Abstract
Objective
There is debate as to the role of inflammatory disease activity in the etiology of rheumatoid arthritis (RA)–related fatigue. We undertook this study to determine the relationship of fatigue to disease activity by examining pathways associated with change in fatigue in subjects starting anti–tumor necrosis factor (anti-TNF) therapy for the first time.
Methods
Participants who had been recruited to the British Society for Rheumatology Biologics Register for RA provided information on fatigue (Short Form 36 [SF-36] vitality scale) and other health status variables at the start of anti-TNF therapy and 6 months later. The Disease Activity Score in 28 joints (DAS28) and inflammation (erythrocyte sedimentation rate [ESR]/C-reactive protein [CRP] level) were also reported. A path analysis model comprising changes in fatigue, pain, disease activity, disability, and mental health, along with effects of sex and a history of depression, was used to examine those with high levels of fatigue at baseline (score of ≤12.5 units on the SF-36 vitality scale). The DAS28 was substituted for ESR/CRP to delineate the specific role of inflammation.
Results
With a total of 2,652 participants, we identified a well-fitting model (χ2 = 0.18, P = 0.98) accounting for 40% of the variance in fatigue change. There was no direct pathway from change in inflammation to change in fatigue; instead, significant pathways to change in fatigue were observed from changes in disease activity, pain, mental health, and disability, along with effects of sex and a history of depression. A total of 82% of the effect of change in disease activity was indirect, of which ∼50% was mediated through a change in pain.
Conclusion
Improvements in fatigue do not appear to be driven by inflammatory disease activity; instead, they appear to result indirectly from improvements in pain. Additional significant pathways through disability and mental health suggest potentially modifiable factors that could be targeted to improve clinically important levels of fatigue.
There is debate as to the role of inflammatory disease activity in the etiology of rheumatoid arthritis (RA)–related fatigue. We undertook this study to determine the relationship of fatigue to disease activity by examining pathways associated with change in fatigue in subjects starting anti–tumor necrosis factor (anti-TNF) therapy for the first time.
Methods
Participants who had been recruited to the British Society for Rheumatology Biologics Register for RA provided information on fatigue (Short Form 36 [SF-36] vitality scale) and other health status variables at the start of anti-TNF therapy and 6 months later. The Disease Activity Score in 28 joints (DAS28) and inflammation (erythrocyte sedimentation rate [ESR]/C-reactive protein [CRP] level) were also reported. A path analysis model comprising changes in fatigue, pain, disease activity, disability, and mental health, along with effects of sex and a history of depression, was used to examine those with high levels of fatigue at baseline (score of ≤12.5 units on the SF-36 vitality scale). The DAS28 was substituted for ESR/CRP to delineate the specific role of inflammation.
Results
With a total of 2,652 participants, we identified a well-fitting model (χ2 = 0.18, P = 0.98) accounting for 40% of the variance in fatigue change. There was no direct pathway from change in inflammation to change in fatigue; instead, significant pathways to change in fatigue were observed from changes in disease activity, pain, mental health, and disability, along with effects of sex and a history of depression. A total of 82% of the effect of change in disease activity was indirect, of which ∼50% was mediated through a change in pain.
Conclusion
Improvements in fatigue do not appear to be driven by inflammatory disease activity; instead, they appear to result indirectly from improvements in pain. Additional significant pathways through disability and mental health suggest potentially modifiable factors that could be targeted to improve clinically important levels of fatigue.
Original language | English |
---|---|
Pages (from-to) | 2303-2310 |
Number of pages | 8 |
Journal | Arthritis & Rheumatology |
Volume | 67 |
Issue number | 9 |
Early online date | 26 Aug 2015 |
DOIs | |
Publication status | Published - Sept 2015 |
Bibliographical note
Funded by:The Institute of Applied Health Sciences, University of Aberdeen
The British Society for Rheumatology Biologics Register for Rheumatoid Arthritis
British Society for Rheumatology to the University of Manchester
Schering-Plough
Wyeth Laboratories
Abbott Laboratories
Amgen
Fingerprint
Dive into the research topics of 'Determining Pathways to Improvements in Fatigue in Rheumatoid Arthritis: Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis'. Together they form a unique fingerprint.Profiles
-
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
-
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