Genes influencing coagulation and the risk of aneurysmal subarachnoid hemorrhage, and subsequent complications of secondary cerebral ischemia and rebleeding

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• 作者：Ynte M. Ruigrok (1)
  Arjen J. C. Slooter (2)
  Gabriel J. E. Rinkel (1)
  Cisca Wijmenga (3) (4)
  Frits R. Rosendaal (5)
  
• 关键词：Intracranial aneurysm ; Subarachnoid hemorrhage ; Genes ; Coagulation
• 刊名：Acta Neurochirurgica
• 出版年：2010
• 出版时间：February 2010
• 年：2010
• 卷：152
• 期：2
• 页码：257-262
• 全文大小：115KB
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• 作者单位：Ynte M. Ruigrok (1)
  Arjen J. C. Slooter (2)
  Gabriel J. E. Rinkel (1)
  Cisca Wijmenga (3) (4)
  Frits R. Rosendaal (5)
  
  1. Department of Neurology, Rudolf Magnus Institute of Neuroscience, University Medical Centre Utrecht, PO Box?85500, 3500 GA, Utrecht, The Netherlands
  2. Department of Intensive Care, University Medical Centre Utrecht, Utrecht, The Netherlands
  3. Department of Biomedical Genetics, University Medical Centre Utrecht, Utrecht, The Netherlands
  4. Department of Genetics, University Medical Centre Groningen, Groningen, The Netherlands
  5. Departments of Clinical Epidemiology and Haematology, University Medical Centre, Leiden, the Netherlands
  

文摘

Background We investigated whether genes influencing coagulation are associated with the occurrence of aneurysmal subarachnoid hemorrhage (SAH) and with secondary cerebral ischemia and rebleeding in patients with aneurysmal SAH. Method Genotyping for factor V Leiden (G1691A), prothrombin G20210A, methylenetetetrahydrofolate reductase (MTHFR) C677T, factor XIII subunit A Val34Leu, Tyr204Phe and Pro564Leu, and factor XIII subunit B His95Arg was performed in 208 patients with aneurysmal SAH and in 925 controls. Secondary cerebral ischemia occurred in 49 (24%) patients and rebleeding in 28 (14%) during their clinical course of 3 months after the aneurysmal SAH. The risk of aneurysmal SAH was assessed as odds ratio (OR) with 95% confidence interval (95% CI). The risk of secondary cerebral ischemia and rebleeding was assessed as hazard ratio (HR) with 95% CI using Cox regression. Findings Carriers of the subunit B His95Arg factor XIII polymorphism had an increased risk of aneurysmal SAH with 23% of the patients homozygous or heterozygous for the variant allele compared to 17% of control subjects (OR 1.5, 95% CI 1.0-.2). For the remaining genetic variants no effect on the risk of aneurysmal SAH could be demonstrated. A clear relation with the risk of secondary cerebral ischemia and of rebleeding could not be established for any of the genetic variants. Conclusions We found that aneurysmal SAH patients are more often carriers of the subunit B His95Arg factor XIII polymorphism compared to controls. This suggests that carriers of the subunit B His95Arg factor XIII polymorphism have an increased risk of aneurysmal SAH. Larger studies should confirm our results. As aneurysmal SAH patients who died soon after admission could not be included in the present study, our results only apply to a population of patients who survived the initial hours after the hemorrhage. For the other studied genetic factors involved in coagulation, no association with the occurrence of aneurysmal SAH or with the occurrence of secondary cerebral ischemia or rebleeding after aneurysmal SAH could be demonstrated.