gms | German Medical Science

59th Annual Meeting of the German Society of Neurosurgery (DGNC)
3rd Joint Meeting with the Italian Neurosurgical Society (SINch)

German Society of Neurosurgery (DGNC)

1 - 4 June 2008, Würzburg

Association of Interleukin-6 and Tumor Necrosis Factor-[alpha] gene polymorphisms and aneurysmal subarachnoid hemorrhage in an Italian population

Meeting Abstract

  • corresponding author M. Fontanella - Division of Neurosurgery, Department of Neuroscience, University of Torino, Italy
  • I. Rainero - Neurology II, Department of Neuroscience, University of Torino, Italy
  • D. Garbossa - Division of Neurosurgery, Department of Neuroscience, University of Torino, Italy
  • C. Benevello - Division of Neurosurgery, Department of Neuroscience, University of Torino, Italy
  • M. Pejrona - Division of Neurosurgery, Department of Neuroscience, University of Torino, Italy
  • A. Ducati - Division of Neurosurgery, Department of Neuroscience, University of Torino, Italy

Deutsche Gesellschaft für Neurochirurgie. Società Italiana di Neurochirurgia. 59. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3. Joint Meeting mit der Italienischen Gesellschaft für Neurochirurgie (SINch). Würzburg, 01.-04.06.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocDI.02.04

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2008/08dgnc154.shtml

Published: May 30, 2008

© 2008 Fontanella et al.
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Outline

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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.