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How Much Is Fatigue Explained by Standard Clinical Characteristics of Disease Activity in Patients With Inflammatory Arthritis? A Longitudinal Study
Author(s) -
Minnock Patricia,
McKee Gabrielle,
Bresnihan Barry,
FitzGerald Oliver,
Veale Douglas J.
Publication year - 2014
Publication title -
arthritis care and research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.032
H-Index - 163
eISSN - 2151-4658
pISSN - 2151-464X
DOI - 10.1002/acr.22387
Subject(s) - medicine , rheumatology , physical therapy , rheumatoid arthritis , arthritis , disease
Objective To determine the relationship between fatigue and the American College of Rheumatology (ACR) core set outcomes in patients with inflammatory arthritis (IA). Methods This prospective longitudinal study evaluated fatigue in patients with active IA commencing tumor necrosis factor (TNF) inhibitor therapy. Fatigue was assessed using the multidimensional assessment of fatigue scale and the ACR core set (swollen and tender joint counts, pain, global health score, Health Assessment Questionnaire [HAQ] disability index [DI], and C‐reactive protein level) was used for standard assessment of disease activity. Results Assessments at baseline, 3 months, and 6 months were completed by 125, 92, and 82 patients, respectively. Fatigue and disease activity improved significantly within the first 3 months, with fatigue improving by 29% (F[2, 118] = 17.14, P < 0.001; repeated‐measures analysis of variance). Using multiple regression, the amount of fatigue explained by the core outcomes differed at each time point: 28% at baseline ( P < 0.001; significant predictors were the HAQ DI, global health, and C‐reactive protein level), 37% at 3 months ( P < 0.001; significant predictors were pain and tender joint count), and 46% at 6 months ( P < 0.001; significant predictor was global health). Regression modelling using the fatigue change score at 3 months explained 17% of fatigue change ( P < 0.012; significant predictors were HAQ DI and global health). Conclusion Fatigue, which improved following treatment with TNF inhibitors, was poorly and inconsistently explained through the core set outcomes. Further, fatigue was least accounted for when the disease was most active, highlighting the need for further research into alternate explanations. These findings suggest further exploration of contributing variables and mechanisms in order to develop targeted symptom management of fatigue in IA.