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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 05650naa a2200493 4500 | |
| 001 | oai:DiVA.org:lnu-32678 | |
| 003 | SwePub | |
| 008 | 140307s2013 | |||||||||||000 ||eng| | |
| 009 | oai:DiVA.org:uu-220567 | |
| 009 | oai:lup.lub.lu.se:c157d69f-2124-48dc-b514-3b14105f111e | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-326782 URI |
| 024 | 7 | a https://doi.org/10.1186/ar43992 DOI |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2205672 URI |
| 024 | 7 | a https://lup.lub.lu.se/record/c157d69f-2124-48dc-b514-3b14105f111e2 URI |
| 040 | a (SwePub)lnud (SwePub)uud (SwePub)lu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Bäck, Jennieu Uppsala universitet,Institutionen för immunologi, genetik och patologi,Bo NiIsson,Uppsala University4 aut0 (Swepub:uu)jenba617 |
| 245 | 1 0 | a Contact activation products are new potential biomarkers to evaluate the risk of thrombotic events in systemic lupus erythematosus |
| 264 | 1 | b Springer Science and Business Media LLC,c 2013 |
| 338 | a print2 rdacarrier | |
| 520 | a Introduction: Patients with systemic lupus erythematosus (SLE) have persistent platelet activation and an increased risk of thrombotic events, which cannot be accounted for by traditional cardiovascular risk factors. Factor (F)XII has a potentially important role in thrombus formation and is triggered by activated platelets. We therefore asked whether the contact system is involved in inflammation and vascular disease (VD) in SLE. Methods: Fibrin clots were incubated with purified FXII or whole blood, and the activation and regulation of FXII were studied. Plasma from SLE patients with (n = 31) or without (n = 38) previous VD and from matched healthy controls (n = 68) were analyzed for the presence of complexes formed between contact system enzymes and antithrombin (AT) or C1 inhibitor (C1INH) and evaluated with regard to clinical data and laboratory parameters. Results: Fibrin clots elicited FXII activation and acted as co-factors for AT. In clotting plasma, the levels of FXIIa-AT increased, and FXIIa-C1INH decreased. A similar reciprocal relationship existed in SLE patients. FXIIa-AT was elevated in the SLE patients with a history of VD, while the corresponding levels of factor FXIIa-C1INH were significantly decreased. FXIIa-AT correlated strongly with platelet parameters. The odds ratio for VD among the SLE patients was 8.9 if they had low levels of FXIIa-C1INH, 6.1 for those with high levels of FXIIa-AT, and increased to 23.4 for those with both decreased levels of FXIIa-C1INH and increased levels of FXIIa-AT. Conclusions: Activation of FXII is elicited by fibrin during thrombotic reactions in vitro and in vivo, and fibrin acts as a heparin-like co-factor and regulates AT. Patients with SLE had altered levels of FXIIa-serpin complexes, supporting that the contact system is involved in this disease. FXIIa-serpin complexes are strongly associated with previous VD in SLE patients, suggesting that these complexes are potential biomarkers for monitoring and assessing the risk of thrombotic events in SLE. | |
| 650 | 7 | a NATURVETENSKAPx Biologix Immunologi0 (SwePub)106052 hsv//swe |
| 650 | 7 | a NATURAL SCIENCESx Biological Sciencesx Immunology0 (SwePub)106052 hsv//eng |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng |
| 653 | a Biomedicinsk vetenskap | |
| 653 | a Biomedical Sciences | |
| 700 | 1 | a Lood, Christianu Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Skåne University Hospital4 aut0 (Swepub:lu)med-ctl |
| 700 | 1 | a Bengtsson, Anders A.u Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Lund SLE Research Group,Forskargrupper vid Lunds universitet,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)reum-abe |
| 700 | 1 | a Nilsson Ekdahl, Kristinau Linnaeus University,Uppsala universitet,Linnéuniversitetet,Institutionen för kemi och biomedicin (KOB),Uppsala University,Linnaeus Ctr Biomat Chem, BMC,Institutionen för immunologi, genetik och patologi,Bo Nilsson4 aut0 (Swepub:uu)krisnil |
| 700 | 1 | a Nilsson, Bou Uppsala universitet,Institutionen för immunologi, genetik och patologi,Bo Nilsson,Uppsala University4 aut0 (Swepub:uu)bonils |
| 710 | 2 | a Uppsala universitetb Institutionen för immunologi, genetik och patologi4 org |
| 773 | 0 | t Arthritis Research & Therapyd : Springer Science and Business Media LLCg 15:6q 15:6x 1478-6362x 1478-6354 |
| 856 | 4 | u https://doi.org/10.1186/ar4399y Fulltext |
| 856 | 4 | u https://arthritis-research.biomedcentral.com/track/pdf/10.1186/ar4399 |
| 856 | 4 | u https://uu.diva-portal.org/smash/get/diva2:706380/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print |
| 856 | 4 | u http://dx.doi.org/10.1186/ar4399x freey FULLTEXT |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-32678 |
| 856 | 4 8 | u https://doi.org/10.1186/ar4399 |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-220567 |
| 856 | 4 8 | u https://lup.lub.lu.se/record/c157d69f-2124-48dc-b514-3b14105f111e |
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