医学
特应性皮炎
贾纳斯激酶
皮肤病科
后遗症
发病机制
脂溢性皮炎
免疫学
免疫系统
头皮
Janus激酶抑制剂
细胞因子
外科
作者
Elena Pastukhova,Alison Spurr,Quentin Nakonechny,Jennifer Lipson
标识
DOI:10.1177/2050313x231164271
摘要
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.
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