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Objective: To evaluate the development of anti-drug antibodies (ADAb) against tumor necrosis factor inhibitors (TNFi) therapy during a 2-year period and search the factors linked to patients with axial spondyloarthritis (axSpA). Methods: Biologic-naive patients with axSpA were included in this observational study. Serum drug levels and ADAb were measured at weeks 12, 24, 52, and 104 of treatment by enzyme-linked immunosorbent assay (ELISA). The development of ADAb and factors related to ADAb over time were investigated using generalized estimating equations (GEE). Results: A total of 180 patients with axSpA (116 male, mean (±SD) 45.6 (±11.9) years) who started TNFi treatment (etanercept (32.2%), adalimumab (27.2%), golimumab (20.6%), infliximab (20%)) were included. In the etanercept treatment group, only 1 patient had ADAb at 12 weeks and 24 weeks. Anti-drug antibodies against TNFi drugs were present in the adalimumab group in 32.7% of patients and in the infliximab group in 21.2% of patients at 12 weeks, and the proportion of ADAb-positive patients were found to be stable throughout the follow-up for adalimumab- and infliximab-treated patients. In the golimumab group, one patient had ADAb against golimumab at 12 weeks and the proportion of ADAb-positive patients increased throughout follow-up. In longitudinal analysis, baseline age, TNFi type, longitudinal Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and ASDAS-CRP scores, serum C-eeactive protein (CRP) levels, presence of adverse events and treatment discontinuation were associated with the presence of ADAb. Conclusion: The development of ADAb against TNFi therapy is associated with younger age, high disease activity, the development of adverse events and more common treatment discontinuation in patients with axSpA during 2-year follow-up. [ABSTRACT FROM AUTHOR]

Objective: To our knowledge, the prevalence of pistol-grip deformity (PGD) has not previously been studied in patients with axial spondyloarthritis (axSpA). This study aimed to evaluate PGD prevalence in patients with axSpA and to assess its relationship with the clinical and demographic factors. Methods: A total of 158 patients with axSpA in whom diagnosis was established according to the Assessment of SpondyloArthritis International Society criteria in rheumatology department and 193 age- and sex-matched controls admitted to the emergency room and had anteroposterior (AP) pelvic X-rays were included in the study. PGD was identified by determining the non-spherical shape of the femoral head on AP hip or pelvic X-rays. Results: Prevalence of PGD was significantly higher in patients with axSpA than in controls (20.3% vs. 8.8%, respectively, p=0.002). PGD was also found to be more frequent in patients with radiographic ax-SpA than in those with non-radiographic axSpA (26/106 [24.5%] vs. 6/52 [11.5%]); however, this difference did not reach statistical significance (p=0.056). The presence of PGD was significantly associated with the presence of hip arthritis (odds ratio [OR], 3.1; 95% confidence interval [CI], 1.2-8.7; p=0.023), ever smoking (OR, 4.5; 95% CI, 1.4-13.6; p=0.008), and male sex (OR, 38.7; 95% CI, 5.1-292.7; p<0.001) in univariate analyses. In multivariate model, ever smoking (OR, 2.9; 95% CI, 1.10-10.05; p=0.03) and male sex (OR, 27.0; 95% CI, 3.5-208.4; p=0.002) were associated with PGD. Conclusion: PGD was significantly more common in patients with axSpA. Presence of PGD correlated significantly with hip arthritis, smoking, and sex. We assume that new bone formation could be the possible reason for increased PGD prevalence. Femoroacetabular impingement should be considered as a secondary cause of hip pain in patients with axSpA. [ABSTRACT FROM AUTHOR]

Objective: The reactivation of hepatitis B virus (HBV) infection is a well-known event in hepatitis B surface antigen (HbsAg)-positive patients receiving immunosuppressive therapy. The objective of this study was to assess the antiviral practice and course of HBV infection in inflammatory arthritis. Material and Methods: Nineteen rheumatology centers participated in this retrospective study. HbsAg-positive patients who were taking disease-modifying antirheumatic drugs and who were being tested for HBV viral load at a minimum of two different time points were included. The case report form (CRF) consisted of demographic data, rheumatic diseases, treatment profiles, transaminase levels, viral hepatitis serological markers, and HBV viral load. The reactivation of HBV was defined as the abrupt rise in HBV replication by an increase in serum HBV DNA levels in a patient with a previously inactive HBV infection. Results: In total, the data of 101 (female 50.5%) patients were included (76 patients with inactive HBV carriers and 25 patients with chronic HBV infection). The mean age of patients was 44±12 years, and the mean follow-up duration was 31±22 months. Of the 101 patients, 70 (69.3%) received antiviral treatment. HBV reactivation was detected in 13 of 76 (17.1%) patients with inactive HBV carriers. HBV reactivation was observed less frequently, not although significantly, in those patients receiving antiviral prophylaxis compared with those not receiving prophylaxis [5/41 (12.2%) vs. 8/33 (24.2%), p=0.17]. Forty-two patients (31 patients had inactive HBV carriers) were using anti-tumor necrosis factor agents. HBV reactivation was detected in 6 of the 31 (19.3%) patients. Twenty-five patients had chronic hepatitis, and five (20%) of them had not received antiviral prophylaxis. HBV viral loads were persistently elevated in 7 (28%) of 25 patients (three patients under and four patients not under antiviral treatment). Conclusion: HBV reactivation was observed in approximately 17% of patients under immunosuppressive treatments. HBV reactivation was more frequently observed in those who did not receive antiviral prophylaxis. [ABSTRACT FROM AUTHOR]