Abstract

BackgroundMagnetic resonance imaging (MRI) and ultrasonography (US) are more sensitive than clinical evaluation in assessing inflammation in rheumatoid arthritis (RA). Data is scarce regarding potential link between patient-reported flares and inflammation on imaging. The aim of the study was to explore the pattern and longitudinal associations of inflammatory lesions detected by serial MRI and US in relation to patient-reported flares in patients with RA.MethodsEighty RA patients with baseline DAS28CRP < 3.2 and no swollen joints were examined at baseline and followed for 1 year. Patients were requested to contact the hospital in case of patient-reported hand flare accompanied by ≥ 1 tender and swollen joint. The 29 patients who reported hand flare had four extra visits within 4 months from flare onset comprising clinical examination, patient-reported outcomes, MRI, and US of wrists and hands. MRI synovitis/tenosynovitis/bone marrow edema (BME) and US synovitis/tenosynovitis were scored. MRI and US scores at and after the flare were compared to baseline before the flare, and associations were explored by linear mixed models for repeated measurements.ResultsSynovitis and tenosynovitis by MRI/US increased significantly at flare onset. Synovitis waned quickly, as did US tenosynovitis. BME showed delayed increase yet persisted, once the patient-reported flare had resolved, as did MRI tenosynovitis. In univariate models, patient-reported flares were associated with all MRI and US inflammatory markers, except for BME, which was only associated with SJC28 and long-lasting flares > 14 days. Independent associations were observed between patient-reported flares and tenosynovitis by MRI and US (p < 0.05).ConclusionsPatient-reported flares were linked to inflammation detected by serial MRI and US. Differential patterns of inflammatory lesion evolution were observed by serial imaging with early synovial and tenosynovial inflammation, followed by delayed-onset BME.

Highlights

  • Magnetic resonance imaging (MRI) and ultrasonography (US) are more sensitive than clinical evaluation in assessing inflammation in rheumatoid arthritis (RA)

  • Patients aged ≥ 18 years were eligible if they met the American College of Rheumatology (ACR) 1987 or ACR/European League Against Rheumatism (EULAR) 2010 criteria for RA, were anti-cyclic citrullinated peptide antibody and/or rheumatoid-factor (RF) positive, had a Disease Activity Score based on C-reactive protein (DAS28CRP) at baseline < 3.2 and no swollen joints, were on stable disease modifying anti-rheumatic drugs (DMARD) treatment with no intra-articular glucocorticoid injections 4 weeks prior to study entry, and had no contraindications for MRI

  • bone marrow edema (BME) evolved with delay, and remained for months, while MRI tenosynovitis raised promptly and persisted after the flare waned

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Summary

Introduction

Magnetic resonance imaging (MRI) and ultrasonography (US) are more sensitive than clinical evaluation in assessing inflammation in rheumatoid arthritis (RA). Patient-reported flares have an impact on everyday life [7], but there is scarce evidence indicating as to whether they are linked to objectively assessed immune-mediated inflammation, functional impairment, and radiographic progression [8]. Imaging modalities such as magnetic resonance imaging (MRI) and ultrasonography (US) are superior to clinical assessment for detecting inflammation and are recommended by the European League Against Rheumatism (EULAR) for more accurate evaluation of inflammation [9]. Clinical flares may be precipitated by incomplete suppression of inflammation, as US-detected persistent synovitis has been shown to predict clinical flares [13,14,15]

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