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Serum pentraxin 3 levels are negatively associated with carotid intima media thickness in non-obese rheumatoid arthritis patients.

Authors :
Kahlow BS
Petisco R
Skare TL
Goeldner I
Nisihara RM
Messias-Reason IJ
Source :
International journal of cardiology [Int J Cardiol] 2016 Oct 15; Vol. 221, pp. 298-301. Date of Electronic Publication: 2016 Jul 06.
Publication Year :
2016

Abstract

Background: Pentraxin-3 (PTX3) is a long pentraxin that is supposed to participate in the inflammatory process and in atherosclerosis.<br />Aim: To study PTX3 serum levels in rheumatoid arthritis (RA) patients to know if its serum levels may reflect disease activity and/or subclinical atherosclerosis.<br />Methods: PTX3 and carotid intima media thickness (IMT) were studied in 85 RA patients (83.5% females, median age of 59years old, median disease duration of 13years) along with its demographic, clinical, serological and lipid profile. For comparison PTX3 was measured in 85 healthy volunteers.<br />Results: PTX3 levels in RA patients were similar to controls (p=0.21) and did not correlate with inflammatory activity measured by ESR (p=0.39) CRP (p=0.18) and DAS28 (p=0.67). Serum PTX3 levels were higher in nonobese RA patients than in obese (BMI vs PTX3 with rho=-0.27; 95%IC=-0.46 to -0.06; p=0.009). In non-obese patients, PTX3 correlated negatively with carotid IMT (rho=-0.40; 95%IC=-0.66 to -0.06; p=0.01) but not in the obese ones (p=0.26). In the obese RA patients there was a negative correlation between PTX3 levels and LDL/HDL ratio (Rho=-0.29; 95%IC=-0.53-0.01; p=0.03).<br />Conclusions: PTX3 levels do not reflect inflammatory process in RA. However, it exerts a protective role in the process of atherogenesis in non-obese RA patients.<br /> (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Details

Language :
English
ISSN :
1874-1754
Volume :
221
Database :
MEDLINE
Journal :
International journal of cardiology
Publication Type :
Academic Journal
Accession number :
27404695
Full Text :
https://doi.org/10.1016/j.ijcard.2016.06.175