The coexistence of PRTH and factor V mutation has been strongly associated with juvenile and recurrent venous thrombo- embolism.6,7 The MTHFR variant increases the risk of deep-vein thrombosis in factor V Leiden carriers.8 Despite the limitations

ground. The frequency of factor V Leiden and of the MTHFR in patients with CVT were 10% (1/10) and 33.3% (3/10), respectively, ie, twice as much as that found in controls (5.8% [15/259] and 17.4% [45/259], respectively). Two patients had the MTHFR genotype and the G20210A PRTH variant simultaneously; 1 carried the PRTH and the factor V Leiden variants. On the whole, 3 patients (33.3%) showed the coexistence of 2 thrombophilic genes; this was significantly different from the prevalence of the coexistence among healthy subjects (5/259, 1.9%; P"0.0019). Three CVT patients had a family history of venous thromboembolism; all were heterozygous for the G20210A PRTH variant. Four patients showed recurrent venous thromboembolism; among them, 3 carried the G20210A PRTH variant and 2 showed the association of the latter with factor V Leiden or with the MTHFR 677TT genotype. In our female patients, 2 of 6 experienced CVT while using oral contraceptives; none of the polymorphisms was present in both cases. The coexistence of PRTH and factor V mutation has been strongly associated with juvenile and recurrent venous thromboembolism.6,7 The MTHFR variant increases the risk of deep-vein thrombosis in factor V Leiden carriers.8 Despite the limitations of the sample size, these data confirm the role of the G20210A PRTH variant as a predisposing factor for CVT. Our data also indicate that thrombophilic genes often coexist in patients with CVT. Whether (and the extent towhich) thrombosis at this unusual site reflects a sustained hypercoagulable state needs to be further evaluated.