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Smoking is another important modifiable environmental factor. Smoking generally has an adverse impact on treatment. In a post hoc analysis of pooled data from phase 2 and 3 trials and a long-term extension study involving 914 patients with PsA and 372 patients with ankylosing spondylitis who received tofacitinib (a Janus kinase inhibitor) or placebo, Ogdie and coworkers assessed the impact of smoking on treatment efficacy and safety. The efficacy rates were generally similar in current/past smokers and never-smokers. The incidence rates of treatment-emergent adverse events were higher in current/past smokers compared with never-smokers. Thus, in contrast to tumor necrosis factor inhibitors, smoking status may not have an impact on tofacitinib efficacy. However, current/past smokers experienced increased rates of adverse events.
Secukinumab, an anti-interleukin (IL)-17A antibody, is an established treatment for PsA and is approved for use as fixed-dose (150/300 mg) subcutaneous injections. The efficacy and safety of weight-based intravenous (IV) therapy is unknown. Kivitz and colleagues recently reported the results of the phase 3 INVIGORATE-2 trial, in which 381 patients with active PsA and either plaque psoriasis or nail psoriasis were randomly assigned to receive IV secukinumab or placebo with crossover to IV secukinumab at week 16. They demonstrated that at week 16, IV secukinumab significantly improved the American College of Rheumatology 50 response rate (ACR50) compared with placebo (31.4% vs 6.3%; adjusted P < .0001). Improvements were observed as early as week 4 and were sustained through week 52. No new safety signals were reported. Thus, IV secukinumab is a safe and efficacious treatment for PsA. This mode of administration of secukinumab is a welcome addition to the PsA therapeutic armamentarium.
There are many targeted therapies available for PsA. However, data on comparative effectiveness is lacking. Kristensen and associates reported the results of an interim analysis of the PRO-SPIRIT real-world study that included 1192 patients with PsA across six countries who initiated or switched to a new biologic or targeted synthetic disease-modifying antirheumatic drug. They showed that at 3 months, ixekizumab significantly improved clinical disease activity in patients with PsA compared with IL-12/23 inhibitors and IL-23 inhibitors. The improvements in the joints were similar to those with TNF inhibitors and JAK inhibitors, but the improvement in psoriasis was higher. Thus, ixekizumab leads to rapid response to active skin and musculoskeletal disease activity in PsA. Comparative data on treatment persistence as well as adverse events are required.
Smoking is another important modifiable environmental factor. Smoking generally has an adverse impact on treatment. In a post hoc analysis of pooled data from phase 2 and 3 trials and a long-term extension study involving 914 patients with PsA and 372 patients with ankylosing spondylitis who received tofacitinib (a Janus kinase inhibitor) or placebo, Ogdie and coworkers assessed the impact of smoking on treatment efficacy and safety. The efficacy rates were generally similar in current/past smokers and never-smokers. The incidence rates of treatment-emergent adverse events were higher in current/past smokers compared with never-smokers. Thus, in contrast to tumor necrosis factor inhibitors, smoking status may not have an impact on tofacitinib efficacy. However, current/past smokers experienced increased rates of adverse events.
Secukinumab, an anti-interleukin (IL)-17A antibody, is an established treatment for PsA and is approved for use as fixed-dose (150/300 mg) subcutaneous injections. The efficacy and safety of weight-based intravenous (IV) therapy is unknown. Kivitz and colleagues recently reported the results of the phase 3 INVIGORATE-2 trial, in which 381 patients with active PsA and either plaque psoriasis or nail psoriasis were randomly assigned to receive IV secukinumab or placebo with crossover to IV secukinumab at week 16. They demonstrated that at week 16, IV secukinumab significantly improved the American College of Rheumatology 50 response rate (ACR50) compared with placebo (31.4% vs 6.3%; adjusted P < .0001). Improvements were observed as early as week 4 and were sustained through week 52. No new safety signals were reported. Thus, IV secukinumab is a safe and efficacious treatment for PsA. This mode of administration of secukinumab is a welcome addition to the PsA therapeutic armamentarium.
There are many targeted therapies available for PsA. However, data on comparative effectiveness is lacking. Kristensen and associates reported the results of an interim analysis of the PRO-SPIRIT real-world study that included 1192 patients with PsA across six countries who initiated or switched to a new biologic or targeted synthetic disease-modifying antirheumatic drug. They showed that at 3 months, ixekizumab significantly improved clinical disease activity in patients with PsA compared with IL-12/23 inhibitors and IL-23 inhibitors. The improvements in the joints were similar to those with TNF inhibitors and JAK inhibitors, but the improvement in psoriasis was higher. Thus, ixekizumab leads to rapid response to active skin and musculoskeletal disease activity in PsA. Comparative data on treatment persistence as well as adverse events are required.
Smoking is another important modifiable environmental factor. Smoking generally has an adverse impact on treatment. In a post hoc analysis of pooled data from phase 2 and 3 trials and a long-term extension study involving 914 patients with PsA and 372 patients with ankylosing spondylitis who received tofacitinib (a Janus kinase inhibitor) or placebo, Ogdie and coworkers assessed the impact of smoking on treatment efficacy and safety. The efficacy rates were generally similar in current/past smokers and never-smokers. The incidence rates of treatment-emergent adverse events were higher in current/past smokers compared with never-smokers. Thus, in contrast to tumor necrosis factor inhibitors, smoking status may not have an impact on tofacitinib efficacy. However, current/past smokers experienced increased rates of adverse events.
Secukinumab, an anti-interleukin (IL)-17A antibody, is an established treatment for PsA and is approved for use as fixed-dose (150/300 mg) subcutaneous injections. The efficacy and safety of weight-based intravenous (IV) therapy is unknown. Kivitz and colleagues recently reported the results of the phase 3 INVIGORATE-2 trial, in which 381 patients with active PsA and either plaque psoriasis or nail psoriasis were randomly assigned to receive IV secukinumab or placebo with crossover to IV secukinumab at week 16. They demonstrated that at week 16, IV secukinumab significantly improved the American College of Rheumatology 50 response rate (ACR50) compared with placebo (31.4% vs 6.3%; adjusted P < .0001). Improvements were observed as early as week 4 and were sustained through week 52. No new safety signals were reported. Thus, IV secukinumab is a safe and efficacious treatment for PsA. This mode of administration of secukinumab is a welcome addition to the PsA therapeutic armamentarium.
There are many targeted therapies available for PsA. However, data on comparative effectiveness is lacking. Kristensen and associates reported the results of an interim analysis of the PRO-SPIRIT real-world study that included 1192 patients with PsA across six countries who initiated or switched to a new biologic or targeted synthetic disease-modifying antirheumatic drug. They showed that at 3 months, ixekizumab significantly improved clinical disease activity in patients with PsA compared with IL-12/23 inhibitors and IL-23 inhibitors. The improvements in the joints were similar to those with TNF inhibitors and JAK inhibitors, but the improvement in psoriasis was higher. Thus, ixekizumab leads to rapid response to active skin and musculoskeletal disease activity in PsA. Comparative data on treatment persistence as well as adverse events are required.