D3.109 - Lichen planus following dupilumab treatment in patients with severe asthma and nasal sinus polyposis

Dupilumab, blocking both interleukin-4 and interleukin-13 signaling, is used to treat moderate-to-severe atopic dermatitis, severe asthma and nasal sinus polyposis. While lichen planus (LP) is an inflammatory, type 1 immune-mediated dermatosis, recent literature has identified a possible correlation between the onset of lichenoid skin injuries and the administration of dupilumab for atopic dermatitis (AD) exclusively.

We report here, for the first time, two original cases of LP occurring after dupilumab administration for severe asthma and nasal polyposis.

The first case report was a 48 years-old woman who developed Lichenoid lesions 9 months after dupilumab employment (200 mg/15 days) to treat severe asthma. Lesions involved upper limbs, trunk, and extremities. Dupilumab was switched for mepolizumab, high-dose dermocorticoids treatment was initiated, and skin lesions regressed within a month.  The second case report was a 29 years-old man, displaying after 8 months of dupilumab used to cure NSP (300 mg/15 days), flat-topped erythematous to violaceous plaques and papules on ankles, wrists and forearms.  Dupilumab was maintened during 2 years, and skin lesions persist despite the use of dermocorticoids.

In both cases, pathological examinations of skin biopsy were consistent with LP. Interestingly, the review of their medical files revealed the presence of AD between childhood and adolescence, then no longer active.

The risk of LP appears to be higher in patients with AD, but not exclusively and to the best of our knowledge, theses case reports are the firsts to describe cutaneous LP in patients treated with dupilumab for severe asthma and nasal sinus polyposis. Although it is a rare event, these observations strengthen the hypothesis that dupilumab by downregulating T2 pathway, may lead to T1/T2 imbalance, facilitating T1 response, to promote the onset of LP. Further research on this topic is necessary to better understand the underlying mechanisms of dupilumab-induced LP development and clinical attention is required in our routine medical practice, especially all the more in patients with  a clinical history of AD.