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Anti-rheumatic treatment is not associated with reduction of pentraxin 3 in rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis

Deyab, Gia; Hokstad, Ingrid; Whist, Jon Elling; Småstuen, Milada Cvancarova; Agewall, Stefan; Lyberg, Torstein; Bottazzi, Barbara; Meroni, Pier Luigi; Leone, Roberto; Hjeltnes, Gunnbjørg; Hollan, Ivana
Journal article, Peer reviewed
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Anti+rheumatic+treatment+is+not+assosiated+with+reduction+of+pentraxin+3+in+rheumatoid+arthritis%2C+psoriatic+artritis+and+ankylosing+spondylitis+%28PLOSONE%29.pdf (1.236Mb)
URI
http://hdl.handle.net/11250/2446683
Date
2017
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  • Artikler [61]
  • Publikasjoner fra Cristin - Sykehuset Innlandet HF [359]
Original version
10.1371/journal.pone.0169830
Abstract
Background

Pentraxin 3 is proposed to be a marker of inflammation and cardiovascular risk, but its role

in inflammatory rheumatic diseases (IRDs) is still uncertain. Therefore, we wanted to examine

if anti-rheumatic treatment reduced serum PTX3 (s-PTX3) levels in IRDs, and if s-PTX3

levels were related to other markers of inflammation and to endothelial function (EF).

Methods

We examined s-PTX3, EF and established inflammatory biomarkers in 114 IRD patients

from the PSARA study before and after 6 weeks and 6 months of treatment with methotrexate

(MTX) or anti-tumor necrosis factor alpha (anti-TNF) therapy with or without MTX comedication.

Results

s-PTX3 levels in all IRD diagnoses were above the upper limit of the reference range. In contrast

to established inflammatory markers, in particular CRP and ESR, s-PTX3 levels did not

change significantly after 6 weeks and 6 months of anti-rheumatic therapy. There was no difference

in change in s-PTX3 levels from baseline to 6 weeks and 6 months between MTX monotherapy and anti-TNF regimens. CRP, ESR and EF were not related to changes in s-

PTX3 neither in crude nor adjusted analyses.

Conclusion

IRD patients have increased s-PTX3 levels, which, in contrast to other inflammatory markers,

do not seem to improve within 6 months of therapy with MTX and/or anti-TNF. Thus, s-

PTX3 might reflect a persisting immune process, even a causal factor of inflammation, not

inhibited by the standard anti-rheumatic treatment. Furthermore, even though s-PTX3 is

thought to be a strong predictor of cardiovascular prognosis, it was not related to EF.
Journal
PLoS ONE

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