Background Palindromic rheumatism (PR) is a recurrent, self-abortive arthritis and/or peri-arthritis which progresses to RA in up to 50% of patients, especially those that are anti-CCP positive (1). Whether PR is truly a prodrome of RA or a distinct syndrome is unclear; the pathological phenotype of PR flare, and whether this changes when RA is imminent, remains unknown
Objectives To describe the clinical and imaging (US and MRI) phenotype during PR flares and to determine whether this changes in PR patients with imminent RA. We hypothesised PR patients with imminent RA would have a RA phenotype during flare
Methods Patients were recruited from a prospective PR cohort. PR flares were defined as ≥2 of pain, swelling, erythema in or around ≥1 joint, that later normalised. Clinical details were recorded during flares. Blinded US assessment (wrists, MCPs, PIPs, elbows, knees, MTPs, ECUs and 2nd-5th finger flexor tendons) was performed during and between flares. Synovitis, tenosynovitis, subcutaneous oedema, peri-articular inflammation and peri-tendinous oedema were reported at each joint. Where possible, MRI was also performed on the most symptomatic region during flare. Patients were followed for progression to RA
Results US was performed in 22 patients during flare. 19 patients also had non-flare US. Mean age was 49 yrs. 16/22 (73%) were anti-CCP+ and 6/22 (27%) anti-CCP-. Six (27%) patients developed RA (mean 23 weeks post flare); these patients had higher frequency of flares and absence of flare trigger (figure) but no difference in distribution of flaring joints. The flare US showed grey scale (GS) synovitis in 13/22 (59%) patients, power Doppler (PD) synovitis in 4/22 (18%) and no erosions. 12/22 (55%) patients had peri-articular inflammation and/or subcutaneous oedema; in 6 patients this was without synovitis/tenosynovitis. Tenosynovitis and/or peri-tendinous oedema were present in 6/22 (27%) patients. Non-flare US demonstrated fewer abnormalities with improvement post flare. In 5 patients multiple flares were imaged with variable US abnormalities identified. The US flare phenotype did not differ (from non-progressors) in patients who progressed to RA, with PD synovitis present in only 17% (table 1) contrasting with our early RA cohort where PD synovitis occurred in 73% of patients (2). MRI was performed on 8 patients (2 flares imaged in 1 patient) and detected more pathology than US. Bone marrow oedema (BME) was found in only 1 patient. No erosions were seen.
Conclusions PR flares have a distinct imaging phenotype characterised by peri-articular inflammation and subcutaneous oedema, often without synovitis. The low prevalence of PD synovitis, BME and erosions distinguishes PR from RA. PR patients with imminent RA have no triggers and more frequent flares, but retain the distinct PR phenotype. This suggests distinct pathological mechanisms in PR and should be of value for potential therapeutic interventions.
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Disclosure of Interest None declared