Omalizumab as an alternative therapeutic tool in the treatment of bullous pemphigoid: A case report

Vico‐Alonso, Cristina; Calleja‐Algarra, Alba; Aragón‐Miguel, Raquel; Sánchez-Velázquez, Alba; Velasco‐Tamariz, Virginia; Ortiz‐Romero, Pablo L.; Monsálvez‐Honrubia, Verónica

doi:10.1111/dth.12829

Cited by 18 publications

(18 citation statements)

References 11 publications

(12 reference statements)

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“…Significant efforts have been devoted to developing novel therapeutics for BP. Omalizumab, a humanized monoclonal antibody of IgE, has been reported to be useful in a pruritic BP patient who was deemed unsuitable for higher doses of glucocorticoids and immunosuppressive agents [ [163] , [164] , [165] , [166] ], and can be an alternative treatment for BP patients. Bertilimumab, a human monoclonal antibody of eotain-1, may decrease the infiltration of eosinophils in the skin of patients with BP.…”

Section: Bullous Pemphigoidmentioning

confidence: 99%

The pathogenesis of bullous skin diseases

Yang

Zhao

et al. 2019

Journal of Translational Autoimmunity

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Bullous skin diseases are a group of dermatoses characterized by blisters and bullae in the skin and mucous membranes. The etiology and pathogenesis of bullous skin diseases are not completely clear. The most common are pemphigus and bullous pemphigoid (BP). Autoantibodies play critical roles in their pathogenesis. Abnormalities in the adhesion between keratinocytes in patients with pemphigus leads to acantholysis and formation of intra-epidermal blisters. Anti-desmoglein autoantibodies are present both in the circulation and skin lesions of patients with pemphigus. The deficient adhesion of keratinocytes to the basement membrane in BP patients gives rise to subepidermal blisters. Autoantibodies against the components of hemidesmosome can be detected in BP patients. Many novel therapeutics based on knowledge of the pathogenesis have emerged in recent years.

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Section: Bullous Pemphigoidmentioning

confidence: 99%

The pathogenesis of bullous skin diseases

Yang

Zhao

et al. 2019

Journal of Translational Autoimmunity

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“…Bullous pemphigoid (BP) is a blistering antibody-mediated autoimmune skin disease. BP is associated with tissue-bound and circulating autoantibodies directed against two hemidesmosomal proteins, BP180 (also called BPAG2, type XVII collagen) and/or BP230 (also called BPAG1-e) (1, 2). For many decades, studies examining the pathogenic mechanisms of BP autoantibodies focused solely on IgG (3).…”

Section: Introductionmentioning

confidence: 99%

“…As a result, humanized monoclonal antibody directed to IgE, omalizumab, an approved treatment for severe asthma and chronic spontaneous urticaria, might represent an alternative drug for BP. Although the clinical effectiveness of omalizumab in treatment of BP has been already demonstrated (1, 2, 12, 15–18), the exact mechanism of action remains elusive. Furthermore, current data suggest that only a subset of BP patients respond favorably to omalizumab treatment.…”

Section: Introductionmentioning

confidence: 99%

Effects of Omalizumab on FcεRI and IgE Expression in Lesional Skin of Bullous Pemphigoid

et al. 2019

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Recent studies suggest an important role of immunoglobulin E (IgE) as an alternative pathogenic pathway in the development of bullous pemphigoid (BP), as the most frequent subepidermal blistering disease of the skin Use of IgE targeted therapies, such as omalizumab, has been shown promising in recent studies. The aim of this study was to assess the effect of omalizumab on FcεRI and IgE expression on circulating basophils and on lesional intradermal cells in BP to generate insight into the immunological effects of omalizumab in BP. We report two cases of BP patients treated with omalizumab. Efficacy of treatment was assessed clinically 4 months after initiation of the therapy. Lesional and non-lesional skin biopsies where taken before and 4 weeks after initiation of omalizumab therapy. In addition, FcεRI expression on circulating cells and IgE levels in serum and in the skin samples, as well as anti-BP180 and anti-BP230 in serum and eosinophils and basophils counts in blood were assessed before and during treatment. Both patients showed a marked improvement after 4 months, with no adverse effects. Down-regulation of FcεRI, IgE in lesional skin and on circulating basophils were observed in parallel with clinical improvement. The current case study supports the role of omalizumab in the treatment of a subset of BP patients. Our observations suggest that omalizumab represents a valuable therapeutic option in the management of BP patients. Its efficacy might be related to reduction in FcεRI+ and IgE+ basophils and intradermal cells.

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“…The significance of IgE autoantibodies in BP however remains controversial as they are not universally detected and are not associated with a specific BP phenotype . Reports demonstrating successful treatment with omalizumab, a humanized monoclonal antibody directed to IgE, have shown modest success in recalcitrant cases of BP . Future investigations may unveil clinical characteristics that afford clinicians early identification of patients responsive to anti‐IgE therapy.…”

Section: Evolving Therapeutic Targetsmentioning

confidence: 99%

“…145 Reports demonstrating successful treatment with omalizumab, a humanized monoclonal antibody directed to IgE, have shown modest success in recalcitrant cases of BP. [146][147][148][149] Future investigations may unveil clinical characteristics that afford clinicians early identification of patients responsive to anti-IgE therapy.…”

Section: Inhibitory Antibodiesmentioning

confidence: 99%

From bench to bedside: evolving therapeutic targets in autoimmune blistering disease

Kridin

Kowalski

Kneiber

et al. 2019

Acad Dermatol Venereol

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Autoimmune blistering diseases comprise a group of heterogenous conditions characterized by the loss of tolerance and subsequent development of autoantibodies targeting epidermal and subepidermal adhesion proteins. Blisters and erosions form on the skin and mucous membranes leading to significant morbidity and mortality. Traditional therapies rely on systemic immunosuppression. Advancements in our understanding of the pathophysiology of pemphigus and pemphigoid have led to the development of molecules which target specific pathways involved in induction and perpetuation of disease. In this review, we outline the novel therapeutic strategies including B‐cell depletion, T‐regulatory cell repletion, cell signalling inhibitors and small molecular inhibitors, inhibitory monoclonal antibodies, as well as complement inhibition. We additionally review their current level of clinical evidence. We lastly review therapeutics targets gleaned from the experimental epidermolysis bullosa acquisita mouse model. These emerging treatments offer an exciting progression from basic science discoveries that have the potential to transform the treatment paradigm in autoimmune blistering diseases.

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Omalizumab as an alternative therapeutic tool in the treatment of bullous pemphigoid: A case report

Cited by 18 publications

References 11 publications

The pathogenesis of bullous skin diseases

The pathogenesis of bullous skin diseases

Effects of Omalizumab on FcεRI and IgE Expression in Lesional Skin of Bullous Pemphigoid

From bench to bedside: evolving therapeutic targets in autoimmune blistering disease

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