Evidence map›Paper›PMID 39380043›Full record

ArticleArthritis research & therapy2024

Contribution of inflammation markers and quantitative sensory testing (QST) indices of central sensitisation to rheumatoid arthritis pain.

Vasileios Georgopoulos, Stephanie Smith, Daniel F McWilliams, Eamonn Ferguson, Richard Wakefield, Dorothy Platts, Susanne Ledbury, Deborah Wilson, David A Walsh

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Vasileios GeorgopoulosDivision of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Nottingham, UK. vasileios.georgopoulos@nottingham.ac.uk.
Stephanie SmithDivision of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Nottingham, UK.
Daniel F McWilliamsDivision of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Nottingham, UK.
Eamonn FergusonPain Centre Versus Arthritis, University of Nottingham, Nottingham, UK.
Richard WakefieldLeeds Institute of Rheumatic and Musculoskeletal Medicine and NIHR Leeds Biomedical Research Centre, University of Leeds, Leeds, UK.
Dorothy PlattsIndependent Consultant, Nottingham, UK.
Susanne LedburyIndependent Consultant, Nottingham, UK.
Deborah WilsonRheumatology, Sherwood Forest Hospitals NHS Foundation Trust, Sutton-in-Ashfield, UK.
David A WalshDivision of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Nottingham, UK.

Funding

Pfizer UK 51708879Versus Arthritis 22462
6 · The paper itself

Abstract

backgroundPain, 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.

methodsThis 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.

resultsIn 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.

conclusionsIn 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.

Indexed as

Arthritis, RheumatoidBiomarkersCentral Nervous System SensitizationInflammationPain MeasurementPain ThresholdAgedCross-Sectional StudiesFemaleHumansMaleMiddle AgedPainSeverity of Illness IndexBiomarkersCentral sensitisationDisease activityInflammationPainQuantitative sensory testingRheumatoid arthritis

Identifiers

PMID39380043
PMCPMC11460083

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.