Observational studyRheumatology (Oxford, England)2025
Neither ultrasound synovitis nor clinical-ultrasound phenotypes of established rheumatoid arthritis predict response to targeted therapy.
Observational study in Rheumatology (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesTo identify patient sub-phenotypes using clinical and imaging measures in established rheumatoid arthritis (RA) and to establish if baseline ultrasound synovitis and/or baseline patient sub-phenotypes predicts response to targeted therapy (TT).
methodsThis was an observational cohort study of consecutively recruited patients with established RA starting TT. Participants received clinical assessment, 38-joint musculoskeletal ultrasound (MSUS), measuring grey scale and power Doppler (PD) synovitis/tenosynovitis, and patient reported outcomes (PRO), prior to and 6 months after treatment. Latent profile analysis of the clinical and MSUS variables identified disease clusters, and multinomial logistic regression models determined whether these and/or baseline synovitis predicted EULAR response.
resultsOf 200 recruited patients, three clusters, low to high inflammatory, were identified with median (IQR) total joint PD 2 (0-4) in cluster 1, 9 (6-13) in cluster 2 and 29.5 (21-45) in cluster 3. A health assessment questionnaire correlated with disease activity, and DAS-P score distributions differed between clusters (P = 0.001) but with identical medians. Other PROs did not differ. At 6 months relative risk ratio of EULAR response in those with baseline synovitis compared with those without was 1.05 (95% CI: 0.38, 2.93) and response compared with the lowest inflammatory cluster [1] was 1.50 (95% CI: 0.61, 3.70) for cluster 2 and 1.24 (95% CI: 0.43, 3.60) for cluster 3.
conclusionThis is the first study to identify RA phenotypes employing 38-joint MSUS. Strikingly, neither baseline synovitis nor inflammatory cluster predicted clinical response. Mechanistic understanding of TT response/non-response is needed and clinical trials need to still capture all these populations.
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