Title : Successful lebrikizumab therapy following tralokinumab in moderate atopic dermatitis with limited systemic treatment options: Implications for sequential IL-13 inhibition
Abstract:
Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease predominantly driven by type 2 inflammation pathways, with interleukin-13 (IL-13) playing a central role. Although targeted biologic therapies have expanded treatment options for moderate-to-severe AD, evidence guiding intra-class switching between IL-13 inhibitors remains limited.
Case presentation: We report a 29-year-old man with lifelong AD. He was a social smoker and had a history of heavy alcohol consumption, hepatic steatosis, with a BMI >25 kg/m2. He had lifelong AD presenting with excoriated, lichenified eczema predominantly affecting the upper body.
Baseline disease severity was moderate, with Eczema Area and Severity Index (EASI) score of 9, Patient-Oriented Eczema Measure (POEM) score of 16, and Dermatology Life Quality Index (DLQI) score 8. Previous treatments included phototherapy, Upadacitinib, methotrexate, ciclosporin, which were discontinued due to contraindications or suboptimal response. JAK inhibitors were contraindicated due to hepatic steatosis and the patient was initiated on tralokinumab. However, only mild and gradual improvements was observed before a significant flare occurred, with no meaningful overall improvement in disease severity.
Following MDT, the decision was made to switch from tralokinumab to lebrikizumab without washout period. At four-month post-switch, he demonstrated marked clinical improvement, with EASI 0, POEM 5, DLQI 7, and pruritus NRS score 3, with only minimal residual eczema involving the face, left antecubital fossa, and right wrist. At six-month follow-up, overall disease control remained substantially improved despite a mild flare (EASI 1.4, DLQI 5, POEM 9).
Discussion: IL-13 is a central driver of inflammation, barrier dysfunction, and pruritus in AD. Despite targeting the same cytokine, lebrikizumab and tralokinumab differ in their mechanisms of receptor interaction, which may contribute to variation in clinical repones. The improvement in pruritus observed in this patient reflects the central role of IL-13 in neuroimmune pathways involved in itch.
Conclusion: Sequential IL-13 inhibition may represent a viable therapeutic strategy in selected patients with AD, particularly when systemic treatment options are limited. Further research is needed to determine whether clinical or molecular factors may help predict response to individual IL-13 inhibitors and guide more personalised treatment strategy in AD.
