Katie Bechman1,2, Lieke Tweehuysen3,4, Toby Garrood3,4, David L Scott3,4, Andrew P Cope3,4, James B Galloway3,4, Margaret H Y Ma3,4. 1. From the Academic Department of Rheumatology, Kings College London, London; Department of Rheumatology, Guy's and St Thomas' UK National Health Service (NHS) Foundation Trust, London, UK; Department of Rheumatology, Sint Maartenskliniek, Nijmegen, the Netherlands. katie.bechman@kcl.ac.uk. 2. K. Bechman, MBChB, BSc, Rheumatology Registrar and Clinical Research Fellow, Academic Department of Rheumatology, Kings College London; L. Tweehuysen, MD, Rheumatology Registrar and Clinical Research Fellow, Department of Rheumatology, Sint Maartenskliniek; T. Garrood, MBBS, MRCP, MSc, PhD, Consultant Rheumatologist, Department of Rheumatology, Guy's and St Thomas' NHS Foundation Trust; D.L. Scott, BSc, MD, FRCP, Professor of Rheumatology, Academic Department of Rheumatology, Kings College London; A.P. Cope, BSc, MBBS, PhD, FRCP, FHEA, Professor of Rheumatology, Academic Department of Rheumatology, Kings College London; J.B. Galloway, MBChB, MSc, CHP, MRCP, PhD, Consultant Rheumatologist/Senior Lecturer, Academic Department of Rheumatology, Kings College London; M.H. Ma, MBBS, BSc, MRCP, MSc, PhD, Consultant Rheumatologist, Academic Department of Rheumatology, Kings College London. katie.bechman@kcl.ac.uk. 3. From the Academic Department of Rheumatology, Kings College London, London; Department of Rheumatology, Guy's and St Thomas' UK National Health Service (NHS) Foundation Trust, London, UK; Department of Rheumatology, Sint Maartenskliniek, Nijmegen, the Netherlands. 4. K. Bechman, MBChB, BSc, Rheumatology Registrar and Clinical Research Fellow, Academic Department of Rheumatology, Kings College London; L. Tweehuysen, MD, Rheumatology Registrar and Clinical Research Fellow, Department of Rheumatology, Sint Maartenskliniek; T. Garrood, MBBS, MRCP, MSc, PhD, Consultant Rheumatologist, Department of Rheumatology, Guy's and St Thomas' NHS Foundation Trust; D.L. Scott, BSc, MD, FRCP, Professor of Rheumatology, Academic Department of Rheumatology, Kings College London; A.P. Cope, BSc, MBBS, PhD, FRCP, FHEA, Professor of Rheumatology, Academic Department of Rheumatology, Kings College London; J.B. Galloway, MBChB, MSc, CHP, MRCP, PhD, Consultant Rheumatologist/Senior Lecturer, Academic Department of Rheumatology, Kings College London; M.H. Ma, MBBS, BSc, MRCP, MSc, PhD, Consultant Rheumatologist, Academic Department of Rheumatology, Kings College London.
Abstract
OBJECTIVE: To investigate predictors of flare in rheumatoid arthritis (RA) patients with low disease activity (LDA) and to evaluate the effect of flare on 12-month clinical outcomes. METHODS: Patients with RA who were taking disease-modifying antirheumatic drugs and had a stable 28-joint count Disease Activity Score (DAS28) < 3.2 were eligible for inclusion. At baseline and every 3 months, clinical (DAS28), functional [Health Assessment Questionnaire-Disability Index (HAQ-DI), EQ-5D, Functional Assessment of Chronic Illness Therapy Fatigue scale (FACIT-F), Medical Outcomes Study Short Form-36 (SF-36)], serum biomarkers [multibiomarker disease activity (MBDA) score, calprotectin, CXCL10], and imaging data were collected. Flare was defined as an increase in DAS28 compared with baseline of > 1.2, or > 0.6 if concurrent DAS28 ≥ 3.2. Cox regression analyses were used to identify baseline predictors of flare. Biomarkers were cross-sectionally correlated at time of flare. Linear regressions were performed to compare clinical outcomes after 1 year. RESULTS: Of 152 patients, 46 (30%) experienced a flare. Functional disability at baseline was associated with flare: HAQ-DI had an unadjusted HR 1.82 (95% CI 1.20-2.72) and EQ-5D had HR 0.20 (95% CI 0.07-0.57). In multivariate analyses, only HAQ-DI remained a significant independent predictor of flare (HR 1.76, 95% CI 1.05-2.93). At time of flare, DAS28 and its components significantly correlated with MBDA and calprotectin, but correlation coefficients were low at 0.52 and 0.49, respectively. Two-thirds of flares were not associated with a rise in biomarkers. Patients who flared had significantly worse outcomes at 12 months (HAQ-DI, EQ-5D, FACIT-F, SF-36, and radiographic progression). CONCLUSION: Flares occur frequently in RA patients with LDA and are associated with worse disease activity, quality of life, and radiographic progression. Higher baseline HAQ-DI was modestly predictive of flare, while biomarker correlation at the time of flare suggests a noninflammatory component in a majority of events.
OBJECTIVE: To investigate predictors of flare in rheumatoid arthritis (RA) patients with low disease activity (LDA) and to evaluate the effect of flare on 12-month clinical outcomes. METHODS:Patients with RA who were taking disease-modifying antirheumatic drugs and had a stable 28-joint count Disease Activity Score (DAS28) < 3.2 were eligible for inclusion. At baseline and every 3 months, clinical (DAS28), functional [Health Assessment Questionnaire-Disability Index (HAQ-DI), EQ-5D, Functional Assessment of Chronic Illness Therapy Fatigue scale (FACIT-F), Medical Outcomes Study Short Form-36 (SF-36)], serum biomarkers [multibiomarker disease activity (MBDA) score, calprotectin, CXCL10], and imaging data were collected. Flare was defined as an increase in DAS28 compared with baseline of > 1.2, or > 0.6 if concurrent DAS28 ≥ 3.2. Cox regression analyses were used to identify baseline predictors of flare. Biomarkers were cross-sectionally correlated at time of flare. Linear regressions were performed to compare clinical outcomes after 1 year. RESULTS: Of 152 patients, 46 (30%) experienced a flare. Functional disability at baseline was associated with flare: HAQ-DI had an unadjusted HR 1.82 (95% CI 1.20-2.72) and EQ-5D had HR 0.20 (95% CI 0.07-0.57). In multivariate analyses, only HAQ-DI remained a significant independent predictor of flare (HR 1.76, 95% CI 1.05-2.93). At time of flare, DAS28 and its components significantly correlated with MBDA and calprotectin, but correlation coefficients were low at 0.52 and 0.49, respectively. Two-thirds of flares were not associated with a rise in biomarkers. Patients who flared had significantly worse outcomes at 12 months (HAQ-DI, EQ-5D, FACIT-F, SF-36, and radiographic progression). CONCLUSION: Flares occur frequently in RApatients with LDA and are associated with worse disease activity, quality of life, and radiographic progression. Higher baseline HAQ-DI was modestly predictive of flare, while biomarker correlation at the time of flare suggests a noninflammatory component in a majority of events.
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