Long‐Term Use of Tralokinumab in Patients With Atopic Dermatitis: A Real‐World Multicentric Case Series

Tralokinumab is a human immunoglobulin G4 monoclonal antibody approved for treating moderate-to-severe atopic dermatitis (AD). Since its regulatory approval, several studies have evaluated the performance of tralokinumab in real-world settings, though results have been limited to the first year of treatment [1-4]. This case series aimed to assess the real-world effectiveness, safety, and tolerability of long-term tralokinumab use in adult patients with AD treated at five dermatology clinics in Austria between August 16, 2021, and July 30, 2024. All patients provided informed consent for inclusion in this study and for their anonymized data to be published in related publications. Effectiveness was evaluated using the Eczema Area and Severity Index (EASI), the Investigator Global Assessment (IGA), and the Peak Pruritus Numerical Rating Scale (PP-NRS). This case series included 13 patients (six male and seven female) with a median age of 33 years (Table 1). Previous AD treatments consisted of topical corticosteroids (85% of patients), phototherapy (54%), dupilumab (54%), systemic corticosteroids (31%), and calcineurin inhibitors (31%). The median (interquartile range [IQR]) treatment duration for tralokinumab was 29 (13–35) months. Most patients (92%) had received tralokinumab for over 1 year, and four had been on treatment for approximately 3 years. Only one patient discontinued tralokinumab, which was due to pregnancy rather than side effects or dissatisfaction with treatment effectiveness. Five patients experienced dry eyes, blepharitis, and/or conjunctivitis with tralokinumab, but these generally resolved over time. Other treatment-emergent adverse events included herpes simplex infection (n = 2), head/neck dermatitis (n = 1), worsening of dust mite allergy (n = 1), hair loss (n = 1), and respiratory infection (n = 1). The hair loss was mild, resolved within three months, and the relationship to tralokinumab was uncertain. Five patients had previously experienced conjunctivitis while on dupilumab. Of these, four reported that the condition had resolved, and one noted an improvement following the transition to tralokinumab. The median (IQR) EASI score dropped from 11.2 (4.4–15.3) at the start of tralokinumab treatment to 1.3 (0.1–3.1) at the most recent EASI assessment (with a median follow-up of 23.5 months). Similar reductions were noted for other parameters, with median (IQR) IGA declining from 3.0 (3.0–4.0) to 1.0 (0.0–1.0) and PP-NRS falling from 4.5 (3.8–8.0) to 1.0 (0.5–2.5) over median follow-up periods of 18.0 and 23.0 months, respectively (Figure 1). Most patients (9 out of 12; 75%) achieved an IGA score of 0 or 1 at their most recent assessment. Of the nine patients with EASI scores at baseline and at least one follow-up visit, EASI 75, EASI 90, and EASI 100 were reached by seven (78%), four (44%), and two (18%) patients, respectively. All patients who had skin assessments more than 2 years after starting tralokinumab maintained EASI scores of ≤ 3.2, and all but one had an IGA score of 0–1. This multicentric case series involved 13 patients with long-standing AD who initiated tralokinumab and received treatment for up to 3 years. Tralokinumab was tolerated well, and symptom suppression was maintained throughout long-term treatment. These results align with data from the ECZTEND study showing long-term control of AD signs and symptoms with tralokinumab [5]. Our study had several limitations. It was a case series study subject to inherent selection bias, lacked a control arm, and has incomplete data. Additionally, the study included only a small number of patients, and the follow-up dates varied among them. Findings from this retrospective case series provide real-world evidence that tralokinumab can be a well-tolerated and effective long-term treatment option for patients with AD. We thank the patients who contributed to this study. B.E. has received fees for speaking and attending conferences from Janssen-Cilag Pharma, Stallergenes Greer, Bristol-Myers Squibb, MEDA Pharma, HAL Allergy, Bencard Allergie, Eli Lilly, Galderma, Novartis, ALK—Abellò, Thermo Fisher Scientific, Pfizer, AbbVie, Leo Pharma, Almirall, La Roche, and L'Oréal. C.B. has been an adviser to and/or received speakers' honoraria from and/or participated in clinical trials for ALK, Almirall, AbbVie, Eli Lilly, Galderma, LEO Pharma, A. Menarini Pharma, Novartis, Pfizer, and Sanofi Genzyme. D.M. has received fees for speaking from Lilly, AbbVie, Almirall, Sanofi, Leo Pharma, Novartis, Janssen-Cilag, Boehringer Ingelheim, UCB, and Bristol-Myers Squibb. J.T. has been a consultant or speaker for Almirall, BMS, Eli Lilly, Johnson & Johnson, LEO Pharma, and Novartis, and has received support for congresses from Eli Lilly, Johnson & Johnson, LEO Pharma, and Novartis. B.G. has no conflicts of interest to declare.