Abstract
To the Editor:
Lebrikizumab is a monoclonal antibody that selectively inhibits interleukin-13 signaling, a cytokine that is dysregulated in atopic dermatitis (AD).1,2
Randomized trials show that lebrikizumab significantly increases the proportion of adults with moderate-to-severe AD achieving clear or almost clear skin.3,4 We describe the efficacy and safety profile of long‐term lebrikizumab treatment in 3 patients with refractory AD.
Patients were identified from a consecutive cohort of individuals with clinician-diagnosed moderate-to-severe, refractory AD who initiated lebrikizumab at a single dermatology practice. Disease severity was assessed at the time of lebrikizumab initiation and at the most recent visit using the Investigator’s Global Assessment (IGA: 0–4, clear to severe) and percent body surface area (BSA) affected (Table 1). Patient-reported disease control was assessed at baseline and follow-up with the Atopic Dermatitis Control Tool (ADCT). A ≥5-point decrease reflects clinically meaningful within-person improvement, and scores <7 indicate well-controlled disease. 5
Characteristics and Outcomes of Refractory AD Patients Treated with Lebrikizumab (Ebglyss)
AD, atopic dermatitis; BSA, body surface area; IGA, Investigator’s Global Assessment; q2w, every 2 weeks; q4w, every 4 weeks; HTN, hypertension.
Three adult patients (2 males, 1 female) were identified with an average age of 43.7 years (range, 33–56). The loading dose for all patients was 500 mg at weeks 0 and 2, followed by 250 mg every 2 weeks. None were spaced to monthly dosing as they had not achieved IGA 0 or 1 status. No adverse events were reported for any of the patients.
Case 1. A 42-year-old man with adult-onset AD and concomitant prurigo nodularis presented with xerosis and severe, widespread eczematous patches involving the trunk and extremities (IGA = 4; BSA = 65%, ADCT = 18). He had been unresponsive to aggressive topicals, dupilumab, and upadacitinib. He was on cyclosporine at 100 mg twice daily. Lebrikizumab was initiated and cyclosporine was weaned over 2 months. After ∼5 months of lebrikizumab therapy, he showed improvement to a moderate score along with a nearly 20% reduction in BSA involvement (IGA = 3; BSA = 46%, ADCT = 12).
Case 2. A 33-year-old man with adult-onset AD presented with widespread severe eczematous patches on the trunk and extremities (IGA = 4; BSA = 57%, ADCT = 20). He was on aggressive topical therapy using wet wraps along with potent topical steroids and several non-steroidal agents. He had failed dupilumab, tralokinumab, upadacitinib, and cyclosporine and had required intermittent prednisone tapers. After ∼8 months of lebrikizumab therapy, involvement was limited to only the upper extremities with marked improvement (IGA = 2; BSA = 19%, ADCT = 8).
Case 3. A 56-year-old woman with adult-onset AD presented with widespread eczematous patches on the trunk, extremities, and face (IGA = 3; BSA = 78%, ADCT = 14). She was on aggressive topical therapy and failed dupilumab, upadacitinib, and cyclosporine. After ∼6 months of lebrikizumab therapy, she showed reduced involvement of BSA and a 5-point improvement in her ADCT score (IGA = 3; BSA = 33%, ADCT = 9).
The results from this retrospective study, along with open‐label phase 3 data,3,4 suggest that lebrikizumab is a promising option for adults with refractory AD. Notably, all cases achieved clinically meaningful ADCT improvement (≥5-point decrease). Prospective, multicenter studies are warranted to define durability of response, optimal maintenance intervals, and predictors of treatment success in refractory disease.