Thromb Haemost 2004; 91(05): 967-976
DOI: 10.1160/TH03-10-0608
Platelets and Blood Cells
Schattauer GmbH

Strong correlation between the prevalence of cerebral infarction and the presence of anti-cardiolipin/β2-glycoprotein I and anti-phosphatidylserine/prothrombin antibodies

Co-existence of these antibodies enhances ADP-induced platelet activation in vitro
Junzo Nojima
1   Laboratory for Clinical Investigation, Osaka University Hospital, Suita, Osaka, Japan
,
Hirohiko Kuratsune
2   Department of Health Science, Faculty of Health Science for Welfare, Kansai University of Welfare Science, Kashiwara, Osaka, Japan
,
Etsuji Suehisa
1   Laboratory for Clinical Investigation, Osaka University Hospital, Suita, Osaka, Japan
,
Teruo Kitani
3   Honorary Professor, Osaka University, Japan
,
Yoshinori Iwatani
4   Division of Biomedical Informatics, Course of Health Science, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
,
Yuzuru Kanakura
1   Laboratory for Clinical Investigation, Osaka University Hospital, Suita, Osaka, Japan
5   Department of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
› Author Affiliations
Further Information

Publication History

Received 01 October 2003

Accepted after resubmission 01 March 2004

Publication Date:
01 December 2017 (online)

Preview

Summary

Cerebral infarction is the most common arterial thromboembolic complication in the anti-phospholipid antibodies (aPL) syndrome. In an effort to clarify the roles of aPL in the pathogenesis of cerebral infarction in patients with SLE, we examined the levels of anti-cardiolipin/β2-glycoprotein I antibodies (antiCL/β2-GPI) and anti-phosphatidylserine/prothrombin antibodies (anti-PS/PT) in addition to lupus anticoagulant (LA) activity in 126 patients with SLE (35 with cerebral infarction and 91 without thrombosis). Both anti-CL/β2-GPI and antiPS/PT strongly correlated with the presence of LA activity. The prevalence of cerebral infarction was obviously higher in the patients who had both anti-CL/β2-GPI and anti-PS/PT (76.5% [26/34 cases], p<0.0001) than in the other patients having antiCL/β2-GPI or anti-PS/PT alone or neither of them (9.8% [9/92 cases]). Furthermore, we studied the in vitro effects of antiCL/β2-GPI and/or anti-PS/PT on the enhancement of platelet activation induced by stimulation with a low concentration of adenosine diphosphate (ADP). The purified IgG containing both anti-CL/β2-GPI and anti-PS/PT caused significant enhancement of platelet activation caused by ADP. However, the purified IgG containing either anti-CL/β2-GPI or anti-PS/PT had no enhancing effects on it. Furthermore, platelet activation was generated by the mixture of anti-CL/β2-GPI-IgG and anti-PS/PT-IgG prepared from individual patients, but not by each fraction alone. These results indicate that anti-CL/β2-GPI and antiPS/PT may cooperate to promote platelet activation, which may contribute to the risk of cerebral infarction in patients with SLE.