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Retrospective cohort study shows long-term IL-23 inhibitors improve drug-free remission in psoriasis, suggesting disease-modifying effects.
INTRODUCTION: Psoriasis is a chronic inflammatory disease that often requires long-term treatment. However, treatment interruption is common. Although several predictors of drug-free remission (DFR) have been reported, the impact of treatment duration remains unclear. In Taiwan, biologics were reimbursed for up to 2.5 years, with re-treatment initiated after relapse. This study compared DFR between reimbursed patients and those enrolled in phase III pivotal trials, where treatment courses were at least 4 years. METHODS: This two-center, retrospective study included patients with moderate-to-severe plaque psoriasis treated with secukinumab, guselkumab, or risankizumab. For reimbursement, patients were required to have Psoriasis Area and Severity Index (PASI) ≥ 10, whereas pivotal trials required PASI ≥ 12 and body surface area ≥ 10%. Patients were classified into short-term (≤ 2.5 years, reimbursed) and long-term (4-6 years, clinical trials) treatment groups. Disease relapse was assessed at each visit, and DFR was evaluated using Kaplan-Meier analysis and Cox regression. RESULTS: Among 164 patients, 51 received long-term therapy and 113 received short-term therapy. Long-term therapy was associated with longer DFR (median 211 vs. 111 days, log-rank p < 0.001). In multivariate analysis, long-term risankizumab reduced relapse risk by 66% (hazard ratio [HR] 0.34, 95% confidence interval [CI] 0.13-0.90, p = 0.03), with a non-significant trend for long-term guselkumab (HR 0.55, 95% CI 0.28-1.06, p = 0.07). In contrast, no significant difference was observed for secukinumab (log-rank p = 0.94). In the guselkumab subgroup, continuous long-term therapy resulted in numerically higher remission days per dose than interrupted sequential short-term therapy (9.61 ± 11.43 vs. 8.23 ± 2.78, p = 0.64). CONCLUSION: Long-term treatment with interleukin (IL)-23 inhibitors (particularly risankizumab), but not anti-IL-17 inhibitors, may prolong DFR, suggesting a potential disease-modifying effect of prolonged IL-23 inhibition. These findings should be considered preliminary and warrant confirmation in larger prospective studies.
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Hsu et al. (2026) studied this question.
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