TY - JOUR
T1 - Patients Receiving Anti-Tumour Necrosis Factor Therapies Experience Clinically Important Improvements in Rheumatoid Arthritis Related Fatigue
T2 - Results from the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis
AU - Druce, Katie
AU - Jones, Gareth
AU - Macfarlane, Gary
AU - Basu, Neil
PY - 2014
Y1 - 2014
N2 - Background – Pro-inflammatory cytokines associated with the development and progression of rheumatoid arthritis (RA) have been linked to fatigue. According to randomised controlled trials, anti-TNF therapy results in modest improvements in fatigue, however no such trials have addressed this symptom as the primary research question and therefore have not specifically evaluated response in those presenting with clinically relevant fatigue. This study aimed to determine changes in fatigue and predictors of its improvement, six months after initiating Anti-TNF therapy, in a cohort of RA patients with high baseline fatigue.
Methods - Participants recruited to a long-term observational cohort study, the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis (BSRBR-RA), between October 2000 and November 2008, provided information on fatigue using the SF 36 Vitality domain (scored 0-100). The prevalence of high fatigue – SF36 Vitality ≤12.5, defined using the 5th percentile of general population data - was calculated at baseline, and changes in fatigue examined six months subsequently. Changes were considered as a) absolute values and b) improvement from high fatigue to low fatigue (SF36 Vitality >12.5). In those with high baseline fatigue, a comprehensive set of putative predictors of fatigue improvement, were evaluated first individually and then considered within a multivariable logistic regression model.
Results - High fatigue at baseline was common (38.8%) among the 6835 subjects (Etanercept n=2441, Infliximab n=1994, Adalimumab n=2400). Of those with high fatigue (n=2652), 70% reported clinically relevant improvements (≥10 SF 36 Vitality units), with a mean improvement of 22.5 units at six month follow up. Further, 66% moved to the “low fatigue” category by follow up and reported a mean change of three times the minimum clinically relevant improvement (32.9 units). Baseline independent predictors of improvement were: female sex (OR 1.3, 95%CI 1.1-1.7), not being unemployed due to ill-health (1.5,1.2-1.7), low disability (1.2,1.0-1.5), rheumatoid factor positive (1.2,1.0-1.4), not using steroids (1.2,1.0-1.5), no history of hypertension (1.4,1.1-1.6) or depression (1.3,1.1-1.5) and good current mental health (1.4,1.2-1.7). Participants who were positive for ≥6 of these variables reported the largest absolute improvement in fatigue, 75% of whom moved to the “low fatigue” category by follow up.
Conclusions – These results demonstrate improvement in fatigue is common and substantial, six months after commencing biologics therapy, in those who have clinically relevant fatigue at baseline. Further, in patients with high baseline fatigue, a number of clinical and psycho-social baseline factors can be used to predict the largest improvement, supporting future stratified approaches to RA related fatigue management.
AB - Background – Pro-inflammatory cytokines associated with the development and progression of rheumatoid arthritis (RA) have been linked to fatigue. According to randomised controlled trials, anti-TNF therapy results in modest improvements in fatigue, however no such trials have addressed this symptom as the primary research question and therefore have not specifically evaluated response in those presenting with clinically relevant fatigue. This study aimed to determine changes in fatigue and predictors of its improvement, six months after initiating Anti-TNF therapy, in a cohort of RA patients with high baseline fatigue.
Methods - Participants recruited to a long-term observational cohort study, the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis (BSRBR-RA), between October 2000 and November 2008, provided information on fatigue using the SF 36 Vitality domain (scored 0-100). The prevalence of high fatigue – SF36 Vitality ≤12.5, defined using the 5th percentile of general population data - was calculated at baseline, and changes in fatigue examined six months subsequently. Changes were considered as a) absolute values and b) improvement from high fatigue to low fatigue (SF36 Vitality >12.5). In those with high baseline fatigue, a comprehensive set of putative predictors of fatigue improvement, were evaluated first individually and then considered within a multivariable logistic regression model.
Results - High fatigue at baseline was common (38.8%) among the 6835 subjects (Etanercept n=2441, Infliximab n=1994, Adalimumab n=2400). Of those with high fatigue (n=2652), 70% reported clinically relevant improvements (≥10 SF 36 Vitality units), with a mean improvement of 22.5 units at six month follow up. Further, 66% moved to the “low fatigue” category by follow up and reported a mean change of three times the minimum clinically relevant improvement (32.9 units). Baseline independent predictors of improvement were: female sex (OR 1.3, 95%CI 1.1-1.7), not being unemployed due to ill-health (1.5,1.2-1.7), low disability (1.2,1.0-1.5), rheumatoid factor positive (1.2,1.0-1.4), not using steroids (1.2,1.0-1.5), no history of hypertension (1.4,1.1-1.6) or depression (1.3,1.1-1.5) and good current mental health (1.4,1.2-1.7). Participants who were positive for ≥6 of these variables reported the largest absolute improvement in fatigue, 75% of whom moved to the “low fatigue” category by follow up.
Conclusions – These results demonstrate improvement in fatigue is common and substantial, six months after commencing biologics therapy, in those who have clinically relevant fatigue at baseline. Further, in patients with high baseline fatigue, a number of clinical and psycho-social baseline factors can be used to predict the largest improvement, supporting future stratified approaches to RA related fatigue management.
M3 - Abstract
SN - 1462-0324
VL - 53
JO - Rheumatology
JF - Rheumatology
IS - Suppl 1
M1 - 035
ER -