Mesh : Humans Dermatitis, Atopic / drug therapy chemically induced Dermatologists Antibodies, Monoclonal, Humanized / adverse effects Antibodies, Monoclonal / adverse effects Treatment Outcome Severity of Illness Index Hyperkeratosis, Epidermolytic

来  源:   DOI:10.1089/derm.2022.0096

Abstract:
Dupilumab, a monoclonal antibody targeting interleukin-4 antibody, is approved for use in many type 2 inflammatory diseases, including atopic dermatitis. It is generally well tolerated with no need of routine laboratory monitoring. However, several adverse events have been reported during real-world practice and in pivotal trials. We conducted a systematic literature research of the PubMed, Medline, and Embase databases to identify articles recording the clinical manifestation and potential pathogenesis of these adverse events with interests (AEIs) to dermatologists. In total, 547 cases from 134 studies have developed 39 AEIs 1 day to 2.5 years after dupilumab treatment. The most common AEIs are facial and neck dermatitis (299 cases), psoriasis (70 cases), arthralgia (56 cases), alopecia (21 cases), cutaneous T cell lymphoma (19 cases), severe ocular diseases (19 cases), and drug eruption (6 cases). Most of the AEIs recorded in this review resolved or improved after dupilumab discontinuation or the addition of another treatment, whereas 3 of the cases died of severe AEI. The potential pathogenesis included T help type 1 (Th1)/T help type 2 (Th2) imbalance, Th2/T help type 17 (Th17) imbalance, immune reconstitution, hypersensitivity reaction, transient hypereosinophilia related, and Th1 suppression. Clinicians should be alert of these AEIs for timely diagnosis and appropriate treatment.
摘要:
Dupilumab,针对白细胞介素-4抗体的单克隆抗体,被批准用于许多2型炎症性疾病,包括特应性皮炎.它通常具有良好的耐受性,无需常规实验室监测。然而,在现实世界的实践和关键试验中已经报告了一些不良事件.我们对PubMed进行了系统的文献研究,Medline,和Embase数据库,以确定记录这些不良事件的临床表现和潜在发病机制的文章与皮肤科医生的利益(AEIs)。总的来说,来自134项研究的547例病例在dupilumab治疗后1天至2.5年发展出39例AEIs。最常见的AEIs是面部和颈部皮炎(299例),银屑病(70例),关节痛(56例),脱发(21例),皮肤T细胞淋巴瘤(19例),严重的眼部疾病(19例),药疹(6例)。本综述中记录的大多数AEIs在dupilumab停药或添加另一种治疗后得到解决或改善,而其中3例死于严重AEI。潜在的发病机制包括T帮助型1(Th1)/T帮助型2(Th2)失衡,Th2/T帮助17型(Th17)失衡,免疫重建,过敏反应,短暂性嗜酸性粒细胞增多相关,Th1抑制临床医生应警惕这些AEIs,以便及时诊断和适当治疗。
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