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran Nabizadeh, Sima , Farajian-Mashhadi، Farzaneh نويسنده Department of Pharmacology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran Farajian-Mashhadi, Farzaneh , Sandoughi، Mahnaz نويسنده Department of Internal Medicine, Clinical Research Development Center, Faculty of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran Sandoughi, Mahnaz
كليدواژه :
Polymorphism , systemic lupus erythematosus , Lupus nephropathy , IRAN , angiotensin-converting enzyme
چكيده لاتين :
Background: Systemic lupus erythematosus (SLE) is a multisystem disease with unknown etiology. We hypothesized that insertion/deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE) gene may influence the development and/or progression of SLE and lupus nephritis.
Materials and Methods: In a crass sectional case-control study, genomic DNA from 106 SLE patients and 103 healthy controls matched for sex, age, and ethnicity, were genotyped for the (I/D) polymorphism of ACE gene by polymerase chain reaction (PCR). Comparison of quantitative variants between two groups was assessed by student t-test and association between qualitative variables was analyzed by the chi-square or Fisher exact tests.
Results: The frequency of DD genotype in SLE patients was significantly higher than control group (25.5 % vs. 14 %), and the risk of SLE was 2.2 times greater in subjects with DD genotype than the individual by DI and II genotypes (OR, 2.2 [95% CI, 1.1 to 4.4]; p=0.023). The distribution of D allele in SLE patients was significantly higher (p=0.021) compare to controls (47 and 36.4, respectively). The Risk of nephropathy in SLE patients with DD genotype was three times more than other genotypes (OR), 3 [95% CI, 1.1 to 8]; p=0.027].
Conclusion: This study demonstrated that ACE DD genotype acts as a risk factor on SLE and Lupus nephropathy in an Iranian population.
