Patterns of angiotensin converting enzyme insertion/deletion gene polymorphism among an Egyptian cohort of patients with rheumatoid arthritis
Article first published online: 4 SEP 2012
© 2012 The Authors International Journal of Rheumatic Diseases © 2012 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd
International Journal of Rheumatic Diseases
Volume 16, Issue 3, pages 284–290, June 2013
How to Cite
Ahmed, A. Z., El-Shahaly, H. A., Omar, A. S. and Ghattas, M. H. (2013), Patterns of angiotensin converting enzyme insertion/deletion gene polymorphism among an Egyptian cohort of patients with rheumatoid arthritis. International Journal of Rheumatic Diseases, 16: 284–290. doi: 10.1111/j.1756-185X.2012.01820.x
- Issue published online: 11 AUG 2013
- Article first published online: 4 SEP 2012
- angiotensin converting enzyme;
- insertion/deletion ACE gene polymorphism;
- rheumatoid arthritis
This case control study was designed to determine the patterns of angiotensin converting enzyme insertion/deletion (ACE I/D) gene polymorphism in rheumatoid arthritis (RA) patients and healthy controls.
The study population was divided into two groups: the study group included 66 RA patients diagnosed according to the American College of Rheumatology (ACR) classification criteria for RA, and the control group included 66 healthy adults who were age-and sex-matched to the RA group. All RA patients were assessed by Disease Activity Score (DAS28), ACR Classification of Global Functional Disability Status and Sharp's score as outcome measures. Gene investigations for ACE I/D polymorphism were performed by polymerase chain reaction (PCR) in both groups.
The ACE I/D polymorphism was the (D/D) genotype in 60.6% (n = 40) of RA patients, the (I/D) genotype in 31.8% (n = 21) and the (I/I) genotype in 7.6% (n = 5). The frequency of (D) carriage was significantly higher in the RA cases than in the control group (76.5% vs. 53.8%, respectively, P = 0.0002). ACE D allele carriers were at higher risk of RA, 2.8 times higher than (I) carriers and those who had the homozygote (DD) genotype had 5.6 times the possibility of having RA. No correlations were observed between the homozygote (DD) genotype and disease activity or severity in RA patients.
Our study suggests that high frequency of the ACE D allele contributes to the heritability of RA susceptibility compared to other ACE alleles. On the other hand, no association was detected between ACE I/D polymorphism and the severity of RA.