Hyperhomocysteinaemia and factor V Leiden mutation are associated with Budd-Chiari syndrome
Küçük Resim Yok
Tarih
2006
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
OBJECTIVES: Budd-Chiari syndrome (BCS) is characterized by hepatic venous outflow obstruction and may be caused by various prothrombotic disorders. We aimed to study the role of hyperhomocysteinaemia, factor V Leiden mutation and G20210A prothrombin gene mutation in the pathogenesis of the syndrome. METHODS: Thirty-two patients (16 male, 16 female, aged 19-45 years) 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 (16.4±8.8 vs 11.0±2.7 µmol/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 14.4±5.9 µmol/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. © 2006 Lippincott Williams & Wilkins.
Açıklama
Anahtar Kelimeler
Budd-Chiari, Factor V Leiden, Hyperhomocysteinaemia, Prothrombin
Kaynak
European Journal of Gastroenterology and Hepatology
WoS Q Değeri
Scopus Q Değeri
Q2
Cilt
18
Sayı
8
