Determining Pathways to Improvements in Fatigue in Rheumatoid Arthritis

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

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

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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.
Original languageEnglish
Pages (from-to)2303-2310
Number of pages8
JournalArthritis & Rheumatology
Volume67
Issue number9
Early online date26 Aug 2015
DOIs
Publication statusPublished - Sep 2015

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Biological Products
Fatigue
Rheumatoid Arthritis
Pain
Mental Health
Blood Sedimentation
Inflammation
C-Reactive Protein
Necrosis
Joints
Depression
Health Status

Cite this

@article{fa79ef4dfbf04c0c98c85764a261ca5a,
title = "Determining Pathways to Improvements in Fatigue in Rheumatoid Arthritis: Results From the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis",
abstract = "ObjectiveThere 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.MethodsParticipants 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.ResultsWith 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.ConclusionImprovements 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.",
author = "Druce, {Katie L} and Jones, {Gareth T} and Macfarlane, {Gary J} and Neil Basu",
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",
year = "2015",
month = "9",
doi = "10.1002/art.39238",
language = "English",
volume = "67",
pages = "2303--2310",
journal = "Arthritis & Rheumatology",
issn = "2326-5191",
publisher = "Wiley",
number = "9",

}

TY - JOUR

T1 - Determining Pathways to Improvements in Fatigue in Rheumatoid Arthritis

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 - 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

PY - 2015/9

Y1 - 2015/9

N2 - ObjectiveThere 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.MethodsParticipants 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.ResultsWith 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.ConclusionImprovements 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.

AB - ObjectiveThere 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.MethodsParticipants 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.ResultsWith 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.ConclusionImprovements 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.

U2 - 10.1002/art.39238

DO - 10.1002/art.39238

M3 - Article

VL - 67

SP - 2303

EP - 2310

JO - Arthritis & Rheumatology

JF - Arthritis & Rheumatology

SN - 2326-5191

IS - 9

ER -