Factor V Leiden and Thrombosis in Patients with Systemic Lupus Erythematosus (SLE): A Meta-analysis

Kaiser, R R; Barton, J.L.; Chang, M. N.; Catanese, JJ.; Li, Y.; Begovich, A.B.; Criswell, LA

doi:10.1038/gene.2009.32

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Factor V Leiden and Thrombosis in Patients with Systemic Lupus Erythematosus (SLE): A Meta-analysis

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Author(s): R. Kaiser ¹ , J.L. Barton ¹ , M. Chang ² , JJ. Catanese ² , Y. Li ² , A.B. Begovich ² , LA. Criswell ¹

Publication date (Electronic): 7 May 2009

Journal: Genes and immunity

Keywords: Systemic lupus erythematosus, factor V Leiden polymorphism, thrombosis, risk factors, antiphospholipid antibodies

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Abstract

To perform a meta-analysis of the association between the factor V Leiden polymorphism (FVL) and thrombosis among patients with SLE and/or antiphospholipid antibody (aPL) positivity. Included studies recruited patients based on SLE or aPL positive status, confirmed subjects' SLE diagnosis as defined by the American College of Rheumatology, and documented thrombotic events. Excluded studies were non-English or considered only arterial thrombosis. Individual patient data, available from five studies, together with unpublished data from 1210 European-American SLE patients from the UCSF Lupus Genetics Collection genotyped for FVL, were further analyzed. Seventeen studies (n=2090 subjects) were included in the initial meta-analysis. Unadjusted odds ratios (OR) were calculated to assess association of FVL with thrombosis. The OR for association of thrombosis with FVL was 2.88 (95% C.I. 1.98-4.20). In the secondary analysis with our individual patient dataset (n=1447 European-derived individuals), SLE subjects with the FVL polymorphism still had more than two times the odds of thrombosis compared to subjects without this polymorphism, even when adjusting for covariates such as gender, age, and aPL status. SLE and/or aPL positive patients with the FVL variant have more than two times the odds of thrombosis compared to those without this polymorphism.

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Most cited references 34

Record: found
Abstract: found
Article: not found

Advances in understanding pathogenic mechanisms of thrombophilic disorders.

Björn Dahlbäck (2008)

Venous thromboembolism is a major medical problem, annually affecting 1 in 1000 individuals. It is a typical multifactorial disease, involving both genetic and circumstantial risk factors that affect a delicate balance between procoagulant and anticoagulant forces. In the last 50 years, the molecular basis of blood coagulation and the anticoagulant systems that control it have been elucidated. This has laid the foundation for discoveries of both common and rare genetic traits that tip the natural balance in favor of coagulation, with a resulting lifelong increased risk of venous thrombosis. Multiple mutations in the genes for anticoagulant proteins such as antithrombin, protein C, and protein S have been identified and constitute important risk factors. Two single mutations in the genes for coagulation factor V (FV Leiden) and prothrombin (20210G>A), resulting from approximately 20,000-year-old mutations with subsequent founder effects, are common in the general population and constitute major genetic risk factors for thrombosis. In celebration of the 50-year anniversary of the American Society of Hematology, this invited review highlights discoveries that have contributed to our present understanding of the systems that control blood coagulation and the genetic factors that are involved in the pathogenesis of venous thrombosis.

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Record: found
Abstract: found
Article: not found

Association of gene variants with incident myocardial infarction in the Cardiovascular Health Study.

Bruce M. Psaty, James Devlin, Olga A. Iakoubova … (2007)

We asked whether single nucleotide polymorphisms (SNPs) that had been nominally associated with cardiovascular disease in antecedent studies were also associated with cardiovascular disease in a population-based prospective study of 4522 individuals aged 65 or older. Based on antecedent studies, we prespecified a risk allele and an inheritance model for each of 74 SNPs. We then tested the association of these SNPs with myocardial infarction (MI) in the Cardiovascular Health Study (CHS). The prespecified risk alleles of 8 SNPs were nominally associated (1-sided P<0.05) with increased risk of MI in White CHS participants. The false discovery rate for these 8 was 0.43, suggesting that about 4 of these 8 are likely to be true positives. The 4 of these 8 SNPs that had the strongest evidence for association with cardiovascular disease before testing in CHS (association in 3 antecedent studies) were in KIF6 (CHS HR=1.29; 90%CI 1.1 to 1.52), VAMP8 (HR=1.2; 90%CI 1.02 to 1.41), TAS2R50 (HR=1.13; 90%CI 1 to 1.27), and LPA (HR=1.62; 90%CI 1.09 to 2.42). Although most of the SNPs investigated were not associated with MI in CHS, evidence from this investigation combined with previous studies suggests that 4 of these SNPs are likely associated with MI.

0 comments Cited 44 times – based on 0 reviews      Review now

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Record: found
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Article: not found

Morbidity and mortality in systemic lupus erythematosus during a 5-year period. A multicenter prospective study of 1,000 patients. European Working Party on Systemic Lupus Erythematosus.

R Cervera, O T Aydintuğ, F Houssiau … (1999)

In the present study we assessed the frequency and characteristics of the main causes of morbidity and mortality in SLE during a 5-year period and analyzed the prognostic significance for morbidity and mortality of the main immunologic parameters used in clinical practice. We started in 1990 a multicenter study of 1,000 patients from 7 European countries. All had medical histories documented and underwent medical interview and routine general physical examination when entered in the study, and all were followed prospectively by the same physicians during the ensuing 5 years (1990-1995). Four hundred thirteen patients (41.3%) presented 1 or more episodes of arthritis, 264 (26.4%) had malar rash, 222 (22.2%) active nephropathy, 139 (13.9%) fever, 136 (13.6%) neurologic involvement, 132 (13.2%) Raynaud phenomenon, 129 (12.9%) serositis (pleuritis and/or pericarditis), 95 (9.5%) thrombocytopenia, and 72 (7.2%) thrombosis. Two hundred seventy patients (27%) presented infections, 113 (11.3%) hypertension, 75 (7.5%) osteoporosis, and 59 (5.9%) cytopenia due to immunosuppressive agents. Sixteen patients (1.6%) developed malignancies, with the most frequent primary localizations the uterus and the breast. Several immunologic parameters (anti-dsDNA or antiphospholipid antibodies) were found to have a predictive value for the development of SLE manifestations during the period of the study. Forty-five patients (4.5%) died; the most frequent causes of death were divided similarly among active SLE (28.9%), infections (28.9%), and thromboses (26.7%). A survival probability of 95% at 5 years was found. A lower survival probability (92%) was detected in those patients who presented at the beginning of the study with nephropathy.

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Author and article information

Journal

Journal ID (nlm-journal-id): 100953417

Journal ID (pubmed-jr-id): 21482

Journal ID (nlm-ta): Genes Immun

Title: Genes and immunity

ISSN (Print): 1466-4879

ISSN (Electronic): 1476-5470

Publication date Nihms-submitted: 31 March 2009

Publication date (Electronic): 7 May 2009

Publication date (Print): July 2009

Publication date PMC-release: 1 January 2010

Volume: 10

Issue: 5

Pages: 495-502

Affiliations

[1 ]Rosalind Russell Medical Research Center for Arthritis, Division of Rheumatology, University of California, San Francisco (UCSF)

[2 ]Celera, Alameda, California

Author notes

[†]

Current address: Roche Diagnostics, Pleasanton, California

Corresponding Author and Requests for Reprints: Lindsey A. Criswell, MD, MPH UCSF Division of Rheumatology 374 Parnassus, 1 ^st Floor Box 0500 San Francisco, CA 94143 Phone (415) 476-9026 Fax (415) 476-9370 Lindsey.Criswell@ 123456ucsf.edu

Article

Manuscript ID: nihpa106580

DOI: 10.1038/gene.2009.32

PMC ID: 2766554

PubMed ID: 19421222

SO-VID: 657c526a-20f3-4388-9e93-4ae971c91e5b