Rheumatology Advance Access published online on January 17, 2006
Rheumatology, doi:10.1093/rheumatology/kel010
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1 Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Japan
* To whom correspondence should be addressed. Objectives. To determine whether autoantibodies to two platelet-specific antigens, glycoprotein IIb/IIIa (GPIIb/IIIa) and thrombopoietin receptor (TPOR), contribute to thrombocytopenia in patients with systemic lupus erythematosus (SLE). Methods. Circulating B cells producing anti-GPIIb/IIIa antibodies and serum anti-TPOR antibodies were measured in 32 SLE patients with thrombocytopenia, 30 SLE patients without thrombocytopenia, 92 patients with idiopathic thrombocytopenia and 60 healthy controls. The megakaryocyte density in bone-marrow smears from all the patients with thrombocytopenia was evaluated. Results. Anti-GPIIb/IIIa and anti-TPOR antibody responses were more frequent in SLE patients with thrombocytopenia than in those without thrombocytopenia (88 vs 17%, P<0.0001; and 22% vs 0%, P=0.01, respectively). The frequencies of these platelet-related antibodies were comparable between SLE patients with thrombocytopenia and patients with idiopathic thrombocytopenia. Twenty-nine (91%) SLE patients with thrombocytopenia had either anti-GPIIb/IIIa or anti-TPOR antibody, and six had both. In SLE patients with thrombocytopenia, the anti-TPOR-positive patients had significantly higher frequencies of megakaryocytic hypoplasia and poorer therapeutic responses to corticosteroids and intravenous immunoglobulin than did the anti-TPOR-negative patients, most of whom had the anti-GPIIb/IIIa antibody alone. Conclusions. Anti-GPIIb/IIIa and anti-TPOR antibodies are major factors contributing to SLE-associated thrombocytopenia, but the clinical presentations associated with these autoantibodies are different.
Received October 17, 2005
Accepted December 8, 2005
Concise Report
Two types of autoantibody-mediated thrombocytopenia in patients with systemic lupus erythematosus
M. Kuwana 1 *,
J. Kaburaki 2,
Y. Okazaki 1,
H. Miyazaki 3,
and
Y. Ikeda 4
2 Department of Internal Medicine, Tokyo Electric Power Company Hospital, Tokyo
3 Kirin Brewery Company Ltd., Takasaki, Japan
4 Division of Haematology, Department of Internal Medicine, Keio University School of Medicine, Japan
M. Kuwana, E-mail: kuwanam{at}sc.itc.keio.ac.jp
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