Examining Changes in Central and Peripheral Pain as Mediates of Fatigue Improvement: Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis

Katie L. Druce, Gareth T. Jones, Gary J. Macfarlane, Neil Basu

Research output: Contribution to journalArticle

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3 Downloads (Pure)

Abstract

Objective
Following anti-TNF therapy, improvements in rheumatoid Arthritis (RA) fatigue are driven by reductions in pain. However, therapies may modify central and peripheral pain. This study sought to examine the hypothesis that reductions in fatigue after anti-TNF therapy reflect changes in central, not peripheral, pain mechanisms.

Methods
Data of patients with severe baseline fatigue (SF36 Vitality ≤12.5; n=2652), recruited to the British Society for Rheumatology Biologics Register for RA for commencing anti-TNF therapies between October 2000 and November 2008, were used. Data of interest comprised change over 6-months in fatigue, pain (SF36 Bodily Pain) and disease activity constituents (DAS28; ESR, global health, swollen and tender joints). Principal components factor analysis with varimax rotation determined latent variables of symptom change; variables were accepted provided they had eigenvalues≥1.

Results
Six factors were identified, of which two met acceptance criteria (eigenvalues 2.39 and 1.14, respectively). Following rotation, loadings indicated that factor 1 comprised markers of peripheral inflammation; change in ESR, swollen and tender joints, and global health. This distinct loading led to factor 1 being labelled ‘peripheral inflammation'. Conversely, factor 2 comprised change in pain, fatigue and global health and an absence of peripheral inflammation markers, and was therefore labelled as ‘central inflammation'.

Conclusions
Following anti-TNF therapies, reductions in fatigue and pain appear to reflect improvements in central, rather than peripheral, inflammation. Therefore, for those seeking to treat fatigue via pain mechanisms, improvements may be maximised by the application of treatment modalities which effectively target central mechanisms.
Original languageEnglish
Pages (from-to)922-926
Number of pages5
JournalArthritis Care & Research
Volume68
Issue number7
Early online date23 Jun 2016
DOIs
Publication statusPublished - Jul 2016

Cite this

@article{176e88e7bee04aee9156d49f530f7fef,
title = "Examining Changes in Central and Peripheral Pain as Mediates of Fatigue Improvement: Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis",
abstract = "ObjectiveFollowing anti-TNF therapy, improvements in rheumatoid Arthritis (RA) fatigue are driven by reductions in pain. However, therapies may modify central and peripheral pain. This study sought to examine the hypothesis that reductions in fatigue after anti-TNF therapy reflect changes in central, not peripheral, pain mechanisms.MethodsData of patients with severe baseline fatigue (SF36 Vitality ≤12.5; n=2652), recruited to the British Society for Rheumatology Biologics Register for RA for commencing anti-TNF therapies between October 2000 and November 2008, were used. Data of interest comprised change over 6-months in fatigue, pain (SF36 Bodily Pain) and disease activity constituents (DAS28; ESR, global health, swollen and tender joints). Principal components factor analysis with varimax rotation determined latent variables of symptom change; variables were accepted provided they had eigenvalues≥1.ResultsSix factors were identified, of which two met acceptance criteria (eigenvalues 2.39 and 1.14, respectively). Following rotation, loadings indicated that factor 1 comprised markers of peripheral inflammation; change in ESR, swollen and tender joints, and global health. This distinct loading led to factor 1 being labelled ‘peripheral inflammation'. Conversely, factor 2 comprised change in pain, fatigue and global health and an absence of peripheral inflammation markers, and was therefore labelled as ‘central inflammation'.ConclusionsFollowing anti-TNF therapies, reductions in fatigue and pain appear to reflect improvements in central, rather than peripheral, inflammation. Therefore, for those seeking to treat fatigue via pain mechanisms, improvements may be maximised by the application of treatment modalities which effectively target central mechanisms.",
author = "Druce, {Katie L.} and Jones, {Gareth T.} and Macfarlane, {Gary J.} and Neil Basu",
note = "ROLE OF THE STUDY SPONSOR The British Society for Rheumatology Biologics Register for Rheumatoid Arthritis data collection, management, and analysis service, funded by UK pharmaceutical companies, is overseen by The University of Manchester. The principal investigators and their team had full academic freedom and were able to work independently of pharmaceutical industry influence. All decisions concerning analyses, interpretation, and publication were made autonomously of any industrial contribution.",
year = "2016",
month = "7",
doi = "10.1002/acr.22803",
language = "English",
volume = "68",
pages = "922--926",
journal = "Arthritis Care & Research",
issn = "0893-7524",
publisher = "Wiley-Blackwell",
number = "7",

}

TY - JOUR

T1 - Examining Changes in Central and Peripheral Pain as Mediates of Fatigue Improvement

T2 - Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis

AU - Druce, Katie L.

AU - Jones, Gareth T.

AU - Macfarlane, Gary J.

AU - Basu, Neil

N1 - ROLE OF THE STUDY SPONSOR The British Society for Rheumatology Biologics Register for Rheumatoid Arthritis data collection, management, and analysis service, funded by UK pharmaceutical companies, is overseen by The University of Manchester. The principal investigators and their team had full academic freedom and were able to work independently of pharmaceutical industry influence. All decisions concerning analyses, interpretation, and publication were made autonomously of any industrial contribution.

PY - 2016/7

Y1 - 2016/7

N2 - ObjectiveFollowing anti-TNF therapy, improvements in rheumatoid Arthritis (RA) fatigue are driven by reductions in pain. However, therapies may modify central and peripheral pain. This study sought to examine the hypothesis that reductions in fatigue after anti-TNF therapy reflect changes in central, not peripheral, pain mechanisms.MethodsData of patients with severe baseline fatigue (SF36 Vitality ≤12.5; n=2652), recruited to the British Society for Rheumatology Biologics Register for RA for commencing anti-TNF therapies between October 2000 and November 2008, were used. Data of interest comprised change over 6-months in fatigue, pain (SF36 Bodily Pain) and disease activity constituents (DAS28; ESR, global health, swollen and tender joints). Principal components factor analysis with varimax rotation determined latent variables of symptom change; variables were accepted provided they had eigenvalues≥1.ResultsSix factors were identified, of which two met acceptance criteria (eigenvalues 2.39 and 1.14, respectively). Following rotation, loadings indicated that factor 1 comprised markers of peripheral inflammation; change in ESR, swollen and tender joints, and global health. This distinct loading led to factor 1 being labelled ‘peripheral inflammation'. Conversely, factor 2 comprised change in pain, fatigue and global health and an absence of peripheral inflammation markers, and was therefore labelled as ‘central inflammation'.ConclusionsFollowing anti-TNF therapies, reductions in fatigue and pain appear to reflect improvements in central, rather than peripheral, inflammation. Therefore, for those seeking to treat fatigue via pain mechanisms, improvements may be maximised by the application of treatment modalities which effectively target central mechanisms.

AB - ObjectiveFollowing anti-TNF therapy, improvements in rheumatoid Arthritis (RA) fatigue are driven by reductions in pain. However, therapies may modify central and peripheral pain. This study sought to examine the hypothesis that reductions in fatigue after anti-TNF therapy reflect changes in central, not peripheral, pain mechanisms.MethodsData of patients with severe baseline fatigue (SF36 Vitality ≤12.5; n=2652), recruited to the British Society for Rheumatology Biologics Register for RA for commencing anti-TNF therapies between October 2000 and November 2008, were used. Data of interest comprised change over 6-months in fatigue, pain (SF36 Bodily Pain) and disease activity constituents (DAS28; ESR, global health, swollen and tender joints). Principal components factor analysis with varimax rotation determined latent variables of symptom change; variables were accepted provided they had eigenvalues≥1.ResultsSix factors were identified, of which two met acceptance criteria (eigenvalues 2.39 and 1.14, respectively). Following rotation, loadings indicated that factor 1 comprised markers of peripheral inflammation; change in ESR, swollen and tender joints, and global health. This distinct loading led to factor 1 being labelled ‘peripheral inflammation'. Conversely, factor 2 comprised change in pain, fatigue and global health and an absence of peripheral inflammation markers, and was therefore labelled as ‘central inflammation'.ConclusionsFollowing anti-TNF therapies, reductions in fatigue and pain appear to reflect improvements in central, rather than peripheral, inflammation. Therefore, for those seeking to treat fatigue via pain mechanisms, improvements may be maximised by the application of treatment modalities which effectively target central mechanisms.

U2 - 10.1002/acr.22803

DO - 10.1002/acr.22803

M3 - Article

VL - 68

SP - 922

EP - 926

JO - Arthritis Care & Research

JF - Arthritis Care & Research

SN - 0893-7524

IS - 7

ER -