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Blood, 15 May 2001, Vol. 97, No. 10, pp. 2979-2982
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Polymorphisms of clotting factors modify the risk for primary
intracranial hemorrhage
Javier Corral,
Juan
Antonio Iniesta,
Rocio González-Conejero,
Marino Villalón, and
Vicente Vicente
From the Emergency Service Hospital Virgen de la
Arrixaca; the Neurology Division and the Hematology and Medical
Oncology Service, Hospital General Universitario, Murcia, Spain.
Intracranial hemorrhage is the third most frequent cause of
cerebrovascular disease, but few genetic risk factors have been associated with its development. Recently, it has been reported that
some polymorphisms that affect clotting factors increase the risk for
thrombosis. However, reports have analyzed the effect of polymorphisms
influencing the hemostatic state in bleeding disorders insufficiently.
A case-control study was conducted of 201 patients with spontaneous
intracranial hemorrhage and 201 control subjects matched for age, race,
sex, and selected risk factors (hypertension, smoking, and alcohol
consumption). Genomic polymerase chain reaction was used to analyze the
prevalence of 4 polymorphisms: factor V Leiden, prothrombin 20210A,
factor VII 323 Del/Ins of a decanucleotide, and factor
XIII V34L. Subjects with factor V Leiden had decreased risk for
spontaneous intracranial hemorrhage (odds ratio, 0.19; 95% confidence
interval, 0.03-0.95). The frequency of the prothrombin 20210A/G
genotype was also lower among patients than controls (1.5% vs 3%,
respectively). Moreover, carriers of the 323 Ins allele of factor VII
had a 1.54-fold risk for intracranial hemorrhage (95% CI, 1.03-2.72).
Finally, no significant differences were observed in the prevalence of factor XIII V34L polymorphism between patients and controls. Therefore, new genetic factors affecting the risk for spontaneous intracranial hemorrhage were identified. These data, together with the relevance of
these polymorphisms in thrombotic diseases, support the idea that a
polymorphism may play opposite roles in thrombosis and hemorrhage,
suggesting an explanation for the high frequency of these polymorphisms
in the general population.
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Factor V Leiden and intracranial hemorrhage
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