D3.155 - Th2–Th17 immune shift following dupilumab therapy

Background

Dupilumab is a monoclonal antibody that blocks IL-4 and IL-13 signaling pathways and represents an effective therapeutic option for severe type 2 asthma and atopic dermatitis. Although it has a favorable safety profile, paradoxical cutaneous reactions have been reported, including psoriasis and psoriasiform dermatitis. The prevalence of these manifestations in patients with atopic dermatitis treated with dupilumab ranges from 1.08% to 3.33%, while in severe asthma it is approximately 1%. The proposed pathophysiological mechanism is an immune shift in which inhibition of the Th2 pathway promotes compensatory activation of the Th17 pathway.

Case Report

A 26-year-old woman, ex-smoker (5 cigarettes/day), with allergic rhinoconjunctivitis, severe persistent asthma, and nut allergy. She showed allergy to grass pollen and subclinical sensitization to cat dander. Since 2023 she was followed due to severe uncontrolled asthma, with 3–4 hospital admissions per year and repeated use of oral corticosteroids. Complementary tests revealed peripheral eosinophilia (400–800/µL) and elevated total IgE levels (135 IU/mL). She was receiving formoterol/beclomethasone and tiotropium, with an ACT score of 17. Due to poor control, dupilumab (300 mg every two weeks) was initiated, achieving marked respiratory improvement. After 6–12 months of treatment, she developed erythematous and scaly lesions on the extremities and scalp, consistent with psoriasiform dermatitis.

Discussion

A multidisciplinary evaluation considered continuation of dupilumab with topical therapy versus discontinuation. Given the impact of the skin reaction and suspected adverse event, dupilumab was stopped and tezepelumab initiated. Following the switch, skin lesions resolved progressively while asthma remained controlled, with no further exacerbations.

Conclusion:

The resolution of the skin lesions after changing the biological therapy assess the relationship between the treatment with dupilumab and the development of psoriasiform dermatitis.