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1
Central Laboratory for Clinical Investigation, Osaka University Hospital, Suita, Osaka 565-0871, Japan.
2
Department of Clinical Laboratory Science, School of
Allied Health Sciences, Faculty of Medicine, Osaka University, Osaka
565-0871, Japan.
3
Department of Hematology and Oncology, Osaka University
Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
aAddress correspondence to this author at: Central 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: Anti-phospholipid (aPL) antibodies (Abs) frequently found in the plasma of patients with systemic lupus erythematosus (SLE) have been associated with thrombotic complications. Our aim was to clarify the roles in thrombosis of aPL Abs that react with complexes of phospholipids and plasma proteins such as ß2-glycoprotein I (ß2-GPI), prothrombin, protein C, protein S, and annexin V.
Methods: We determined the prevalence of aPL Abs to various
phospholipid-binding plasma proteins in SLE patients with arterial
thrombosis (30 cases), venous thrombosis (19 cases), thrombocytopenia
(14 cases), fetal loss (14 cases), and patients without complications
(91 cases). The aPL Abs were measured by an ELISA system in which human
plasma proteins (ß2-GPI, prothrombin, protein C, protein
S, and annexin V) were immobilized on 
-irradiated or plain
polystyrene plates.
Results: All types of aPL Abs were frequently observed in the
patients with SLE when -irradiated polystyrene plates were used (51
of 168 cases positive for anti-ß2-GPI, 94 of 168 cases
positive for anti-prothrombin, 36 of 168 cases positive for
anti-protein C, 47 of 168 cases positive for anti-protein S, and 50 of
168 cases positive for anti-annexin V), whereas no Abs to these plasma
proteins were detected when plain polystyrene plates were used.
Multivariate analysis confirmed that both anti-ß2-GPI and
anti-prothrombin Abs were significant risk factors for arterial
thrombosis [odds ratios (ORs), 8.8 and 14.5, respectively; 95%
confidence intervals (CIs), 3.2–25 and 1.8–116, respectively] but
not for venous thrombosis. The presence of anti-protein S Abs was a
significant risk factor for venous thrombosis (OR, 30.4; CI, 3.3–281)
but not for arterial thrombosis. The only significant risk factor for
fetal loss was the presence of anti-annexin V Abs (OR, 5.9; CI,
1.4–14.8).
Conclusions: Patients with SLE frequently have some aPL Abs to ß2-GPI, prothrombin, protein C, protein S, and annexin V. Thrombotic complications in SLE may depend on the antigenic specificities of these Abs, alone or in combination.
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