2013年10月
Neuropsychiatric systemic lupus erythematosus: Pathophysiology and the future of treatment
International Journal of Clinical Rheumatology
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- 巻
- 8
- 号
- 5
- 開始ページ
- 585
- 終了ページ
- 595
- 記述言語
- 英語
- 掲載種別
- 書評論文,書評,文献紹介等
- DOI
- 10.2217/ijr.13.48
Systemic lupus erythematosus (SLE) is characterized by the presence of several autoantibodies, including anti-dsDNA. Among types of SLE, neuropsychiatric (NP)-SLE accounts for significant morbidity and mortality. Cerebrovascular disease, which could account for most of the serious permanent neurological damage, is a common presentation of NP-SLE. The pathophysiology of NP-SLE involves several factors, including vasculitis, thrombosis, and inflammation and/or apoptosis of neuronal and glial cells. The current treatment strategy is immunosuppressive therapy, which is occasionally insufficient for patients with NP-SLE. Recent studies have revealed that autoantibodies, such as anti-NR2, pass from the peripheral blood to the brain through the blood-brain barrier, cross-react with human brain tissue and cause increased intracellular Ca2+ in SLE. Regulating blood-brain barrier permeability, inhibiting autoantibody deposition in tissues and modulating intracellular Ca2+ may be new concepts for the treatment with NP-SLE. © 2013 Future Medicine Ltd.
- リンク情報
- ID情報
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- DOI : 10.2217/ijr.13.48
- ISSN : 1758-4272
- ISSN : 1758-4280
- SCOPUS ID : 84885576807