Objective: CT-P13, a biosimilar of infliximab, is widely used for treating ankylosing spondylitis (AS). However, the formation of anti-drug antibodies (ADAs) can reduce its efficacy. This study aimed to identify risk factors associated with high ADA levels in AS patients treated with CT-P13. Methods: A prospective observational study enrolled patients with intravenous CT-P13. Clinical data and disease activity was assessed at baseline, 24 weeks, and 54 weeks after CT-P13 treatment. Blood concentrations of CT-P13 and ADAs were measured at 24 and 54 weeks, and their correlation was investigated. Patients were grouped by ADA levels at 54 weeks. Univariable and multivariable logistic regression identified factors associated with high ADA concentrations. Results: A total of 34 patients was enrolled. Significant decreases in Bath Ankylosing Spondylitis Disease Activity Index and Bath Ankylosing Spondylitis Functional Index scores were observed relative to baseline after 24 weeks of CT-P13 therapy. Serum concentrations of CT-P13 and ADA levels increased following treatment. The median serum CT-P13 concentration was 17.6 [12.8, 22.7] µg/mL at 24 weeks and 23.5 [11.7, 34.2] µg/mL at 54 weeks. ADA levels were 6.7 [6.5, 9.1] AU/mL at 24 weeks and 11.4 [9.0, 28.4] AU/mL at 54 weeks. The serum concentrations of CT-P13 and ADA exhibited a negative correlation. In multivariable analysis, current smoking was associated with high ADA production at 54 weeks. Conclusion Smoking is identified as a significant risk factor for elevated ADAs in AS patients treated with CT-P13. The findings underscore the importance of smoking-cessation strategies in the management of AS patients.

Objective: CT-P13, a biosimilar of infliximab, is widely used for treating ankylosing spondylitis (AS). However, the formation of anti-drug antibodies (ADAs) can reduce its efficacy. This study aimed to identify risk factors associated with high ADA levels in AS patients treated with CT-P13. Methods: A prospective observational study enrolled patients with intravenous CT-P13. Clinical data and disease activity was assessed at baseline, 24 weeks, and 54 weeks after CT-P13 treatment. Blood concentrations of CT-P13 and ADAs were measured at 24 and 54 weeks, and their correlation was investigated. Patients were grouped by ADA levels at 54 weeks. Univariable and multivariable logistic regression identified factors associated with high ADA concentrations. Results: A total of 34 patients was enrolled. Significant decreases in Bath Ankylosing Spondylitis Disease Activity Index and Bath Ankylosing Spondylitis Functional Index scores were observed relative to baseline after 24 weeks of CT-P13 therapy. Serum concentrations of CT-P13 and ADA levels increased following treatment. The median serum CT-P13 concentration was 17.6 [12.8, 22.7] µg/mL at 24 weeks and 23.5 [11.7, 34.2] µg/mL at 54 weeks. ADA levels were 6.7 [6.5, 9.1] AU/mL at 24 weeks and 11.4 [9.0, 28.4] AU/mL at 54 weeks. The serum concentrations of CT-P13 and ADA exhibited a negative correlation. In multivariable analysis, current smoking was associated with high ADA production at 54 weeks. Conclusion Smoking is identified as a significant risk factor for elevated ADAs in AS patients treated with CT-P13. The findings underscore the importance of smoking-cessation strategies in the management of AS patients.

Objective: CT-P13, a biosimilar of infliximab, is widely used for treating ankylosing spondylitis (AS). However, the formation of anti-drug antibodies (ADAs) can reduce its efficacy. This study aimed to identify risk factors associated with high ADA levels in AS patients treated with CT-P13. Methods: A prospective observational study enrolled patients with intravenous CT-P13. Clinical data and disease activity was assessed at baseline, 24 weeks, and 54 weeks after CT-P13 treatment. Blood concentrations of CT-P13 and ADAs were measured at 24 and 54 weeks, and their correlation was investigated. Patients were grouped by ADA levels at 54 weeks. Univariable and multivariable logistic regression identified factors associated with high ADA concentrations. Results: A total of 34 patients was enrolled. Significant decreases in Bath Ankylosing Spondylitis Disease Activity Index and Bath Ankylosing Spondylitis Functional Index scores were observed relative to baseline after 24 weeks of CT-P13 therapy. Serum concentrations of CT-P13 and ADA levels increased following treatment. The median serum CT-P13 concentration was 17.6 [12.8, 22.7] µg/mL at 24 weeks and 23.5 [11.7, 34.2] µg/mL at 54 weeks. ADA levels were 6.7 [6.5, 9.1] AU/mL at 24 weeks and 11.4 [9.0, 28.4] AU/mL at 54 weeks. The serum concentrations of CT-P13 and ADA exhibited a negative correlation. In multivariable analysis, current smoking was associated with high ADA production at 54 weeks. Conclusion Smoking is identified as a significant risk factor for elevated ADAs in AS patients treated with CT-P13. The findings underscore the importance of smoking-cessation strategies in the management of AS patients.

Purpose: This study aimed to establish baseline morphological and functional data for normal mouse kidneys via a clinical 33 MHz ultra-high-frequency (UHF) transducer, compare the data with the findings from fibrotic mice, and assess correlations between ultrasonography (US) parameters and fibrosis-related markers. Methods: This retrospective study aggregated data from three separate experiments (obstructive nephropathy, diabetic nephropathy, and acute-to-chronic kidney injury models). Morphological parameters (kidney size, parenchymal thickness [PT]) and functional (shear-wave speed [SWS], stiffness, resistive index [RI], and microvascular imaging-derived vascular index [VI]) were assessed and compared between normal and fibrotic mouse kidneys. Semi-quantitative histopathologic scores were calculated and molecular markers (epithelial cadherin), Collagen 1A1 [Col1A1], transforming growth factor-β, and α-smooth muscle actin [α-SMA]) were evaluated using western blots. Correlations with US parameters were explored. Results: Clinical UHF US successfully imaged the kidneys of the experimental mice. A three-layer configuration was prevalent in the normal mouse kidney parenchyma (34/35) but was blurred in most fibrotic mouse kidneys (33/40). US parameters, including size (11.14 vs. 10.70 mm), PT (2.07 vs. 1.24 mm), RI (0.64 vs. 0.77), VI (22.55% vs. 11.47%, only for non-obstructive kidneys), SWS (1.67 vs. 2.06 m/s), and stiffness (8.23 vs. 12.92 kPa), showed significant differences between normal and fibrotic kidneys (P<0.001). These parameters also demonstrated strong discriminative ability in receiver operating characteristic curve analysis (area under the curve, 0.76 to 0.95; P<0.001). PT, VI, and RI were significantly correlated with histological fibrosis markers (ρ=-0.64 to -0.68 for PT and VI, ρ=0.71-0.76 for RI, P<0.001). VI exhibited strong negative correlations with Col1A1 (ρ=-0.76, P=0.006) and α-SMA (ρ=-0.75, P=0.009). Conclusion Clinical UHF US effectively distinguished normal and fibrotic mouse kidneys, indicating the potential of US parameters, notably VI, as noninvasive markers for tracking fibrosis initiation and progression in mouse kidney fibrosis models.

Purpose: This study aimed to establish baseline morphological and functional data for normal mouse kidneys via a clinical 33 MHz ultra-high-frequency (UHF) transducer, compare the data with the findings from fibrotic mice, and assess correlations between ultrasonography (US) parameters and fibrosis-related markers. Methods: This retrospective study aggregated data from three separate experiments (obstructive nephropathy, diabetic nephropathy, and acute-to-chronic kidney injury models). Morphological parameters (kidney size, parenchymal thickness [PT]) and functional (shear-wave speed [SWS], stiffness, resistive index [RI], and microvascular imaging-derived vascular index [VI]) were assessed and compared between normal and fibrotic mouse kidneys. Semi-quantitative histopathologic scores were calculated and molecular markers (epithelial cadherin), Collagen 1A1 [Col1A1], transforming growth factor-β, and α-smooth muscle actin [α-SMA]) were evaluated using western blots. Correlations with US parameters were explored. Results: Clinical UHF US successfully imaged the kidneys of the experimental mice. A three-layer configuration was prevalent in the normal mouse kidney parenchyma (34/35) but was blurred in most fibrotic mouse kidneys (33/40). US parameters, including size (11.14 vs. 10.70 mm), PT (2.07 vs. 1.24 mm), RI (0.64 vs. 0.77), VI (22.55% vs. 11.47%, only for non-obstructive kidneys), SWS (1.67 vs. 2.06 m/s), and stiffness (8.23 vs. 12.92 kPa), showed significant differences between normal and fibrotic kidneys (P<0.001). These parameters also demonstrated strong discriminative ability in receiver operating characteristic curve analysis (area under the curve, 0.76 to 0.95; P<0.001). PT, VI, and RI were significantly correlated with histological fibrosis markers (ρ=-0.64 to -0.68 for PT and VI, ρ=0.71-0.76 for RI, P<0.001). VI exhibited strong negative correlations with Col1A1 (ρ=-0.76, P=0.006) and α-SMA (ρ=-0.75, P=0.009). Conclusion Clinical UHF US effectively distinguished normal and fibrotic mouse kidneys, indicating the potential of US parameters, notably VI, as noninvasive markers for tracking fibrosis initiation and progression in mouse kidney fibrosis models.