Single‐center experience with bimekizumab in psoriasis patients with previous exposure to interleukin‐17 inhibitors

The therapeutic options for patients suffering from moderate-to-severe plaque psoriasis have expanded considerably in recent years. Despite that, treatment failure can be expected in a considerable number of patients, constantly challenging physicians to choose the next best alternative. According to the available literature, switching within the class of interleukin (IL)-17 inhibitors (intra-class switching) has proved to be a successful tactic.1 Data regarding the recently approved IL-17A/F inhibitor bimekizumab in patients with previous exposure to an IL-17 inhibitor remain limited. Therefore, we aimed to assess whether switching to bimekizumab after the failure of a previous IL-17 inhibitor is an effective and safe option in a real-world setting over 1 year. We retrospectively identified 102 adult patients with moderate-to-severe plaque psoriasis under bimekizumab treatment, of which 39 (21 males and 18 females) were pre-exposed to another IL-17 inhibitor. Their baseline characteristics are presented in Table 1. Thirty patients were directly switched after a previous failure of an IL-17 inhibitor (3–4 weeks after direct previous biological agent injection). The remaining 9 patients had utilized an IL-17 inhibitor, followed by a different biological agent directly before switching to bimekizumab. The mean follow-up period for the whole cohort was 10.72 months. The available clinical outcomes at each follow-up visit (12/16, 24, and 52 weeks) include the Psoriasis Area Severity Index (PASI) 75/90/100 (reduction in baseline PASI score by 75/90/100%, respectively), PASI ≤ 3 and PASI ≤ 1 (Table 2). PASI 75/90/100 was achieved by 84.4/71.9/65.6% of the evaluated patients at Weeks 12/16, by 76.5/67.6/67.6% at Week 24, and by 94.4/94.4/88.9% at Week 52. As reflected by PASI ≤1, minimal disease activity was achieved by 75% and 70.6% at Weeks 12/16 and 24, respectively. During follow-up, six patients discontinued bimekizumab, two of them due to adverse events (AEs) (one recurrent intertriginous fungal infection and one widespread staphylococcal infection) and four due to secondary drug failure. Four treatment-related AEs occurred, three of which were fungal infections (two oral infections and one intertrigo) and one staphylococcal infection. Two patients with AEs who continued treatment were promptly managed and were event-free at the last follow-up. Overall, our results are encouraging regarding the use of bimekizumab in patients with prior exposure and failure of an IL-17 inhibitor, even in cases where more than one IL-17 inhibitor was utilized. A real-world multicenter study by Sood et al.2 demonstrated favorable outcomes of bimekizumab despite prior IL-17 inhibitor exposure over 16 weeks. Our results at Weeks 12/16 are slightly inferior to those reported by Sood et al.2 but still within the range reported in clinical trials.3, 4 Regarding safety, we observed a higher incidence of AEs (10.3% vs. 4.7%), but our follow-up period was significantly longer.1 Additionally, in a previous short- and mid-term real-world study of our centre that included bimekizumab patients irrespective of previous biologic exposure, the probability of achieving PASI90 and PASI100 at Week 16 did not seem to be affected by the status of previous IL-17 inhibitor exposure.5 In the BE RADIANT open-label clinical trial, patients who received secukinumab initially and did not meet PASI90 (PASI90 non-responders) were switched to bimekizumab, with PASI90 being achieved by 79% of patients after 48 weeks of treatment without additional safety findings reported.4 The main limitations of our study include the small sample size, the retrospective design, and the fact that not all patients had available clinical data at all follow-ups. Additionally, not all patients reached the 52-week time point, thus not allowing for stronger conclusions on the long-term efficacy of bimekizumab in this IL-17 inhibitor-exposed population. Our results agree with previously published real-world2 and clinical trial4 data and demonstrate the effectiveness and safety of bimekizumab, irrespective of prior exposure to IL-17 inhibitors, for a long follow-up period of up to 1 year. Additionally, extensive sample studies with prospective designs and longer follow-ups are needed to validate these results and draw firmer conclusions. All patients have given informed consent to the use and publication their case details. The data supporting the findings in this study will be made available upon reasonable request.

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Publication Details

Journal
International Journal of Dermatology
Published
2024-12-30
DOI
https://doi.org/10.1111/ijd.17630
Citations
1
Primary Topic
Psoriasis: Treatment and Pathogenesis
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article
Field-Weighted Citation Impact
0.24
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article

Single‐center experience with bimekizumab in psoriasis patients with previous exposure to interleukin‐17 inhibitors

Irene Stefanaki, Ioannis‐Alexios Koumprentziotis, Marina Papoutsaki, Natalia Rompoti et al.
1 citations
International Journal of Dermatology
Psoriasis: Treatment and Pathogenesis
0.24
article

Single‐center experience with bimekizumab in psoriasis patients with previous exposure to interleukin‐17 inhibitors

Irene Stefanaki, Ioannis‐Alexios Koumprentziotis, Marina Papoutsaki, Natalia Rompoti, Charitomeni Vavouli, Maria Politou, Electra Nicolaidou, Alexander Stratigos
article en
1 citations

Abstract

The therapeutic options for patients suffering from moderate-to-severe plaque psoriasis have expanded considerably in recent years. Despite that, treatment failure can be expected in a considerable number of patients, constantly challenging physicians to choose the next best alternative. According to the available literature, switching within the class of interleukin (IL)-17 inhibitors (intra-class switching) has proved to be a successful tactic.1 Data regarding the recently approved IL-17A/F inhibitor bimekizumab in patients with previous exposure to an IL-17 inhibitor remain limited. Therefore, we aimed to assess whether switching to bimekizumab after the failure of a previous IL-17 inhibitor is an effective and safe option in a real-world setting over 1 year. We retrospectively identified 102 adult patients with moderate-to-severe plaque psoriasis under bimekizumab treatment, of which 39 (21 males and 18 females) were pre-exposed to another IL-17 inhibitor. Their baseline characteristics are presented in Table 1. Thirty patients were directly switched after a previous failure of an IL-17 inhibitor (3–4 weeks after direct previous biological agent injection). The remaining 9 patients had utilized an IL-17 inhibitor, followed by a different biological agent directly before switching to bimekizumab. The mean follow-up period for the whole cohort was 10.72 months. The available clinical outcomes at each follow-up visit (12/16, 24, and 52 weeks) include the Psoriasis Area Severity Index (PASI) 75/90/100 (reduction in baseline PASI score by 75/90/100%, respectively), PASI ≤ 3 and PASI ≤ 1 (Table 2). PASI 75/90/100 was achieved by 84.4/71.9/65.6% of the evaluated patients at Weeks 12/16, by 76.5/67.6/67.6% at Week 24, and by 94.4/94.4/88.9% at Week 52. As reflected by PASI ≤1, minimal disease activity was achieved by 75% and 70.6% at Weeks 12/16 and 24, respectively. During follow-up, six patients discontinued bimekizumab, two of them due to adverse events (AEs) (one recurrent intertriginous fungal infection and one widespread staphylococcal infection) and four due to secondary drug failure. Four treatment-related AEs occurred, three of which were fungal infections (two oral infections and one intertrigo) and one staphylococcal infection. Two patients with AEs who continued treatment were promptly managed and were event-free at the last follow-up. Overall, our results are encouraging regarding the use of bimekizumab in patients with prior exposure and failure of an IL-17 inhibitor, even in cases where more than one IL-17 inhibitor was utilized. A real-world multicenter study by Sood et al.2 demonstrated favorable outcomes of bimekizumab despite prior IL-17 inhibitor exposure over 16 weeks. Our results at Weeks 12/16 are slightly inferior to those reported by Sood et al.2 but still within the range reported in clinical trials.3, 4 Regarding safety, we observed a higher incidence of AEs (10.3% vs. 4.7%), but our follow-up period was significantly longer.1 Additionally, in a previous short- and mid-term real-world study of our centre that included bimekizumab patients irrespective of previous biologic exposure, the probability of achieving PASI90 and PASI100 at Week 16 did not seem to be affected by the status of previous IL-17 inhibitor exposure.5 In the BE RADIANT open-label clinical trial, patients who received secukinumab initially and did not meet PASI90 (PASI90 non-responders) were switched to bimekizumab, with PASI90 being achieved by 79% of patients after 48 weeks of treatment without additional safety findings reported.4 The main limitations of our study include the small sample size, the retrospective design, and the fact that not all patients had available clinical data at all follow-ups. Additionally, not all patients reached the 52-week time point, thus not allowing for stronger conclusions on the long-term efficacy of bimekizumab in this IL-17 inhibitor-exposed population. Our results agree with previously published real-world2 and clinical trial4 data and demonstrate the effectiveness and safety of bimekizumab, irrespective of prior exposure to IL-17 inhibitors, for a long follow-up period of up to 1 year. Additionally, extensive sample studies with prospective designs and longer follow-ups are needed to validate these results and draw firmer conclusions. All patients have given informed consent to the use and publication their case details. The data supporting the findings in this study will be made available upon reasonable request.

International Journal of DermatologyVol. 64(6)
National and Kapodistrian University of Athens (GR), Andreas Sygros Hospital (GR)
Good health and well-being
Openalex Percentile: Top 39%
Psoriasis: Treatment and Pathogenesis
0.24
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