title: Interleukin-1 cluster gene polymorphisms and aneurysmal subarachnoid hemorrhage.
abstract: BACKGROUND
  Emerging data indicate that proinflammatory cytokines may be involved in the pathogenesis of intracranial aneurysms. Interleukin (IL)-1 is a proinflammatory cytokine that plays a pivotal role in both acute and chronic central nervous system injuries.
  
  
  OBJECTIVE
  To investigate whether select polymorphisms in the IL-1alpha, IL-1beta, and IL-1 receptor antagonist genes are associated with both susceptibility to and clinical characteristics of subarachnoid hemorrhage due to intracranial aneurysm rupture.
  
  
  METHODS
  Allelic and genotypic frequencies of the IL-1alpha (-889), IL-1beta (-511), and IL-1 receptor antagonist (VNTR) genes were determined in 215 patients and 155 healthy controls. Patient files were reviewed for the clinical characteristics at hospital admission and at 6-month follow-up.
  
  
  RESULTS
  No association between aneurysmal subarachnoid hemorrhage susceptibility and the examined cytokine gene polymorphisms was found. Haplotype analysis did not show any significant difference between cases and controls. However, aneurysmal subarachnoid hemorrhage patients carrying the T/T genotype of the IL-1beta gene showed a significant (P = .034) increase in the Hunt and Hess scores at hospital admission and a significant (P = .026) reduction in 6-month Glasgow Outcome Scale scores. The remaining polymorphisms showed no effect on the clinical features examined.
  
  
  CONCLUSIONS
  Our results do not support the hypothesis that genetic variation in select polymorphisms of the IL-1 cluster genes is associated with aneurysmal subarachnoid cerebral hemorrhage. However, the IL-1beta gene may modify disease severity and may be regarded as disease severity gene.
authors.affiliation: Division of Neurosurgery, Department of Neuroscience, University of Torino, Torino, Italy. marco.fontanella@tin.it
authors.forename: Marco
authors.initials: M
authors.lastname: Fontanella
authors.forename: Innocenzo
authors.initials: I
authors.lastname: Rainero
authors.forename: Salvatore
authors.initials: S
authors.lastname: Gallone
authors.forename: Elisa
authors.initials: E
authors.lastname: Rubino
authors.forename: Riccardo
authors.initials: R
authors.lastname: Fornaro
authors.forename: Pierpaola
authors.initials: P
authors.lastname: Fenoglio
authors.forename: Walter
authors.initials: W
authors.lastname: Valfrè
authors.forename: Giovanna
authors.initials: G
authors.lastname: Vaula
authors.forename: Chiara
authors.initials: C
authors.lastname: Benevello
authors.forename: Alessandro
authors.initials: A
authors.lastname: Ducati
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Pinessi
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D014644:Genetic Variation / Q000276:immunology; D005838:Genotype; D023261:Glasgow Outcome Scale; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics* / Q000378:metabolism*; D053582:Interleukin-1alpha / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D005810:Multigene Family / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D017472:Receptors, Interleukin-1 / Q000235:genetics / Q000378:metabolism; D012720:Severity of Illness Index; D013345:Subarachnoid Hemorrhage / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D017472:Receptors, Interleukin-1