Dupilumab as a novel therapy for bullous pemphigoid: A multicenter case series

Abdat, Rana; Waldman, Reid A.; Bedout, Valeria De; Czernik, Annette; McLeod, Michael P.; King, Brett; Gordon, Samantha; Ahmed, Razzaque; Nichols, Anna; Rothe, Marti Jill; Rosmarin, David

doi:10.1016/j.jaad.2020.01.089

Cited by 147 publications

(145 citation statements)

References 12 publications

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“…Furthermore, the majority of patients with BP have an increased number of cells producing IL-4 and IL-13 in blood and lesional skin. The latter have been shown to decline with disease improvement (7,11). Based on this knowledge, dupilumab thus provides an option to target these disease-driving mechanisms inhibiting IL-4 and IL-13 signaling.…”

Section: Discussionmentioning

confidence: 99%

“…Based on this knowledge, dupilumab thus provides an option to target these disease-driving mechanisms inhibiting IL-4 and IL-13 signaling. It also indirectly downregulates IgE secretion and eosinophil activity (7,11).…”

Section: Discussionmentioning

confidence: 99%

“…Presence of tissue-bound and circulating anti-BP180 and anti-BP230 IgE autoantibodies in BP patients and findings in mouse models of BP have provided evidence that IgE autoantibodies have a pathogenicity role in BPs (2)(3)(4)(5)(6). Furthermore, type 2 pro inflammatory cytokines, including IL-4 and IL-13 contribute to tissue inflammation and damage in BP (7). Therefore, omalizumab, as a humanized monoclonal antibody directed to IgE, and dupilumab, as an interleukin (IL)-4 receptor alpha antagonist, might have a beneficial effect in BP (2,4,5,(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, type 2 pro inflammatory cytokines, including IL-4 and IL-13 contribute to tissue inflammation and damage in BP (7). Therefore, omalizumab, as a humanized monoclonal antibody directed to IgE, and dupilumab, as an interleukin (IL)-4 receptor alpha antagonist, might have a beneficial effect in BP (2,4,5,(7)(8)(9)(10). Here, we describe a patient with severe recalcitrant BP successfully treated with a combination therapy with omalizumab and dupilumab, as add-on therapy.…”

Section: Introductionmentioning

confidence: 99%

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Case Report: Combination of Omalizumab and Dupilumab for Recalcitrant Bullous Pemphigoid

et al. 2021

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Bullous pemphigoid (BP) is a blistering autoimmune skin disease. Omalizumab, a monoclonal antibody directed to IgE, showed a beneficial effect in treatment of recalcitrant BP in case series. More recently, dupilumab, an interleukin (IL)-4-receptor alpha antagonist, also showed promising preliminary results. We describe a patient with refractory BP who showed a complete response to a combination therapy with omalizumab and dupilumab.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Case Report: Combination of Omalizumab and Dupilumab for Recalcitrant Bullous Pemphigoid

et al. 2021

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“…BP-associated pruritus is also mediated by IL-31 expressing eosinophils, which are a major source of this pruritogenic cytokine in the skin and serum of BP patients [98,99]. Personal experience and preliminary evidence indicates a good clinical response to dupilumab in BP patients [100]. Phase II and phase III trials using dupilumab, mepolizumab, or benralizumab (two anti-IL-5 monoclonal antibodies) are also underway to test its efficacy and safety in patients with BP [101,102].…”

Section: Bullous Pemphigoidmentioning

confidence: 99%

Pruritus as a Distinctive Feature of Type 2 Inflammation

et al. 2021

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Pruritus is a common symptom of several skin diseases, both inflammatory and neoplastic. Pruritus might have a tremendous impact on patients’ quality of life and strongly interfere with sleep, social, and work activities. We review the role of type-2 inflammation and immunity in the pathogenesis of chronic pruritic conditions of the skin. Type 2 cytokines, including IL-4, IL-13, thymic stromal lymphopoietin, periostin, IL-31, IL-25, and IL-33 are released by mast cells, innate lymphoid cells 2, keratinocytes, and type 2 T lymphocytes, and are master regulators of chronic itch. These cytokines might act as direct pruritogen on primary sensory neurons (pruriceptors) or alter the sensitivity to other itch mediators Type 2 inflammation- and immunity-dominated skin diseases, including atopic dermatitis, prurigo nodularis, bullous pemphigoid, scabies, parasitic diseases, urticaria, and Sézary syndrome are indeed conditions associated with most severe pruritus. In contrast, in other skin diseases, such as scleroderma, lupus erythematosus, hidradenitis suppurativa, and acne, type 2 inflammation is less represented, and pruritus is milder or variable. Th2 inflammation and immunity evolved to protect against parasites, and thus, the scratching response evoked by pruritus might have developed to alert about the presence and to remove parasites from the skin surface.

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