Abstract
Rheumatoid arthritis (RA) is characterized by persistent synovitis. Conventional inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) inadequately reflect synovial inflammation, particularly under interleukin-6 pathway inhibition. Pentraxin 3 (PTX3), an extrahepatic acute-phase protein produced in inflamed tissues, may better reflect local inflammation and angiogenesis in RA joints. We enrolled 80 RA patients and 80 age-sex-matched healthy controls. Clinical data, inflammatory markers, and disease activity scores (DAS28) were collected. Serum PTX3 levels were quantified by ELISA. Musculoskeletal ultrasound assessed bilateral wrists and metacarpophalangeal/proximal interphalangeal joints for synovial hypertrophy, effusion, color Doppler flow, and bone erosion. Eight patients received tocilizumab at baseline and week 12. PTX3 levels were significantly higher in RA patients than in controls. Serum PTX3 concentrations showed a progressive increase from remission to moderate-to-high disease activity groups. PTX3 showed no significant reduction after tocilizumab treatment. PTX3 correlated positively with CRP, ESR, DAS28-CRP, and rheumatoid factor, but not with anti-cyclic citrullinated peptide antibodies. PTX3 levels were elevated in patients with ultrasound-detected synovial blood flow compared to those without. Receiver operating characteristic analysis demonstrated superior diagnostic performance of PTX3 for predicting synovial blood flow compared to CRP and ESR. In multivariable logistic regression, PTX3 was the only significant predictor of synovial blood flow positivity. PTX3 demonstrates superior diagnostic performance over traditional inflammatory markers in detecting synovial vascularity and independently correlates with disease activity. PTX3 may serve as a valuable complementary biomarker for assessing local synovial inflammation and angiogenesis, particularly when conventional markers are inadequate.
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