Arteriosclerosis obliterans associated with anti-cardiolipin antibody β2-glycoprotein I antibodies as a strong risk factor for ischaemic heart disease in patients with systemic lupus erythematosus

被引:20
作者
Nojima, J. [1 ]
Masuda, Y. [1 ]
Iwatani, Y. [2 ]
Kuratsune, H. [3 ]
Watanabe, Y. [4 ]
Suehisa, E. [1 ]
Takano, T. [1 ]
Hidaka, Y. [1 ]
Kanakura, Y. [5 ]
机构
[1] Osaka Univ Hosp, Clin Invest Lab, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Grad Sch Med, Div Biomed Informat, Suita, Osaka, Japan
[3] Kansai Univ Welfare Sci, Fac Hlth Sci Welfare, Dept Hlth Sci, Kashihara, Nara, Japan
[4] Osaka City Univ, Grad Sch Med, Dept Physiol, Abeno Ku, Suita, Osaka, Japan
[5] Osaka Univ Hosp, Dept Hematol & Oncol, Suita, Osaka, Japan
关键词
systemic lupus erythematosus; anti-phospholipid antibodies; arteriosclerosis obliterans; ischaemic heart disease; cerebral vascular disorder;
D O I
10.1093/rheumatology/ken124
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective. The main objective of this study was to clarify the role of aPLs in the pathogenesis of arteriosclerosis obliterans (ASO), ischaemic heart disease (IHD) and cerebral vascular disorder (CVD) in patients with SLE. Methods. We evaluated 155 patients with SLE by using objective tests for diagnosing ASO, IHD and CVD and laboratory tests including ELISA for aCL/beta 2-glycoprotein I antibodies (aCL/beta 2-GPI) and anti-phosphatidylserine/prothrombin antibodies (anti-PS/PT). Results. Twenty-five ( 16.1%) of the 155 SLE patients were diagnosed with ASO. Both aCL/beta 2-GPI and anti-PS/PT levels were significantly higher in SLE patients with ASO ( mean +/- S. E.,104.3 +/- 38.8 U/ ml foraCL/beta 2-GPI, P < 0.01; 72.6 +/- 48.9 U/ ml for anti-PS/PT, P < 0.05) than in SLE patients without ASO ( 22.8 +/- 9.9 U/ ml for aCL/beta 2-GPI; 18.3 +/- 4.4 U/ ml for anti-PS/PT). Multivariate logistic analysis including aCL/beta 2-GPI, anti-PS/PT and traditional risk factors ( hypercholesterolaemia, hypertension and diabetes mellitus) confirmed that the presence of aCL/beta 2-GPI was the most significant risk factor for ASO in SLE patients [ odds ratio ( OR) 3.45; 95% CI 1.40, 8.56; P < 0.01]. Furthermore, the prevalence of ASO was associated strongly with IHD ( OR 11.8; 95% CI 3.45, 40.1; P < 0.0001) but not CVD ( OR 1.84; 95% CI 0.65, 5.21; P= 0.25). Conclusions. The presence of aCL/beta 2-GPI contributes to the risk of development of ASO, which may represent an important mechanism for the pathogenesis of IHD in patients with SLE.
引用
收藏
页码:684 / 689
页数:6
相关论文
共 41 条
[1]   Subelinical atherosclerosis in systemic lupus erythematosus (SLE): the relative contribution of classic risk factors and the lupus phenotype [J].
Ahmad, Y. ;
Shelmerdine, J. ;
Bodill, H. ;
Lunt, M. ;
Pattrick, M. G. ;
Teh, L. S. ;
Bernstein, R. M. ;
Walker, M. G. ;
Bruce, I. N. .
RHEUMATOLOGY, 2007, 46 (06) :983-988
[2]   The role of the tissue factor pathway in the hypercoagulable state in patients with the antiphospholipid syndrome [J].
Amengual, O ;
Atsumi, T ;
Khamashta, MA ;
Hughes, GRV .
THROMBOSIS AND HAEMOSTASIS, 1998, 79 (02) :276-281
[3]   Management of dyslipidemia in children and adolescents with systemic lupus erythematosus [J].
Ardoin, S. P. ;
Sandborg, C. ;
Schanberg, L. E. .
LUPUS, 2007, 16 (08) :618-626
[4]  
Atsumi T, 2000, ARTHRITIS RHEUM-US, V43, P1982, DOI 10.1002/1529-0131(200009)43:9<1982::AID-ANR9>3.0.CO
[5]  
2-2
[6]  
BEVERS EM, 1991, THROMB HAEMOSTASIS, V66, P629
[7]   Risk factors for coronary heart disease in women with systemic lupus erythematosus -: The Toronto Risk Factor Study [J].
Bruce, IN ;
Urowitz, MB ;
Gladman, DD ;
Ibañez, D ;
Steiner, G .
ARTHRITIS AND RHEUMATISM, 2003, 48 (11) :3159-3167
[8]  
Dobado-Berrios PM, 1999, THROMB HAEMOSTASIS, V82, P1578
[9]   Enhanced monocyte expression of tissue factor by oxidative stress in patients with antiphospholipid antibodies:: effect of antioxidant treatment [J].
Ferro, D ;
Saliola, M ;
Meroni, PL ;
Valesini, G ;
Caroselli, C ;
Praticò, D ;
Fitzgerald, GA ;
Shoenfeld, Y ;
Violi, F .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2003, 1 (03) :523-531
[10]   SLE, atherosclerosis and cardiovascular disease [J].
Frostegård, J .
JOURNAL OF INTERNAL MEDICINE, 2005, 257 (06) :485-495