Abstract
Atopic dermatitis is a chronic, pruritic inflammatory cutaneous condition that can carry significant morbidity. Severe or recalcitrant atopic dermatitis is often treated with immunosuppressants, biologics, or immune-modulating small molecule therapies. The Janus kinase-signal transducer and activator of transcription pathway is highly implicated in atopic dermatitis pathogenesis, and agents that inhibit Janus kinase signalling are new to the atopic dermatitis landscape. Upadacitinib is a JAK1 inhibitor that has a good safety and efficacy profile and is increasingly being prescribed for atopic dermatitis. We report a case of a 35-year-old male with extensive atopic dermatitis that initially improved significantly on upadacitinib, then after 6 months developed a severe crusted dermatitic eruption on the head favouring a seborrheic distribution. While the pathogenesis of this paradoxical reaction is unclear, this phenomenon may involve a shift to a more Th1/Th17-mediated immune response.