Methods: Fifty-eight patients (41 males, 17 females; mean age 62.9±6.5 years; range 45 to 78 years) operated on our clinic between May 2008 and March 2009 with the diagnosis of AAA, and 58 healthy volunteers (38 males, 20 females; mean age 58.8±11.6 years; range 30 to 79 years) with normal aortic diameters measured by computed tomography were included in this study. Thirty-two base p deletions in the CCR5 gene were screened after obtaining genomic DNAs from peripheral blood samples of the patients.

Results: When the groups were compared with the predisposing risk factors for the development of AAA, no significant difference was observed (p>0.05). Eleven patients (19.0%) had heterozygote CCR5 gene mutation in the AAA group, however, only one patient (1.7%) had heterozygote CCR5 gene mutation in the control group. While the CCR5 homozygote was normal in 47 (81.0%) patients, the CCR5 homozygote was normal in 57 (98.3%) volunteers in the control group. Chemokine receptor 5 Δ32 heterozygote gene mutation was significantly higher in the AAA group. (p=0.004).

Conclusion: Consequently, a relationship between CCR5 gene polymorphism and AAA was demonstrated in this study. We think that hereditary factors considered between unchanged etiologic factors play a role in the development of AAA and we believe that AAA can be treated before serious complications occur with frequent clinical check ups in people with hereditary predisposition.