The Leiden mutation of coagulation factor V in Hungarian SLE patients

Citation
N. Regeczy et al., The Leiden mutation of coagulation factor V in Hungarian SLE patients, CL APPL T-H, 6(1), 2000, pp. 41-45
Citations number
34
Categorie Soggetti
Hematology
Journal title
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS
ISSN journal
10760296 → ACNP
Volume
6
Issue
1
Year of publication
2000
Pages
41 - 45
Database
ISI
SICI code
1076-0296(200001)6:1<41:TLMOCF>2.0.ZU;2-E
Abstract
We studied the prevalence and the effect of coagulation factor V Leiden mut ation on the occurrence of thrombotic episodes in 120 Hungarian patients ha ving systemic lupus erythematosus (SLE) with or without antiphospholipid an tibody. The frequency of the factor V Leiden mutation in Hungarian SLE pati ents was 13%, which is comparable with those found previously in a healthy Caucasian population. The incidence of venous thrombosis among factor V Lei den carriers has been found to be higher (odds ratio [OR] 1.7) than it is i n patients without Leiden mutation (38% vs 29%). In addition, the frequency of venous thrombosis in the heterozygous SLE patients (OR 8.4 [confidence interval (CI) 0.8-83.9] P = 0.06) is dependent on the coexistence of other risk factors, such as antiphospholipid antibody. Moreover, among heterozygo us factor V SLE patients, the Leiden mutation could explain the tendency to have significantly higher prevalence of fetal losses (OR 3.9 [CI 1.2-12.0] P = 0.02) and higher prevalence of cerebrovascular lesions, cardiac valvul ar abnormalities, and Raynaud's syndrome than that found in individuals wit hout factor V Leiden mutation or those having antiphospholipid antibody. Sy stemic lupus erythematosus patients with combined defects suffer more sever ely from thrombosis than those with a single risk factor do, suggesting tha t thrombophilia is a multifactorial disorder in SLE, also. Although, the fa ctor V Leiden mutation does not seem to be a significant risk factor for ve nous thrombosis in SLE, these data demonstrate that Leiden mutation can be regarded as an additive thrombogenic factor providing higher predisposition to several vasoocclusive disorders in SLE.