RESEARCH - Arteriosclerosis obliterans associated with aCL/â2-GPI antibodies as a strong risk factor for IHD in SLE

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Rheumatology Advance Access published online on March 27, 2008

Rheumatology, doi:10.1093/rheumatology/ken124

Arteriosclerosis obliterans associated with anti-cardiolipin antibody

/ â2-glycoprotein I antibodies as a strong risk factor for ischaemic

heart disease in patients with systemic lupus erythematosus

J. Nojima1, Y. Masuda1, Y. Iwatani2, H. Kuratsune3, Y. Watanabe4, E.

Suehisa1, T. Takano1, Y. Hidaka1 and Y. Kanakura1

1Laboratory for Clinical Investigation, Osaka University Hospital,

Suita, Osaka, 2Division of Biomedical Informatics, Course of Health

Science, Osaka University Graduate School of Medicine, Suita,

3Department of Health Science, Faculty of Health Science for Welfare,

Kansai University of Welfare Science, Kashihara, 4Department of

Physiology, Osaka City University Graduate School of Medicine,

Abeno-ku and 5Department of Hematology and Oncology, Osaka University

Graduate School of Medicine, Suita, Osaka, Japan.

Abstract

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/â2-glycoprotein I antibodies (aCL/â2-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/â2-GPI and anti-PS/PT levels were significantly

higher in SLE patients with ASO (mean ± S.E., 104.3 ± 38.8 U/ml for

aCL/â2-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/â2-GPI; 18.3 ±

4.4 U/ml for anti-PS/PT). Multivariate logistic analysis including

aCL/â2-GPI, anti-PS/PT and traditional risk factors

(hypercholesterolaemia, hypertension and diabetes mellitus) confirmed

that the presence of aCL/â2-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/â2-GPI contributes to the risk of

development of ASO, which may represent an important mechanism for the

pathogenesis of IHD in patients with SLE.

http://rheumatology.oxfordjournals.org/cgi/content/abstract/ken124v1

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