Abstract
ObjectivesTo investigate whether anti-CCP2-positive at-risk individuals with musculoskeletal (MSK) symptoms but without clinical synovitis (CCP2+ at-risk) develop US subclinical synovitis before inflammatory arthritis and if US subclinical synovitis can be predicted.MethodsFirst, US scans of CCP2+ at-risk individuals who developed inflammatory arthritis (‘progressors’) were reviewed for subclinical synovitis prior to inflammatory arthritis development. Patients in whom the pre-progression US scan was negative but the scan was conducted >6 months before progression were excluded. Subsequently, regression analyses were performed to identify predictors of US synovitis in CCP2+ at-risk individuals without baseline US abnormalities who had one or more longitudinal US scan and a complete dataset.ResultsUS subclinical synovitis was detected in one or more scan in 75 of 97 progressors (77.3%) {median time to inflammatory arthritis development from first evidence of US synovitis 26.5 weeks [interquartile range (IQR) 7–60]}, in whom one or more scan was available, excluding those with a negative scan >6 months from inflammatory arthritis development (n = 38). In 220 CCP2+ at-risk individuals with normal baseline US scans, who had one or more longitudinal US scan and a complete dataset, US synovitis was detected in 69/220 (31.4%) [median time to first developing US synovitis 56.4 weeks (IQR 33.0–112.0)]. In the multivariable analysis, only anti-CCP3 antibodies were predictive for the development of US synovitis [odds ratio 4.75 (95% CI 1.97, 11.46); P < 0.01].ConclusionsIn anti-CCP2+ at-risk individuals, a stage of subclinical synovitis usually precedes the development of inflammatory arthritis. Anti-CCP2+/CCP3+ individuals without clinical or US subclinical synovitis may represent the optimal window of opportunity for intervention to prevent joint disease.
Highlights
The concept of early RA has recently evolved
A total of 155/620 (25.0%) anti-CCP2þ at-risk individuals progressed to inflammatory arthritis [median time to develop inflammatory arthritis from the baseline visit: 51 weeks (IQR 24–107.2)]
US subclinical synovitis was detected in the following anatomical areas: wrists in 45/75 (60.0%) CCP2þ individuals, MCP joints in 30/75 (40.0%), MTP joints in 22/75 (29.3%), PIP joints in 17/75 (22.7%), knees in 6/ 75 (8.0%), elbows in 1/75 (1.3%) and ankles in 1/75 (1.3%)
Summary
The concept of early RA has recently evolved It is considered a ‘disease continuum’ rather than a fixed phenotype, in which individuals with risk factors progress through different stages before the development of clinical arthritis [1,2,3]. Several studies have highlighted the presence of another important population along this ‘continuum’, which sits between phases D and E This is represented by at-risk individuals (i.e. those with systemic autoimmunity and MSK symptoms but without clinical arthritis) who have subclinical joint inflammation on US or MRI [5,6,7]. Symptoms in the absence of clinical or subclinical inflammation may represent the critical time point for preventive treatments, for joint disease
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