Objective
Dactylitis has been identified as an important feature of psoriatic arthritis (PsA) with poorer prognosis. Moreover, ultrasound can reveal subclinical dactylitis, however its significance is unclear. Therefore, in this study, we aimed to determine the impact of subclinical dactylitis on PsA severity.
Methods
The study was performed based on the PKUPsA cohort. Patients with complete ultrasound assessment on synovitis, tenosynovitis, and soft tissue of both hands and feet were recruited. They were further classified into subgroups based on the presence of clinical or ultrasound evidence of dactylitis. Their clinical characteristics were compared.
Results
Among the 223 PsA patients enrolled, there were 90 (40.4%) patients with clinical manifestations of dactylitis (clinical dactylitis group), 26 (11.7%) with evidence of dactylitis on ultrasound however not on physical examination (subclinical dactylitis group), and 107 (47.9%) patients with neither clinical nor ultrasound evidence of dactylitis (no-dactylitis group). Compared with no-dactylitis group, patients in clinical dactylitis group had more swollen joint count (4 vs. 2, P < 0.01), tender joint count (4 vs. 3, P < 0.05), and greater median disease activity index in PsA (DAPSA) (25.0 vs. 18.3, P < 0.05). Moreover, 116 PsA patients in clinical dactylitis or subclinical dactylitis groups also had more tender joint count (4 vs. 2, P < 0.01), swollen joint count (4 vs 3, P < 0.001), median C-reactive protein levels (18.1 vs. 11.8, P < 0.05) and median DAPSA scores (25.5 vs. 16.1, P < 0.01). Even excluding the digits with dactylitis from counting, the swollen joint count of 116 patients with dactylitis remained significantly greater than that of no-dactylitis group (3 vs. 2, P < 0.01). 26 patients in subclinical dactylitis group also showed significantly higher DAPSA scores (27.2 vs. 16.1, P < 0.05), more swollen joint count (4.5 vs. 2, P < 0.01) and tender joint count (5 vs. 3, P < 0.05) than no-dactylitis group.
Conclusion
Subclinical dactylitis also represents a more active phenotype of PsA, which calls for more attention and probably more aggressive therapy.