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    Hyperhomocysteinaernia and factor V Leiden mutation are associated with Budd-Chiari syndrome
    (Lippincott Williams & Wilkins, 2006) Colak, Yusuf; Karasu, Zeki; Oruc, Nevin; Can, Cenk; Balym, Zuhal; Akarca, UlusSalih; Gunsar, Fulya; Ersoz, Galip; Tokat, Yarnan; Batur, Yucel
    Objectives Budd-Chiarl syndrome (BCS) is characterized by hepatic venous outflow obstruction and may be caused by various prothrombotic disorders. We aimed to study the role of hyperhomocysteinaernia, factor V Leiden mutation and G20210A prothrombin gene mutation in the pathogenesis of the syndrome. Methods Thirty-two patients (16 male, 16 female, aged 19-45years) with angiographically verified BCS and 33 age-matched and sex-matched voluntary healthy controls (15 male, 18 female, aged 19-45 years) were included into the study. Factor V Leiden and prothrombin gene mutations were determined in extracted DNA from peripheric mononuclear cells, using a light cycler amplification system. Plasma homocysteine levels were measured by fluorescence polarization immunoassay. Results The homozygote factor V Leiden mutation was diagnosed in four BCS patients and the heterozygote mutation was diagnosed in five. The frequency of the mutant allele was 20.3% in BCS patients and 7.6% in the controls (P < 0.05). There was no significant difference in prothrombin gene mutation frequency between the two groups. Serum homocysteine levels were significantly higher in the BCS group than in the controls (116.4 +/- 8.8 vs 11.0 +/- 2.7 pmol/l; P < 0.01). BCS patients with the mutant factor V Leiden allele have significantly higher levels of serum homocysteine (22.1 +/- 13.3 vs 14.40 +/- 5.91mol/l; P < 0.05). Conclusions Hyperhomocysteinaemia, especially when associated with the factor V Leiden mutation, is an important risk factor for the development of BCS.