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RESEARCH PRODUCT
Superficial venous thrombosis: Prevalence of common genetic risk factors and their role on spreading to deep veins
Salvatore NovoSergio SiragusaStefania GrimaudoAmato CEgle CorradoGlauco MilioChiara Minàsubject
AdultMalemedicine.medical_specialtyAdolescentDeep veinThrombophiliaGastroenterologyVeinsCohort StudiesVaricose VeinsYoung AdultRisk FactorsInternal medicineVaricose veinsmedicinePrevalenceHumansGenetic Predisposition to DiseaseMethylenetetrahydrofolate Reductase (NADPH2)Venous ThrombosisColor-duplex-Ultrasonography Genetic Risk Factors Superficial Venous Thrombosis Venous ThromboembolismVascular diseasebusiness.industryFactor VHematologyMiddle Agedmedicine.diseaseThrombosisSettore MED/11 - Malattie Dell'Apparato CardiovascolarePulmonary embolismVenous thrombosismedicine.anatomical_structureEmbolismMutationFemaleProthrombinRadiologymedicine.symptombusinessPhlebitisPulmonary Embolismdescription
Introduction. Superficial venous thrombosis (SVT) has been considered for a long time a limited clinical condition with a low importance, but this approach has changed in recent years, when several studies demonstrated spreading to deep veins occurring from 7.3 to 44%, with high prevalence of pulmonary embolism . Materials and Methods. To evaluate the prevalence of genetic risk factors for VTE in patients suffering from SVT on both normal and varicose vein, and to evaluate their role on spreading to deep veins, we studied 107 consecutive outpatients with symptomatic SVT. Ultrasound examination was performed, and the presence of FV Leiden, Prothrombin G20210A mutation, MTHFR C677T mutation were researched. Results. In patients with SVT on healthy veins, the prevalence of thrombophilic conditions was consistent among all three mutations. In particularly, FV Leiden was more frequent in patients with venous progression to the deep system (60%) than in those without venous extension (23.6%). Similar results were found regarding FII G20210A and MTHFR C677T mutations in patients with (23.7% and 40%, respectively) or without thrombotic progression to the venous system (7.9% and 20%, respectively). Instead, in patients with SVT on varicose veins, the prevalence of FVL, FII and MTHFR mutations was low (6.7%, 4.4% and 6.7% respectively). However, even in these patients, the prevalence of FVL, FII and MTHFR C677T was higher in those with thrombus extension to the deep system (35.7%, 7.4% and 21.4% respectively) in comparison to those without. (6.7%, 4.4% and 6.7% respectively). Conclusions. Our data show the high prevalence of inherited thrombophilic states in patients with SVT on normal veins and their role in the progression to the deep vein system.
year | journal | country | edition | language |
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2008-12-01 |