Rheumatology (Oxford, England) · 2025
Anti-pentraxin 3 antibodies and residual disease activity in rheumatoid arthritis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Salvato Mariangela, Frizzera Francesca, Ghirardello Anna, Calligaro Antonia, Botsios Costantino, Zen Margherita, Doria Andrea, Giollo Alessandro
Аннотация
OBJECTIVES: This study quantified anti-PTX3 antibodies in the serum of seropositive and seronegative RA patients, examining their associations with disease activity and patient-reported outcome measures (PROMs).
METHODS: In this cross-sectional study, RA patients diagnosed per ACR/EULAR 2010 criteria were recruited. Seronegative RA was defined as ACPA <7 kU/L. Data on demographics, clinical characteristics, medications, and PROMs were collected. Serum anti-PTX3 antibodies were measured using an in-house ELISA method. Comparative analyses were conducted with historical controls having PsA and FM.
RESULTS: The cohort included 83 RA patients (42 seropositive, 41 seronegative). Seropositive patients had lower anti-PTX3 antibody levels than PsA (P = 0.001) and FM (P = 0.004) controls. Seronegative patients had higher levels than seropositive ones (P = 0.032). Anti-PTX3 antibodies correlated with CDAI (r = 0.255), PtGA (r = 0.257), VAS-GH (r = -0.235), VAS-pain (r = 0.233), and HAQ (r = 0.311), but not with joint counts, inflammatory markers, or physician's global assessment. The PtGA association remained significant when adjusted for BMI, SJC28, ESR, and prednisone dosage (β = 0.206, P = 0.042). Patients with near-controlled RA (SJC28 ≤ 2, PtGA > 2) had higher anti-PTX3 levels than those with controlled disease (SJC28 ≤ 2, PtGA ≤ 2; P = 0.048). Tocilizumab or abatacept-treated patients had lower levels compared with those on TNFi or JAKi.
CONCLUSION: Elevated anti-PTX3 antibodies in RA indicate residual active disease despite controlled inflammation. They may serve as a biomarker for true active disease, especially in seronegative RA patients who might be undertreated.
METHODS: In this cross-sectional study, RA patients diagnosed per ACR/EULAR 2010 criteria were recruited. Seronegative RA was defined as ACPA <7 kU/L. Data on demographics, clinical characteristics, medications, and PROMs were collected. Serum anti-PTX3 antibodies were measured using an in-house ELISA method. Comparative analyses were conducted with historical controls having PsA and FM.
RESULTS: The cohort included 83 RA patients (42 seropositive, 41 seronegative). Seropositive patients had lower anti-PTX3 antibody levels than PsA (P = 0.001) and FM (P = 0.004) controls. Seronegative patients had higher levels than seropositive ones (P = 0.032). Anti-PTX3 antibodies correlated with CDAI (r = 0.255), PtGA (r = 0.257), VAS-GH (r = -0.235), VAS-pain (r = 0.233), and HAQ (r = 0.311), but not with joint counts, inflammatory markers, or physician's global assessment. The PtGA association remained significant when adjusted for BMI, SJC28, ESR, and prednisone dosage (β = 0.206, P = 0.042). Patients with near-controlled RA (SJC28 ≤ 2, PtGA > 2) had higher anti-PTX3 levels than those with controlled disease (SJC28 ≤ 2, PtGA ≤ 2; P = 0.048). Tocilizumab or abatacept-treated patients had lower levels compared with those on TNFi or JAKi.
CONCLUSION: Elevated anti-PTX3 antibodies in RA indicate residual active disease despite controlled inflammation. They may serve as a biomarker for true active disease, especially in seronegative RA patients who might be undertreated.