Phenotypic switch to eczema in patients receiving biologics for plaque psoriasis: a systematic review

Abstract

The use of biologic therapies for the treatment of chronic plaque psoriasis has been linked to the development of atopic eczema, amongst other cutaneous adverse events. This can cause diagnostic confusion and create difficulty in the management of patients with plaque psoriasis. The main objective of this systematic review was to review all cases of eczema, including atopic eczema, reported in patients treated with biologics for chronic plaque psoriasis. PubMed, Medline and Embase databases were used to identify studies reporting eczema in patients treated with biologic therapy for chronic plaque psoriasis. A total of 92 patients were identified from 24 studies, with patients treated with either: adalimumab; etanercept; infliximab; ixekizumab; secukinumab; or ustekinumab. Factors common to some reported cases include: a prior history of atopy; eosinophilia; raised serum immunoglobulin E. Twenty‐three had documented treatment outcomes; 14 had biologic therapy discontinued or switched. Management strategies included topical or oral corticosteroids, and treatment with alternative systemic agents such as ciclosporin or apremilast. This adverse event occurred in 1.0–12.1% of patients within trial data and observational studies. This review demonstrates that there are consistent reports of a switch to an atopic eczema phenotype from psoriasis in patients taking biologics inhibiting tumour necrosis factor alpha and the interleukin (IL)‐17/IL‐23 axis. The majority stopped the implicated biologic, but conservative management was successful in some cases. Those with an atopic diathesis may be more at risk. Elucidation of mechanisms and risk factors would contribute to optimal therapy selection for individual patients.

Cutaneous Adverse Reactions to COVID-19 Vaccines: Insights from an Immuno-Dermatological Perspective

“…This appears counterintuitive at first, but the chronically skewed cutaneous immune reaction in AD patients predisposes them to perpetuation of inflammatory loops sparked by different triggers. For example, shifting between Th1-polarized and Th2-polarized dermatoses with different treatments, including targeted biologicals, has been a topic of debate for some years now [ 62 , 63 ]. This phenomenon demonstrates the difficulty of rebalancing lost homeostasis in skin immunity.…”

The IL-23/IL-17 Pathway in Inflammatory Skin Diseases: From Bench to Bedside

“…Both the Th1 and Th2 responses are involved in the pathogenesis of eczema. This may be due to the anti-IL-17 biologics mainly inhibit the Th17 cytokines and mediate an imbalance in the Th2/Th17 immune response, thus leading to eczematous eruptions (102)(103)(104). The deficiency of Th17 cells, IL-17RA, and IL-17F are essential for host defense against fungal pathogens in mucocutaneous and oral epithelial cells (105)(106)(107)(108)(109).…”

Pathophysiology of psoriasis: A review

“…The administration of IL-17 or IL-23 inhibitors occasionally induces AD-like eczema. 81,82 An elevation of immunoglobulin E in the skin has been reported in psoriasis patients after treatment with an IL-17 inhibitor. 83 In a mouse study, IL-17-deficient mice exhibited AD-like dermatitis spontaneously, possibly due to changes in the skin microbiota and subsequent increase in thymic stromal lymphopoietin in the skin.…”

“…Conversely, blockade of the IL‐23/IL‐17 axis may shift the immunological balance to type 2 inflammation. The administration of IL‐17 or IL‐23 inhibitors occasionally induces AD‐like eczema 81,82 . An elevation of immunoglobulin E in the skin has been reported in psoriasis patients after treatment with an IL‐17 inhibitor 83 .…”