| Increased level of tumor necrosis factor-α in patients with antiphospholipid syndrome: marker not only of inflammation but also of the prothrombotic state. | |
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MedLine Citation:
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PMID: 20012959 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Connections between inflammation and thrombosis are intriguing, especially in a condition such as an antiphospholipid syndrome (APS), a disease characterized by immune-mediated thrombosis. Tumor necrosis factor alpha (TNF-α) is a cytokine which shares proinflammatory and prothrombotic actions, while a soluble form of interlukin-2 receptor (sIL-2R) is considered a typical marker of (auto)immune inflammation with not known direct links to thrombosis. The differences in the pathogenesis of APS as compared to other autoimmune diseases might be connected with different serum levels of both mediators. To answer this question, we studied 147 patients with systemic lupus erythematosus (SLE), 21 with SLE-like syndrome (SLE-LS), 20 with isolated APS (primary antiphospholipid syndrome, PAPS), and 32 healthy controls. Thirty-six patients from the SLE group fulfilled the updated APS criteria (secondary APS, SAPS). In comparison to healthy subjects, TNF-α concentration was increased in all patients, while sIL-2R rose significantly in the SLE group only. APS (both SAPS and PAPS) was characterized by the highest levels of TNF-α. Moreover, patients with lupus anticoagulant or elevated levels of IgG anticardiolipin or IgG anti-β(2)-glycoprotein I antibodies had higher TNF-α levels than patients without the presence of any type of antiphospholipid antibodies (aPL). In conclusion, the presence of aPL is associated with higher TNF-α level, whereas increased level of sIL-2R is rather connected with definite SLE where inflammatory processes prevail. It might be hypothesized that TNF-α plays a major role in pathogenesis of APS thrombotic phenomena. |
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Authors:
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Jakub Swadzba; Teresa Iwaniec; Jacek Musial |
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Publication Detail:
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Type: Journal Article Date: 2009-12-15 |
Journal Detail:
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Title: Rheumatology international Volume: 31 ISSN: 1437-160X ISO Abbreviation: Rheumatol. Int. Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-02-21 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8206885 Medline TA: Rheumatol Int Country: Germany |
Other Details:
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Languages: eng Pagination: 307-13 Citation Subset: IM |
Affiliation:
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Department of Medicine, Jagiellonian University Medical College, Krakow, Poland, swadzba@diag.pl. |
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