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Therapeutic effect of mizoribine on pemphigus vulgaris and pemphigus foliaceus

We evaluated the effectiveness of mizoribine, a newly developed immunosuppressive agent, as an adjuvant therapy in the treatment of both pemphigus vulgaris and pemphigus foliaceus. Eleven pemphigus patients (eight pemphigus vulgaris and three pemphigus foliaceus) received the combination therapy of

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Efficacy of low-dose rituximab in a refractory acquired factor VIII inhibitor case secondary to pemphigus.

Acquired factor VIII (FVIII) inhibitor induces a bleeding disorder caused by specific antibodies to FVIII. The cause of approximately one fifth of cases can be attributed to autoimmune disorders, such as pemphigus. Here, we describe a case of refractory acquired

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Lack of relationship between blood groups and clinical outcome (body surface area affected) in patients with pemphigus vulgaris

IndianJDermatol_2012_57_5_411_100513_u2

Associations between blood groups and several diseases are observed in the literature. Some of these have scientific support suggesting a rationale, statistical relation. The association between ABO groups with several malignancies, hypercholesterolemia, thrombosis, myocardial infarction, duodenal ulcer, infections, and autoimmune

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Is there an emergent need to modify the Desmoglein compensation theory in pemphigus on the basis of ELISA data and alternative pathogenic mechanisms ?

We read with interest the study by Koga H et al1 and we believe that in light of recent observations including our data (Table 1) the “desmoglein compensation theory” as a explanation for localization of blisters should be revisited 2,3,4.

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Enrichment of total serum IgG4 in pemphigus patients.

Background:  Pemphigus vulgaris (PV) and pemphigus foliaceus (PF) are potentially fatal blistering diseases caused by autoantibodies targeting desmoglein adhesion proteins. Previous studies have shown an IgG4>IgG1 predominance of anti-desmoglein antibodies in pemphigus; however, no studies have examined total serum IgG4

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IgA pemphigus associated with diffuse large B-cell lymphoma showing unique reactivity with desmocollins: Unusual clinical and histopathological features.

Authors: Asahina A, Koga H, Suzuki Y, Hashimoto T Abstract IgA pemphigus includes subcorneal pustular dermatosis (SPD)-type and intraepidermal neutrophilic IgA dermatosis (IEN)-type. Cases of IgG/IgA pemphigus have recently been documented(1) . Nonetheless, individual reports of IgA pemphigus indicate considerable

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Profile of Trypanosoma cruzi Reactivity in a Population at High Risk for Endemic Pemphigus Foliaceus (Fogo Selvagem).

Fogo Selvagem (FS) is an autoimmune bullous disease with pathogenic IgG autoantibodies recognizing desmoglein 1 (Dsg1), a desmosomal glycoprotein. In certain settlements of Brazil, a high prevalence of FS (3%) is reported, suggesting environmental factors as triggers of the autoimmune

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Ultrastructure of acantholysis in pemphigus foliaceus reexamined from the current perspective

Background  Pemphigus foliaceus (PF) is a chronic cutaneous autoimmune blistering disease that is characterized by superficial blistering of the skin, and according to the current perspective is caused by autoantibodies directed against desmoglein 1 (Dsg1). Objectives  To examine early acantholysis

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IgA pemphigus associated with diffuse large B-cell lymphoma showing unique reactivity with desmocollins: Unusual clinical and histopathological features

IgA pemphigus includes subcorneal pustular dermatosis (SPD)-type and intraepidermal neutrophilic IgA dermatosis (IEN)-type. Cases of IgG/IgA pemphigus have recently been documented1. Nonetheless, individual reports of IgA pemphigus indicate considerable heterogeneity. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2133.2012.11127.x/abstract

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Mycophenolate Mofetil for the Management of Autoimmune Bullous Diseases

This article reviews the use of MMF for the treatment of several bullous conditions, and assesses the evidence gathered from clinical trials and case series. According to numerous case series, MMF could be of value in treating refractory disease.

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