OBJECTIVE: Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G>C and -572 G>C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. METHODS: A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G<C and the -572 G<C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. RESULTS: Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. CONCLUSIONS: Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.
OBJECTIVE: Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G>C and -572 G>C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. METHODS: A total of 179 consecutive aneurysmalSAHpatients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G<C and the -572 G<C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. RESULTS: Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. CONCLUSIONS: Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmalSAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmalSAH.
Authors: Sanish Sathyan; Linda V Koshy; Lekshmy Srinivas; Lekshmi Srinivas; H V Easwer; S Premkumar; Suresh Nair; R N Bhattacharya; Jacob P Alapatt; Moinak Banerjee Journal: J Neuroinflammation Date: 2015-07-22 Impact factor: 8.322