Bimekizumab in the Treatment of Psoriasis After Failure of (Not Only) Anti-IL-17A Antibodies – Case Reports
German authors last year described the first 2 cases of patients with psoriasis in whom treatment with, among other things, anti-IL-17A antibodies failed, but who responded to the blockade of interleukins IL-17A/IL-17F with bimekizumab after its approval by the European Medicines Agency (EMA).
Case Report 1
The first patient was a 38-year-old man with a 21-year history of severe psoriasis affecting all areas of the body, including the scalp and groin, with an initial Psoriasis Area and Severity Index (PASI) of 28.8 and a Dermatology Life Quality Index (DLQI) of 16. In addition to psoriasis, he also suffered from depression and hypothyroidism. Both of his parents also had a history of psoriasis.
After 10 weeks of treatment with ixekizumab, he was admitted to the clinic, where he underwent intensive local therapy during hospitalization, including dithranol ointment, calcitriol, topical steroids, and 13 sessions of narrowband UVB phototherapy (311 nm). He continued using ixekizumab for another 2 weeks. After 3 months of ixekizumab treatment, his skin condition improved only slightly (PASI 16.4; DLQI 16), and predominant scalp involvement persisted. Previous treatments included methotrexate, secukinumab, adalimumab, ustekinumab, brodalumab, tildrakizumab, risankizumab, and etanercept. The best results were achieved with secukinumab and adalimumab, with a loss of treatment response occurring only after 3 years. Therefore, it was decided to use IL-17 inhibition again in further treatment and to initiate bimekizumab (an inhibitor of IL-17A/IL-17F) at a dose of 320 mg s.c.
Treatment started 3 weeks after the last dose of ixekizumab, with injections administered every 4 weeks during the first 4 months and then every 8 weeks. Within 4 weeks after the first bimekizumab injection, there was a dramatic improvement in skin condition. Psoriatic lesions on the forehead and scalp almost disappeared, PASI decreased to 7.8, and DLQI to 6. At the 1-year follow-up after starting bimekizumab treatment, the patient had clear skin (PASI 0) and psoriasis no longer impacted his quality of life (DLQI 0). No adverse effects were observed during the entire treatment period.
Case Report 2
The second patient was a 35-year-old obese man (BMI 44.3 kg/m2) with severe psoriasis since the age of 10. The first examination at the clinic occurred due to a loss of response to risankizumab after 2 years of treatment. The current PASI value was 19.5 and DLQI 21. This man also had psoriatic arthritis, enthesitis, and inflammatory back pain, which had worsened over the past 2 years. The diagnosis of axial spondyloarthritis was not confirmed. He described morning stiffness, pain in the carpal and metacarpal joints, finger joints, lumbar spine, and Achilles tendons. His medical history also included depression and asthma. Previous psoriasis treatments included topical agents, phototherapy, nonsteroidal anti-inflammatory drugs, methotrexate, etanercept, adalimumab, ustekinumab, secukinumab, and guselkumab.
Biological treatment needed to be changed due to loss of response. Given that 2 IL-23 antibodies, guselkumab and risankizumab, had failed in long-term disease control, it was decided to change the class of biologics and start bimekizumab treatment at a dose of 320 mg. The drug was administered according to the SPC and within 4 weeks of the first injection, there was a marked improvement in skin condition (PASI 3.7; DLQI 7) and significant relief of joint pain. Morning stiffness and joint swelling were no longer present, and the patient described only mild pain in the Achilles tendons. At the 1-year follow-up after starting bimekizumab treatment, both PASI and DLQI reached 0, and back and joint pain had completely disappeared. No adverse effects were observed. The patient's mobility increased, and his BMI decreased to 40.9 kg/m2 due to increased physical activity.
Summary and Conclusion
Bimekizumab is a new antibody for the treatment of psoriasis that concurrently neutralizes interleukins IL-17A and IL-17F. In the presented patients, there was a loss of response to various biologics (secukinumab, ixekizumab, or brodalumab). Both had, in addition to plaque psoriasis, difficult-to-treat scalp psoriasis, groin skin involvement, or psoriatic arthritis. A response to bimekizumab was observed in them within 4 weeks after the first injection, and a year later, complete lesion resolution (PASI 100) persisted. No adverse effects occurred. This rapid response underscores the role of IL-17F in the pathogenesis of psoriasis and demonstrates that bimekizumab, due to its new mechanism of action, may be beneficial even in patients with a loss/lack of response to other anti-IL-17 antibodies.
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Source: Kokolakis G., Ghoreschi K. The clinical significance of simultaneous IL-17A and IL-17F blockade in psoriasis non-responding to anti-IL17A therapy. J Clin Med 2022 Dec 21; 12 (1): 35, doi: 10.3390/jcm12010035.
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