Consensus Statement on the Use of Intravenous Immunoglobulin Therapy in the Treatment of Autoimmune Mucocutaneous Blistering Diseases

Ahmed, A. Razzaque; Dahl, Mark V.

doi:10.1001/archderm.139.8.1051

Cited by 156 publications

(137 citation statements)

References 100 publications

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“…In PF and PV mice, the HDIG/anti-Dsg1 or HDIG/anti-Dsg3 IgG ratio was 1 mg HDIG/g body weight versus 1:640 anti-Dsg1 or anti-Dsg3 IgG titer. In IVIG-treated patients (BP, PF, and PV), the IVIG/patients' autoantibody ratio is approximately 0.7 g IVIG/kg body weight/day/3-day cycle versus 1:160 (1:40 to 1:640 for most patients' sera) autoantibody titers (34). The ratio of IVIG levels/autoantibody levels in the serum of treated patients is compatible with that of the treated mice.…”

Section: Figurementioning

confidence: 65%

“…Intravenous Ig (IVIG) has been shown to be effective for the treatment of a variety of immune-mediated inflammatory diseases (25), including autoimmune cytopenias, GuillainBarré syndrome, multiple sclerosis, myasthenia gravis, anti-factor VIII autoimmune disease, dermatomyositis, Kawasaki disease, vasculitis, uveitis, and graft-versus-host disease (26)(27)(28)(29)(30)(31)(32). Recently, IVIG has also been reported to treat a small group of patients with human autoimmune blistering diseases, including pemphigus and pemphigoid (33,34). However, the use of IVIG in these blistering diseases is still controversial, and no controlled study has been done on the efficacy of IVIG in the treatment of these diseases.…”

Section: Introductionmentioning

confidence: 99%

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Complete FcRn dependence for intravenous Ig therapy in autoimmune skin blistering diseases

Zhao²,

Hilario-Vargas³

et al. 2005

Journal of Clinical Investigation

226

189

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Numerous mechanisms of action have been proposed for intravenous Ig (IVIG). In this study, we used IgG passive transfer murine models of bullous pemphigoid (BP), pemphigus foliaceus (PF), and pemphigus vulgaris (PV) to test the hypothesis that the effect of IVIG in autoantibody-mediated cutaneous bullous diseases is to accelerate the degradation of pathogenic IgG by saturation of the MHC-like Fc receptor neonatal Fc receptor (FcRn). BP, PF, and PV are organ-specific antibody-mediated diseases in which autoantibodies target the hemidesmosomal antigen BP180 and desmosomal antigens Dsg1 and Dsg3, respectively. Antibodies against BP180, Dsg1, and Dsg3, when injected into neonatal mice, induce the BP, PF, and PV disease phenotypes, respectively. We found that FcRn-deficient mice were resistant to experimental BP, PF, and PV. Circulating levels of pathogenic IgG in FcRndeficient mice were significantly reduced compared with those in WT mice. Administration of high-dose human IgG (HDIG) to WT mice also drastically reduced circulating pathogenic IgG levels and prevented blistering. In FcRn-deficient mice, no additional protective effect with HDIG was realized. These data demonstrate that the therapeutic efficacy of HDIG treatment in the pemphigus and pemphigoid models is dependent on FcRn. Thus, FcRn is a promising therapeutic target for treating such IgG-mediated autoimmune diseases.

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Section: Figurementioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Complete FcRn dependence for intravenous Ig therapy in autoimmune skin blistering diseases

Zhao²,

Hilario-Vargas³

et al. 2005

Journal of Clinical Investigation

226

189

View full text Add to dashboard Cite

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“…most often azathioprine or mycophenolate, although only a few randomized clinical trials have proven their efficacy (49,50). Treatment can be augmented with intravenous immunoglobulin (51) or plasmapheresis (52)(53)(54), which aims to reduce circulating autoantibody levels. Treatment with the anti-CD20 antibody rituximab has been shown to be effective in inducing short-term disease remission in 95%-100% of PV patients (55,56) associated with a decrease in anti-DSG antibody titers, while antibody titers to tetanus toxoid or Pneumococcal polysaccharides remain constant (57)(58)(59).…”

Section: Current Pv Treatment and Implications For The Development Ofmentioning

confidence: 99%

Setting the target for pemphigus vulgaris therapy

Ellebrecht¹,

Payne²

2017

JCI Insight

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“…As aplicações mensais deverão ser mantidas até remissão clínica, depois aumentar os intervalos das infusões para seis, oito,10, 12 e 14 semanas, e suspender o tratamento após obtenção da remissão clínica com intervalo superior a 16 semanas. 56,57 Há relatos recentes de tratamentos de casos graves resistentes a outras terapêuticas com Rituximab (anticorpo monoclonal quimérico antiCD20) na dose 375mg/m 2 EV semanalmente, durante quatro semanas consecutivas. O tratamento é bem tolerado, com relatos de remissão prolongada da doença com ciclo único de tratamento.…”

Section: Tratamentounclassified

Dermatoses bolhosas auto-imunes

Cunha

Barraviera²

2009

An. Bras. Dermatol.

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Resumo: Dermatoses bolhosas autoimunes são doenças cuja manifestação cutânea primária e fundamental consiste em vesículas e bolhas. Classificam-se conforme a localização da bolha, em intraepidérmica e subepidérmica. Os pacientes produzem autoanticorpos contra estruturas específicas da pele detectáveis por técnicas de imunofluorescência, immunobloting e Elisa. Os recentes avanços da biologia molecular e celular têm permitido conhecer esses autoantígenos, contra os quais os pacientes se sensibilizam e que estão localizados na epiderme ou na junção dermoepidérmica. São doenças de baixa incidência, porém de elevada morbidade e por vezes letais. O objetivo deste trabalho é revisar e descrever os progressos nos conhecimentos de quatro doenças vésico-bolhosas autoimunes: pênfigo foliáceo endêmico (fogo selvagem), pênfigo vulgar, penfigóide bolhoso e dermatite herpetiforme. Palavras-chave: Alergia e imunologia; Dermatite herpetiforme; Dermatopatias vesiculobolhosas; Penfigo; Penfigóide bolhoso Abstract: Abstract: Autoimmune bullous dermatoses are diseases in which blisters and vesicles are the primary and fundamental types of skin lesion. Their classification is based on the location of the blister: intraepidermal and subepidermal. Patients produce autoantibodies against self-specific structures of the skin detectable by immunofluorescence techniques, immunoblotting and ELISA. Recent advances in molecular and cellular biology have brought to knowledge these self-antigens, against which patients are sensitized, and which are found in epidermis or in the dermo-epidermal junction. These are low incidence, but high morbidity diseases that may be fatal. The aim of this article is to review and describe the progress of four autoimmune vesiculobullous disorders: endemic pemphigus foliaceous (wild fire), pemphigus vulgaris, bullous pemphigoid and dermatitis herpetiformis. Keyword: Allergy and immunology; Bullous pemphigoid; Dermatitis herpetiformis; Pemphigus; Skin diseases vesiculobullous histológicas comuns e ambos apresentam autoanticorpos da subclasse IgG4, cujo antígeno-alvo é a desmogleína 1, antígeno desmossomal de 160kd.O FS acomete mais frequentemente crianças, adolescentes e adultos jovens que vivem nas áreas rurais de regiões endêmicas, e é comum a ocorrência

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Consensus Statement on the Use of Intravenous Immunoglobulin Therapy in the Treatment of Autoimmune Mucocutaneous Blistering Diseases

Cited by 156 publications

References 100 publications

Complete FcRn dependence for intravenous Ig therapy in autoimmune skin blistering diseases

Complete FcRn dependence for intravenous Ig therapy in autoimmune skin blistering diseases

Setting the target for pemphigus vulgaris therapy

Dermatoses bolhosas auto-imunes

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