Anti-p200 pemphigoid

Goletz, Stephanie; Hashimoto, Takashi; Zillikens, Detlef; Schmidt, Enno

doi:10.1016/j.jaad.2014.02.036

Cited by 101 publications

(133 citation statements)

References 46 publications

Supporting

Mentioning

114

Contrasting

Unclassified

Order By: Relevance

“…The clinical course of anti‐p200 pemphigoid was considered to be of a benign nature as compared with other subepidermal AIBDs . Yet, the rarity of the disease and the lack of large‐scale longitudinal studies restrict a precise assessment of the true clinical outcomes of these patients.…”

Section: Introductionmentioning

confidence: 99%

Treatment and clinical outcomes in anti‐p200 pemphigoid: a systematic review

Britva

Amber

Cohen

et al. 2019

Acad Dermatol Venereol

View full text Add to dashboard Cite

Background Current treatment paradigms in anti‐p200 pemphigoid rely on low levels of evidence, primarily originating from case reports and case series. Objective To systematically review the utilized treatment modalities for anti‐p200 pemphigoid and to synthesize the available clinical outcomes of treated patients. Methods We conducted a systematic review of the literature using Ovid‐Medline (1946–2018), Embase (1947–2018) and Web of Science (1900–2018) databases with a broad and inclusive search strategy along with a subsequent search of retrieved articles. All case reports and case series of patients with anti‐p200 pemphigoid were included. Results Sixty‐eight eligible studies comprising 113 anti‐p200 pemphigoid patients with a mean age of 65.5 years were included in the qualitative synthesis. The clinical outcome of patients following treatment was reported for 91 (80.5%) patients, of whom 83 (91.2%) had achieved complete remission at least once. Complete remission on‐therapy was observed in 51 (56.0%) and complete remission off‐therapy in 12 (13.2%) patients. Thirty‐six (39.6%) patients had experienced at least one flare during the duration of follow‐up. A combination of systemic corticosteroids and adjuvant immunomodulatory agents was the leading therapeutic approach (63.0%) required for disease control. Systemic and topical corticosteroids as monotherapy were sufficient to control the disease in 19.6% and 13.0% of cases, respectively. Dapsone was the most commonly used (41.3%) adjuvant agent. The highest rates of complete remission were achieved in patients managed by systemic corticosteroids as monotherapy (100%) and in those managed by systemic corticosteroids with adjuvant agents (90.7%). Conversely, 45.5% of patients treated only by topical corticosteroids experienced at least one relapse during follow‐up. Conclusion The vast majority of patients had reached a complete remission during the course of the disease, whereas a considerable proportion of patients experienced at least one relapse. A combination of systemic corticosteroids and adjuvant immunomodulatory agents was the most frequently utilized therapeutic approach.

show abstract

Section: Introductionmentioning

confidence: 99%

Treatment and clinical outcomes in anti‐p200 pemphigoid: a systematic review

Britva

Amber

Cohen

et al. 2019

Acad Dermatol Venereol

View full text Add to dashboard Cite

show abstract

“…In our case, the patient has pemphigoid with antibodies to three different antigens; BP180, BP230 and laminin γ1. It was reported that approximately 25% of patients with anti‐laminin γ1 pemphigoid have reactivity against other autoantigens . Simultaneous autoimmune response to laminin γ1 and BP180 has been reported in four cases including our case, although other three cases did not have psoriasis .…”

Section: Discussionmentioning

confidence: 51%

Pemphigoid with antibodies to laminin γ1, BP180 and BP230, associated with psoriasis vulgaris: Successful disease control with cyclosporin

Imanishi

Tateishi

Imanishi

et al. 2015

The Journal of Dermatology

Self Cite

View full text Add to dashboard Cite

Both anti-laminin γ1 pemphigoid and bullous pemphigoid are autoimmune subepidermal blistering diseases. The former is rare and characterized by autoantibodies to laminin γ1, a 200-kDa dermal protein, while the latter is common among the elderly and characterized by autoantibodies to BP180 and BP230, both of which are hemidesmosomal proteins. We experienced a 69-year-old Japanese male patient with blister formation secondary to erythrodermic psoriasis, which was successfully treated with cyclosporin. The histopathology of erythema corresponded with psoriasis and that of a blistering lesion showed infiltration of neutrophils and eosinophils in and around the subepidermal blisters. Patient immunoglobulin G antibodies labeled both the epidermal and dermal sides of 1 mol/L NaCl-split human skin by indirect immunofluorescent microscopy and recognized laminin γ1, BP180 and BP230 by immunoblotting. To the best of our knowledge, this is the first report of coexistence of psoriasis and atypical pemphigoid with these three autoantibodies.

show abstract

“…This technique, however, is tricky and may result in the complete destruction of the skin sample. Moreover, patients with antip200/laminin γ1 pemphigoid and anti-laminin 332 pemphigoid also reveal autoantibodies bound at the blister floor and cannot be differentiated from EBA by this technique [4,127].…”

Section: Direct If Microscopymentioning

confidence: 99%

“…By indirect IF microscopy of human salt-split skin, antitype VII collagen antibodies label the floor of the artificial blister ( Figure 7) [138]. However, antibodies against laminin 332 and the p200 protein/ laminin γ1 also bind to the floor of the blister [3,127,139,140]. In latter two diseases, however, direct IF microscopy reveals an n-serrated pattern.…”

Section: Indirect If Microscopymentioning

confidence: 99%

Clinical features and diagnosis of epidermolysis bullosa acquisita

Vorobyev

Ludwig

Schmidt

2016

Expert Review of Clinical Immunology

Self Cite

100

View full text Add to dashboard Cite

Introduction: Epidermolysis bullosa acquisita (EBA) is a rare autoimmune blistering disease of skin and mucous membranes. EBA is caused by autoantibodies against type VII collagen, which is a major component of anchoring fibrils, attaching epidermis to dermis. Binding of autoantibodies to type VII collagen leads to skin fragility and, finally, blister formation. The clinical picture of EBA is polymorphic, with several distinct phenotypes being described. Despite recent progress in understanding the pathophysiology of EBA, its diagnosis is still challenging. Areas covered: This review provides an update on the clinical manifestations and diagnostic methods of EBA. We searched PubMed using the terms 'epidermolysis bullosa acquisita' covering articles in English between 1 January 2005 and 31 May 2016. Relevant older publications were retrieved form cited literature. Expert commentary: While the clinical picture is highly variable, diagnosis relies on direct immunofluorescence (IF) microscopy of a perilesional skin biopsy. Linear deposits of IgG, IgA and/or C3 along the dermal-epidermal junction with an u-serrated pattern are diagnostic for EBA alike the detection of serum autoantibodies against type VII collagen. Several test systems for the serological diagnosis of EBA have recently become widely available. In some patients, sophisticated diagnostic approaches only available in specialized centers are required. ARTICLE HISTORY

show abstract

Anti-p200 pemphigoid

Cited by 101 publications

References 46 publications

Treatment and clinical outcomes in anti‐p200 pemphigoid: a systematic review

Treatment and clinical outcomes in anti‐p200 pemphigoid: a systematic review

Pemphigoid with antibodies to laminin γ1, BP180 and BP230, associated with psoriasis vulgaris: Successful disease control with cyclosporin

Clinical features and diagnosis of epidermolysis bullosa acquisita

Contact Info

Product

Resources

About