Clinical Chemistry AACC Online Job Center
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 51: 545-552, 2005. First published January 6, 2005; 10.1373/clinchem.2004.043414
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
clinchem.2004.043414v1
51/3/545    most recent
Right arrow Submit an electronic Letter to
the Editor about this paper
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nojima, J.
Right arrow Articles by Kanakura, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nojima, J.
Right arrow Articles by Kanakura, Y.
Related Collections
Right arrow Hemostasis and Thrombosis
(Clinical Chemistry. 2005;51:545-552.)
© 2005 American Association for Clinical Chemistry, Inc.

Hemostasis and Thrombosis

Acquired Activated Protein C Resistance Associated with IgG Antibodies against ß2-Glycoprotein I and Prothrombin as a Strong Risk Factor for Venous Thromboembolism

Junzo Nojima1,a, Hirohiko Kuratsune2, Etsuji Suehisa1, Yoshinori Iwatani3 and Yuzuru Kanakura1,4

1 Laboratory for Clinical Investigation, Osaka University Hospital, Osaka, Japan.
2 Department of Health Science, Faculty of Health Science for Welfare, Kansai University of Welfare Science, Osaka, Japan.
3 Division of Biomedical Informatics, Course of Health Science, and 4 Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.

aAddress correspondence to this author at: Laboratory for Clinical Investigation, Osaka University Hospital, 2-15 Yamadaoka, Suita, Osaka 565-0871, Japan. Fax 81-6-6879-6635; e-mail nojima{at}hp-lab.med.osaka-u.ac.jp.

Background: Venous thromboembolic events such as deep vein thrombosis and pulmonary embolism are common manifestations of antiphospholipid syndrome. Our aim was to clarify the roles of anti-phospholipid (aPL) antibodies in the pathogenesis of venous thromboembolism (VTE) in patients with systemic lupus erythematosus (SLE).

Methods and Results: We examined anti-cardiolipin/ß2-glycoprotein I (anti-CL/ß2-GPI) antibody concentrations, anti-phosphatidylserine/prothrombin (anti-PS/PT) antibody concentrations, and lupus anticoagulant (LA) activity in 87 patients with SLE (21 with VTE and 66 without thrombosis). Both anti-CL/ß2-GPI and anti-PS/PT antibodies strongly correlated with LA activity. Multivariate logistic analysis confirmed that both anti-CL/ß2-GPI and anti-PS/PT antibodies were significant independent risk factors for VTE (odds ratios = 4.98 and 7.54, respectively; 95% confidence intervals, 1.51–16.4 and 2.30–24.7, respectively). We therefore studied the in vitro effects of IgG fractions containing anti-CL/ß2-GPI or anti-PS/PT antibodies on the anticoagulant activity of activated protein C (APC) and found that purified IgG containing anti-CL/ß2-GPI or anti-PS/PT antibodies significantly hampered the anticoagulant activity of APC. We also studied the ability of IgG fractions to impede the anticoagulant activity of APC before and after complete removal of anti-CL/ß2-GPI or anti-PS/PT antibodies by adsorption. Removal of anti-CL/ß2-GPI or anti-PS/PT antibodies from all positive IgG samples clearly decreased the inhibitory effect of those samples on APC anticoagulant activity.

Conclusions: Anti-CL/ß2-GPI and anti-PS/PT antibodies independently cause APC resistance, which may contribute to risk of VTE in patients with SLE.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the American Association for Clinical Chemistry.