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.
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 language | English |
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Pages (from-to) | 922-926 |
Number of pages | 5 |
Journal | Arthritis Care & Research |
Volume | 68 |
Issue number | 7 |
Early online date | 23 Jun 2016 |
DOIs | |
Publication status | Published - Jul 2016 |
Bibliographical note
ROLE OF THE STUDY SPONSORThe 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.
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Gareth Jones
- School of Medicine, Medical Sciences & Nutrition, Applied Health Sciences - Professor in Epidemiology
- School of Medicine, Medical Sciences & Nutrition, MRC/Versus Arthritis Centre for Musculoskeletal Health and Work
- Institute of Applied Health Sciences
- School of Medicine, Medical Sciences & Nutrition, Aberdeen Centre for Arthritis and Musculoskeletal Health (ACAMH)
- School of Medicine, Medical Sciences & Nutrition, Epidemiology Group
Person: Academic
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Gary Macfarlane
- School of Medicine, Medical Sciences & Nutrition, Applied Health Sciences - Clinical Chair in Epidemiology
- School of Medicine, Medical Sciences & Nutrition, MRC/Versus Arthritis Centre for Musculoskeletal Health and Work
- School of Medicine, Medical Sciences & Nutrition, Aberdeen Centre for Arthritis and Musculoskeletal Health (ACAMH)
- School of Medicine, Medical Sciences & Nutrition, Epidemiology Group
Person: Clinical Academic