ObjectivesClinically evident tenosynovitis can be seen in established rheumatoid arthritis (RA). Imaging research has recently shown that tenosynovitis at small joints occurs in early RA, contributes to typical RA symptoms (including joint swelling) and is infrequent in healthy controls. Imaging-detectable tenosynovitis is often not recognisable at joint examination, hence its prevalence can therefore be underestimated. We hypothesised that if MRI-detectable tenosynovitis is a true RA feature, the sensitivity for RA is high, in both anti-citrullinated protein antibodies (ACPA)-positive and ACPA-negative RA, and lower in other diseases that are associated with enthesitis (such as spondyloarthritis (SpA) and psoriatic arthritis (PsA)). So far, no large MRI study addressed these questions.MethodsConsecutive patients with early arthritis (n=1211) from one healthcare region underwent contrast-enhanced 1.5T MRI of hand and foot at diagnosis. MRIs were scored for synovitis and tenosynovitis by two readers blinded for clinical data. All included patients with ACPA-positive RA (n=250), ACPA-negative RA (n=282), PsA (n=88), peripheral SpA (n=24), reactive arthritis (n=30) and self-limiting undifferentiated arthritis (UA; n=76) were studied. Sensitivity was calculated.ResultsThe sensitivity of tenosynovitis in RA was 85%; 88% for ACPA-positive RA and 82% for and ACPA-negative RA (p=0.19). The sensitivity for RA was significantly higher than for PsA (65%; p=0.001), SpA (53%; p<0.001), reactive arthritis (36%; p<0.001) and self-limiting UA (42%; p<0.001). The observed sensitivity of MRI synovitis was 91% in RA and ranged from 83% to 54% in other groups.ConclusionsMRI-detected tenosynovitis has a high sensitivity for early ACPA-positive and ACPA-negative RA. This supports that both juxta-articular (tenosynovitis) and intra-articular synovial involvement is characteristic of RA.

OBJECTIVES Identifying patients that will develop rheumatoid arthritis(RA) among those presenting with undifferentiated-arthritis(UA) remains a clinical dilemma. Although magnetic-resonance-imaging(MRI) is helpful according to EULAR-recommendations, this has only been determined in UA-patients not fulfilling 1987-RA-criteria, whilst some of these patients are currently considered as RA because they fulfill the 2010-criteria. Therefore, we studied the predictive value of MRI for progression to RA in the current UA-population: i.e. not fulfilling RA-classification-criteria (neither 1987- or 2010-criteria) and not having an alternate diagnosis. Additionally, the value of MRI was studied in patients with a clinical diagnosis of UA, regardless of the classification-criteria. METHODS Two UA-populations were studied: criteria-based-UA as described above(n = 405) and expert-opinion-based-UA(n = 564), i.e. UA indicated by treating rheumatologists. These patients were retrieved from a large cohort of consecutively included early arthritis patients that underwent contrast-enhanced MRI-scans of hand-and-foot at baseline. MRIs were scored for osteitis, synovitis and tenosynovitis. Patients were followed for RA-development during 1-year. Test-characteristics of MRI were determined separately for subgroups based on joint-involvement and autoantibody-status. RESULTS Among criteria-based-UA-patients(n = 405), 21% developed RA. MRI-detected synovitis and MRI-detected tenosynovitis were predictive. MRI-detected tenosynovitis was independently associated with RA-progression(OR 2.79; 95%CI 1.40–5.58), especially within ACPA-negative UA-patients(OR 2.91; 1.42–5.96). Prior risks of RA-development for UA-patients with mono-/oligo-/polyarthritis were 3%, 19%, 46%, respectively. MRI-results changed this risk most within the oligoarthritis-subgroup: PPV was 27% and NPV 93%. Similar results were found in expert-opinion-based-UA(n = 564). CONCLUSION This large cohort-study showed that MRI is most valuable in ACPA-negative UA-patients with oligoarthritis; a negative MRI could aid in preventing overtreatment.

ObjectiveFatigue in rheumatoid arthritis (RA) is hypothesised to be caused by inflammation. Still ~50% of the variance of fatigue in RA cannot be explained by the Disease Activity Score (DAS), nor by background or psychological factors. Since MRI can detect joint inflammation more sensitively than the clinical joint counts as incorporated in the DAS, we hypothesised that inflammation detected by MRI could aid in explaining fatigue in RA at diagnosis and during the follow-up.Methods526 consecutive patients with RA were followed longitudinally. Fatigue was assessed yearly on a Numerical Rating Scale. Hand and foot MRIs were performed at inclusion, after 12 and 24 months in 199 patients and were scored for inflammation (synovitis, tenosynovitis and osteitis combined). We studied whether patients with RA with more MRI-inflammation were more fatigued at diagnosis (linear regression), whether the 2-year course of MRI-inflammation associated with the course of fatigue (linear mixed models) and whether decrease in MRI-inflammation in year 1 associated with subsequent improvement in fatigue in year 2 (cross-lagged models). Similar analyses were done with DAS as inflammation measure.ResultsAt diagnosis, higher DAS scores were associated with more severe fatigue (p<0.001). However, patients with more MRI-inflammation were not more fatigued (p=0.94). During 2-year follow-up, DAS decrease associated with improvement in fatigue (p<0.001), but MRI-inflammation decrease did not (p=0.96). DAS decrease in year 1 associated with fatigue improvement in year 2 (p=0.012), as did MRI-inflammation decrease (p=0.039), with similar effect strength.ConclusionSensitive measurements of joint inflammation did not explain fatigue in RA at diagnosis and follow-up. This supports the concept that fatigue in RA is partly uncoupled from inflammation.

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