Dr VASILEIOS GEORGOPOULOS VASILEIOS.GEORGOPOULOS@NOTTINGHAM.AC.UK
RESEARCH FELLOW
Contribution of inflammation markers and quantitative sensory testing (QST) indices of central sensitisation to rheumatoid arthritis pain
Georgopoulos, Vasileios; Smith, Stephanie; McWilliams, Daniel F.; Ferguson, Eamonn; Wakefield, Richard; Platts, Dorothy; Ledbury, Susanne; Wilson, Deborah; Walsh, David A.
Authors
Dr STEPHANIE SMITH STEPHANIE.SMITH2@NOTTINGHAM.AC.UK
SENIOR RESEARCH FELLOW
Dr DANIEL MCWILLIAMS DAN.MCWILLIAMS@NOTTINGHAM.AC.UK
SENIOR RESEARCH FELLOW
Professor EAMONN FERGUSON eamonn.ferguson@nottingham.ac.uk
PROFESSOR OF HEALTH PSYCHOLOGY
Richard Wakefield
Dorothy Platts
Susanne Ledbury
Deborah Wilson
Professor DAVID WALSH david.walsh@nottingham.ac.uk
PROFESSOR OF RHEUMATOLOGY
Abstract
Background: Pain, the primary complaint in rheumatoid arthritis (RA), is multifaceted, and may be driven by inflammatory disease activity and central sensitisation. We aimed to ascertain what proportion of RA pain severity is explained by markers of inflammation and quantitative sensory testing (QST) indices of central sensitisation.
Methods: This was a cross-sectional analysis of data from individuals with clinically active RA. Pain severity was assessed using numerical rating scales and inflammation via 28-joint Disease Activity Score (DAS28) and Ultrasound (Greyscale, Power Doppler). Pain sensitivity was assessed by 'static' (tibialis anterior or brachioradialis pressure pain detection threshold-PPT-TA/PPT-BR) and 'dynamic' (temporal summation-TS, conditioned pain modulation-CPM) QST. Bivariate associations used Spearman's correlation coefficients, and multivariable linear regression models determined relative contributions to pain severity.
Results: In bivariate analyses of N = 96 (age 65 ± 10y, 77% females) people with RA, pain severity was significantly associated with inflammation indices (r = 0.20 to 0.55), and CPM (r=-0.26). In multivariable models that included TS, CPM, age, sex, and body mass index, inflammation indices remained significantly associated with pain severity. Multivariable models explained 22 to 27% of pain variance. Heterogeneity was apparent for associations with pain between subscores for pain now, strongest or average over the past 4-weeks.
Conclusions: In individuals with clinically active RA, markers of inflammatory disease activity best explain RA pain with only marginal contributions from QST indices of central sensitisation. Although inflammation plays a key role in the experience of RA pain, the greater proportion of pain severity remains unexplained by DAS28 and ultrasound indices of inflammation.
Citation
Georgopoulos, V., Smith, S., McWilliams, D. F., Ferguson, E., Wakefield, R., Platts, D., Ledbury, S., Wilson, D., & Walsh, D. A. (2024). Contribution of inflammation markers and quantitative sensory testing (QST) indices of central sensitisation to rheumatoid arthritis pain. Arthritis Research and Therapy, 26(1), Article 175. https://doi.org/10.1186/s13075-024-03407-5
Journal Article Type | Article |
---|---|
Acceptance Date | Sep 24, 2024 |
Online Publication Date | Oct 8, 2024 |
Publication Date | Oct 8, 2024 |
Deposit Date | Oct 8, 2024 |
Publicly Available Date | Oct 8, 2024 |
Journal | Arthritis Research & Therapy |
Print ISSN | 1478-6354 |
Electronic ISSN | 1478-6362 |
Publisher | BioMed Central |
Peer Reviewed | Peer Reviewed |
Volume | 26 |
Issue | 1 |
Article Number | 175 |
DOI | https://doi.org/10.1186/s13075-024-03407-5 |
Keywords | Rheumatoid arthritis; Disease activity; Inflammation; Central sensitisation; Quantitative sensory testing; Pain |
Public URL | https://nottingham-repository.worktribe.com/output/40551601 |
Publisher URL | https://link.springer.com/article/10.1186/s13075-024-03407-5?utm_source=rct_congratemailt&utm_medium=email&utm_campaign=oa_20241008&utm_content=10.1186%2Fs13075-024-03407-5 |
Additional Information | Received: 18 June 2024; Accepted: 24 September 2024; First Online: 8 October 2024; : ; : Ethical approval were obtained from the North of Scotland Research Ethics Committee of the Health Research Authority, United Kingdom (REC: 20/NS/0036) and the University of Nottingham (Sponsor).; : Not applicable.; : Daniel McWilliams has grant support from Eli Lilly and Company and Union Chimique Belge; and active research collaborations with Orion Pharma and GSK. David Walsh has grant support from Eli Lilly and Company, Pfizer Inc., Union Chimique Belge, Orion Pharma, and GlaxoSmithKline plc. Other authors have no conflict of interests to declare. |
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