Akademik Veri Yönetim Sistemi
Medical Journal of İzmir Hospital, cilt.29, sa.1, ss.27-34, 2025 (Hakemli Dergi)
ntroduction: This study investigates the frequency of antinuclear antibody (ANA) positivity in psoriatic arthritis(PsA) patients and examines its relationship with clinical features and biological disease-modifying antirheumaticdrug (bDMARD) treatments.Material and Method: A total of 240 PsA patients meeting the CASPAR criteria we re retrospectively analyzed.demographic, clinical, and serological data, including ANA, anti-extractable nuclear antigen antibodies (ENAs),rheumatoid factor (RF), and anti-cyclic citrullinated peptide (anti-CCP), were reviewed. ANA titers were classifiedas 1+, 2+ or 3+. Disease activity was assessed using t he Disease Activity in Psoriatic Arthritis (DAPSA) score.Treatment details included bDMARDs and targeted synthetic DMARDs (tsDMARDs).Results: ANA positivity was observed in 36.3% of PsA patients, with a higher prevalence in females (90.8%, p <0.001). Clinical features suggestive of connective tissue diseases (CTD) were significantly more common in theANA-positive group (71.3% vs. 4.6%, p< 0.001), including Raynaud's phenomenon and Sicca syndrome. ANAtiters increased in 26 patients after bDMARD initiation, predominantly in those using tumor necrosis factor (TNF)inhibitors (88.5%). Drug-induced l upus did not develop in any patient who developed ANA positivity. ThetsDMARDs were initiated more frequently in ANA-positive patients (10.3% vs. 2%, p=0.004), while DAPSA scoreswere comparable between ANA-positive and ANA-negative groups.Conclusion: ANA positivity in PsA is associated with female sex and CTD-related features. Although clinicalmanifestations are rare, biological therapies, particularly TNF inhibitors, can induce ANA positivity. This study'sfindings suggest that routine ANA monitoring is not necessary unless autoimmune symptoms develop, providingvaluable insights for clinical practice. Future studi es should explore the clinical implications of ANAseroconversion and its impact on treatment outcomes in PsA, further enhancing our understanding of thiscomplex disease.Introduction: This study investigates the frequency of antinuclear antibody (ANA) positivity in psoriatic arthritis(PsA) patients and examines its relationship with clinical features and biological disease-modifying antirheumaticdrug (bDMARD) treatments.Material and Method: A total of 240 PsA patients meeting the CASPAR criteria we re retrospectively analyzed.demographic, clinical, and serological data, including ANA, anti-extractable nuclear antigen antibodies (ENAs),rheumatoid factor (RF), and anti-cyclic citrullinated peptide (anti-CCP), were reviewed. ANA titers were classifiedas 1+, 2+ or 3+. Disease activity was assessed using t he Disease Activity in Psoriatic Arthritis (DAPSA) score.Treatment details included bDMARDs and targeted synthetic DMARDs (tsDMARDs).Results: ANA positivity was observed in 36.3% of PsA patients, with a higher prevalence in females (90.8%, p <0.001). Clinical features suggestive of connective tissue diseases (CTD) were significantly more common in theANA-positive group (71.3% vs. 4.6%, p< 0.001), including Raynaud's phenomenon and Sicca syndrome. ANAtiters increased in 26 patients after bDMARD initiation, predominantly in those using tumor necrosis factor (TNF)inhibitors (88.5%). Drug-induced l upus did not develop in any patient who developed ANA positivity. ThetsDMARDs were initiated more frequently in ANA-positive patients (10.3% vs. 2%, p=0.004), while DAPSA scoreswere comparable between ANA-positive and ANA-negative groups.Conclusion: ANA positivity in PsA is associated with female sex and CTD-related features. Although clinicalmanifestations are rare, biological therapies, particularly TNF inhibitors, can induce ANA positivity. This study'sfindings suggest that routine ANA monitoring is not necessary unless autoimmune symptoms develop, providingvaluable insights for clinical practice. Future studi es should explore the clinical implications of ANAseroconversion and its impact on treatment outcomes in PsA, further enhancing our understanding of thiscomplex diseasIntroduction: This study investigates the frequency of antinuclear antibody (ANA) positivity in psoriatic arthritis(PsA) patients and examines its relationship with clinical features and biological disease-modifying antirheumaticdrug (bDMARD) treatments.
Material and Method: A total of 240 PsA patients meeting the CASPAR criteria we re retrospectively analyzed.demographic, clinical, and serological data, including ANA, anti-extractable nuclear antigen antibodies (ENAs),rheumatoid factor (RF), and anti-cyclic citrullinated peptide (anti-CCP), were reviewed. ANA titers were classifiedas 1+, 2+ or 3+. Disease activity was assessed using t he Disease Activity in Psoriatic Arthritis (DAPSA) score.Treatment details included bDMARDs and targeted synthetic DMARDs (tsDMARDs).
Results: ANA positivity was observed in 36.3% of PsA patients, with a higher prevalence in females (90.8%, p <0.001). Clinical features suggestive of connective tissue diseases (CTD) were significantly more common in theANA-positive group (71.3% vs. 4.6%, p< 0.001), including Raynaud's phenomenon and Sicca syndrome. ANAtiters increased in 26 patients after bDMARD initiation, predominantly in those using tumor necrosis factor (TNF)inhibitors (88.5%). Drug-induced l upus did not develop in any patient who developed ANA positivity. ThetsDMARDs were initiated more frequently in ANA-positive patients (10.3% vs. 2%, p=0.004), while DAPSA scoreswere comparable between ANA-positive and ANA-negative groups.
Conclusion: ANA positivity in PsA is associated with female sex and CTD-related features. Although clinicalmanifestations are rare, biological therapies, particularly TNF inhibitors, can induce ANA positivity. This study'sfindings suggest that routine ANA monitoring is not necessary unless autoimmune symptoms develop, providingvaluable insights for clinical practice. Future studi es should explore the clinical implications of ANAseroconversion and its impact on treatment outcomes in PsA, further enhancing our understanding of thiscomplex disease