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Sökning: id:"swepub:oai:DiVA.org:lnu-100287" > Complement depositi...

Complement deposition, C4d, on platelets is associated with vascular events in systemic lupus erythematosus

Svenungsson, Elisabet (författare)
Karolinska Institutet
Gustafsson, Johanna T. (författare)
Karolinska Institute,Karolinska University Hospital
Grosso, Giorgia (författare)
Karolinska Institutet,Karolinska Institute,Karolinska University Hospital
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Rossides, Marios (författare)
Karolinska Institutet,Karolinska Institute
Gunnarsson, Iva (författare)
Karolinska Institutet,Karolinska Institute,Karolinska University Hospital
Jensen-Urstad, Kerstin (författare)
Karolinska Institute,Stockholm South General Hospital
Larsson, Anders (författare)
Uppsala universitet,Klinisk kemi,Uppsala University, Sweden
Nilsson Ekdahl, Kristina (författare)
Linnaeus University,Uppsala universitet,Linnéuniversitetet,Institutionen för kemi och biomedicin (KOB),Uppsala University, Sweden,Linnaeus Ctr Biomat Chem, BMC,Klinisk immunologi,Linnaeus Center of Biomaterials Chemistry, Linnaeus University, Kalmar
Nilsson, Bo (författare)
Uppsala universitet,Klinisk immunologi,Uppsala University, Sweden
Bengtsson, Anders A. (författare)
Lund University,Lunds universitet,Lund SLE Research Group,Forskargrupper vid Lunds universitet,Lund University Research Groups
Lood, Christian (författare)
Univ Washington, USA,Department of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, USA
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 (creator_code:org_t)
2020-04-07
2020
Engelska.
Ingår i: Rheumatology. - : Oxford University Press. - 1462-0324 .- 1462-0332. ; 59:11, s. 3264-3274
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • Objective. Complement components, including C4d, can be found on activated platelets, a process associated with vascular disease in SLE. We investigated whether platelet C4d (PC4d) adds additional value to traditional and known lupus-associated risk factors when identifying SLE patients with vascular disease. Methods. This cross-sectional study included 308 well-characterized SLE patients and 308 matched general population controls. PC4d deposition was analysed using flow cytometry. Values >95% of controls were considered as PC4d positive (+). aPL were determined by Luminex, and the LA test was performed by DRVVT. History of vascular disease (composite and as separate outcomes) was defined at inclusion. Results. SLE patients had increased PC4d deposition as compared with population controls (50 vs 5%, P < 0.0001). PC4d+ positively associated with any vascular events, and separately with venous and cerebrovascular events, and also with all investigated aPL profiles. The association for any vascular event remained statistically significant after adjustment for traditional and SLE-associated risk factors (odds ratio: 2.3, 95% CI: 1.3, 4.3, P = 0.008). Compared with patients negative for both PC4d and LA, patients with double positivity were more likely to have vascular disease (odds ratio: 12.3, 95% CI: 5.4, 29.3; attributable proportion due to interaction 0.8, 95% CI: 0.4, 1.1) Conclusion. PC4d+ is associated with vascular events in SLE, independently of traditional and SLE-associated risk factors. Concurrent presence of PC4d and LA seem to interact to further increase the odds for vascular events. Prospective studies should examine whether the aPL/PC4d combination can improve prediction of vascular events in SLE and/or APS.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Reumatologi och inflammation (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Rheumatology and Autoimmunity (hsv//eng)

Nyckelord

systemic lupus erythematosus
antiphospholipid syndrome
C4d
vascular events
antibodies
risk factors
Immunologi
Immunology
antibodies
antiphospholipid syndrome
C4d
risk factors
systemic lupus erythematosus
vascular events

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