To the Editor:
Atopic dermatitis (AD) presents with several phenotypes, among which the prurigo nodularis (PN)-like phenotype is particularly resistant to treatment.1 PN-like phenotype of AD is characterized by multiple widespread pruritic nodules and intense and persistent itch, sometimes accompanied by pain.1 Interleukin (IL)-13 is a type-2 cytokine that plays a central role in skin inflammation, barrier disruption, and pruritus associated with AD, including PN-like phenotype.2
Lebrikizumab is a high-affinity humanized immunoglobulin G4 monoclonal antibody that specifically inhibits IL-13. Clinical trials and real-world studies have demonstrated its effectiveness and good tolerability for moderate-to-severe AD.3,4,5 However, data on the effectiveness of lebrikizumab are currently lacking for the PN-like phenotype of AD. Therefore, we retrospectively evaluated the effectiveness and safety of lebrikizumab in 26 patients aged ≥ 12 years with PN-like phenotype of AD who were treated for at least 4 weeks (up to 48 weeks) from May 2024 to July 2025. At baseline, all patients had ≥ 20 excoriated and hyperkeratotic nodules primarily on the trunk and extremities. Lebrikizumab was administered subcutaneously at 500 mg at weeks 0 and 2, followed by 250 mg every 2 weeks together with topical corticosteroids of moderate‑to‑strongest potency. After week 16, all patients received lebrikizumab every 4 weeks. Written informed consent was obtained from all patients.
Baseline features of patients are as follows: male 57.7%, aged mean ± standard deviation 58.3 ± 13.8 years; investigator global assessment (IGA) 3.4 ± 0.6, eczema area and severity index (EASI) 24.0 ± 9.2, peak pruritus numerical rating scale (PPNRS) 7.1 ± 2.9, sleep quality NRS 6.7 ± 3.0, and dermatology life quality index (DLQI) 8.8 ± 6.5. Nine patients previously received systemic therapy (1 patient with baricitinib 4 mg, 3 with upadacitinib 15 mg, 1 with upadacitinib 30 mg, 2 with dupilumab, and 3 with tralokinumab).
EASI, PP-NRS, sleep quality NRS, and DLQI were assessed at weeks 4, 12, 16, 24, 36, and 48. All these scores rapidly decreased by week 12, thereafter plateaued or gradually decreased through week 48 (Figure 1). The rates achieving IGA 0/1, ≥ 4-point improvement of PP-NRS, ≥ 4-point improvement of sleep quality NRS, and DLQI 0/1 continued to increase and reached 50.0%, 64.3%, 80.0%, and 66.7%, respectively, at week 48 (Figure 1). Simultaneously, PN lesions became flattened and decreased over time in most patients. Mild-to-moderate conjunctivitis occurred in three patients. There were no serious adverse events or adverse events leading to discontinuation of lebrikizumab.
In conclusion, this study demonstrated the effectiveness and tolerability of lebrikizumab for the PN-like phenotype of AD. Limitations were the small sample size and inability to precisely track the number of PN-like lesions. Further investigation in larger cohorts with longer follow-up periods and precise counting of PN is required to confirm the long-term effectiveness of lebrikizumab for the PN-like phenotype of AD.
Atopic dermatitis (AD) presents with several phenotypes, among which the prurigo nodularis (PN)-like phenotype is particularly resistant to treatment.1 PN-like phenotype of AD is characterized by multiple widespread pruritic nodules and intense and persistent itch, sometimes accompanied by pain.1 Interleukin (IL)-13 is a type-2 cytokine that plays a central role in skin inflammation, barrier disruption, and pruritus associated with AD, including PN-like phenotype.2
Lebrikizumab is a high-affinity humanized immunoglobulin G4 monoclonal antibody that specifically inhibits IL-13. Clinical trials and real-world studies have demonstrated its effectiveness and good tolerability for moderate-to-severe AD.3,4,5 However, data on the effectiveness of lebrikizumab are currently lacking for the PN-like phenotype of AD. Therefore, we retrospectively evaluated the effectiveness and safety of lebrikizumab in 26 patients aged ≥ 12 years with PN-like phenotype of AD who were treated for at least 4 weeks (up to 48 weeks) from May 2024 to July 2025. At baseline, all patients had ≥ 20 excoriated and hyperkeratotic nodules primarily on the trunk and extremities. Lebrikizumab was administered subcutaneously at 500 mg at weeks 0 and 2, followed by 250 mg every 2 weeks together with topical corticosteroids of moderate‑to‑strongest potency. After week 16, all patients received lebrikizumab every 4 weeks. Written informed consent was obtained from all patients.
Baseline features of patients are as follows: male 57.7%, aged mean ± standard deviation 58.3 ± 13.8 years; investigator global assessment (IGA) 3.4 ± 0.6, eczema area and severity index (EASI) 24.0 ± 9.2, peak pruritus numerical rating scale (PPNRS) 7.1 ± 2.9, sleep quality NRS 6.7 ± 3.0, and dermatology life quality index (DLQI) 8.8 ± 6.5. Nine patients previously received systemic therapy (1 patient with baricitinib 4 mg, 3 with upadacitinib 15 mg, 1 with upadacitinib 30 mg, 2 with dupilumab, and 3 with tralokinumab).
EASI, PP-NRS, sleep quality NRS, and DLQI were assessed at weeks 4, 12, 16, 24, 36, and 48. All these scores rapidly decreased by week 12, thereafter plateaued or gradually decreased through week 48 (Figure 1). The rates achieving IGA 0/1, ≥ 4-point improvement of PP-NRS, ≥ 4-point improvement of sleep quality NRS, and DLQI 0/1 continued to increase and reached 50.0%, 64.3%, 80.0%, and 66.7%, respectively, at week 48 (Figure 1). Simultaneously, PN lesions became flattened and decreased over time in most patients. Mild-to-moderate conjunctivitis occurred in three patients. There were no serious adverse events or adverse events leading to discontinuation of lebrikizumab.
In conclusion, this study demonstrated the effectiveness and tolerability of lebrikizumab for the PN-like phenotype of AD. Limitations were the small sample size and inability to precisely track the number of PN-like lesions. Further investigation in larger cohorts with longer follow-up periods and precise counting of PN is required to confirm the long-term effectiveness of lebrikizumab for the PN-like phenotype of AD.
DISCLOSURES
Hidehisa Saeki, Teppei Hagino, and Naoko Kanda received lecture fees from Eli Lilly. The remaining authors report no conflicts of interest. Funding sources: This work is partly supported by 2025 scholarship grants from Maruho Takagi Dermatology Foundation and Torii Pharmaceutical Co., Ltd. This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committees of Nippon Medical School Chiba Hokusoh Hospital and Nippon Medical School. Written informed consent was obtained from all participants. Data availability statement: The data that support the findings of this study are available from the corresponding author upon reasonable request.
