Survey of factor V Leiden and prothrombin gene mutations in systemic lupus erythematosus


Topaloglu R., Akierli C. , Bakkaloglu A., Aydintug O., Ozen S., Besbas N., et al.

CLINICAL RHEUMATOLOGY, cilt.20, ss.259-261, 2001 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 20 Konu: 4
  • Basım Tarihi: 2001
  • Doi Numarası: 10.1007/s100670170040
  • Dergi Adı: CLINICAL RHEUMATOLOGY
  • Sayfa Sayısı: ss.259-261

Özet

The two most common hereditary risk factors for thrombosis are factor V Leiden mutation and a prothrombin gene mutation. There is indeed a thrombotic tendency in patients with systemic lupus erythematosis (SLE) and it is not always associated with antiphospholipid antibodies. We aimed to determine the relationship between both factor V Leiden and prothrombin gene mutations and SLE. Using polymerase chain reaction (PCR) the factor V Leiden and prothrombin gene mutations were evaluated in 55 patients (20 children and 35 adults) with SLE. Although seven patients were found to have factor V Leiden mutation in the heterozygous state, two had the heterozygous G --> A (20210) prothrombin gene mutation. Although one had these two mutations concurrently, these two patients did not have thrombosis. The factor V Leiden mutation frequency (12.7%) was higher than that of our general population (7.1%). On the other hand, seven of the patients with SLE had a thrombotic event. Although of these seven, four (57%) had factor V Leiden mutation, three (43%) had no mutation. Of 48 patients with no thrombotic history, only three had the factor V mutation (6.25%). The prevalence of the factor V Leiden mutation in SLE patients with and without thrombosis was significantly different by Fisher's exact test (p <0.05). The risk of venous thrombosis in patients with factor V Leiden increased threefold compared to that in those without factor V Leiden mutation (odds ratio 20.1; Cl 2.99-133.6). Although factor V Leiden mutation seems to play a role in the development of venous thrombosis in SLE, the development of thrombosis in SLE is multifactorial.