Article
Association of Interleukin-6 and Tumor Necrosis Factor-[alpha] gene polymorphisms and aneurysmal subarachnoid hemorrhage in an Italian population
Search Medline for
Authors
Published: | May 30, 2008 |
---|
Outline
Text
Objective: Immunological factors may play a role in pathogenesis of intracranial aneurysms. Recent studies have suggested that tumor necrosis factor-[alpha] (TNF-[alpha]), and interleukin-6 (IL-6), two of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study was to evaluate the association of a functionally active polymorphism (-308 GC and -572 G>C) in the promoter region of the IL-6 gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage.
Methods: A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Patients and controls were genotyped for the-308 biallelic (G<A) polymorphism of the TNF-[alpha] gene and for the -174 G<C and the -572 G<C biallelic polymorphisms of the IL-6 gene. The frequencies of different haplotypes were compared between cases and controls.
Results: The TNF-[alpha] G allele was significantly more frequent in patients than in controls ([chi]2=5.59; P=0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio =2.20; 95% confidence interval =1.29<odds ratio<3.75). Allelic and genotypic frequencies of the TNF-[alpha] polymorphism were not significantly different in disease subgroups. Allelic and genotypic frequencies of the -174 G<C and the -572 G<C biallelic polymorphisms of the IL-6 gene were not significantly different between cases and controls. Finally, the different TNFalpha and IL-6 genotypes do not seem to significantly modify the main clinical features of the disease.
Conclusions: Our data suggests that the TNF-[alpha] gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage, but do not confirm, in an Italian population, the association between functionally active polymorphisms in the IL-6 gene and the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.