Plasmapheresis therapy of pemphigus

Bystryn, J. C.

doi:10.1001/archderm.124.11.1702

Cited by 24 publications

(17 citation statements)

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“…8 These findings are consistent with those of our group's prior studies, which have shown that this rebound can be reduced in animals 11 and in humans 12 by using immunosuppressive agents that inhibit antibody synthesis. Our results are nearly identical to those reported previously that the rebound in antibody levels that follows pemphigus antibody depletion by plasmapheresis was suppressed by the concurrent administration of an immunosuppressive agent.…”

Section: Commentsupporting

confidence: 89%

“…The rebound can be suppressed in animals by the coadministration of a cytotoxic drug such as cyclophosphamide. 11 This strategy has been applied to improve the effectiveness of the plasmapheresis treatment of pemphigus, 12 a procedure that also rapidly lowers serum levels of pathogenic antibodies. We have speculated that the coadministration of an immunosuppressive agent will similarly improve the effectiveness of IVIg in pemphigus and other autoantibody-mediated blistering diseases.…”

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confidence: 99%

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Improvement of Intravenous Immunoglobulin Therapy for Bullous Pemphigoid by Adding Immunosuppressive Agents

Czernik¹,

Bystryn²

2008

Arch Dermatol

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Section: Commentsupporting

confidence: 89%

mentioning

confidence: 99%

Improvement of Intravenous Immunoglobulin Therapy for Bullous Pemphigoid by Adding Immunosuppressive Agents

Czernik¹,

Bystryn²

2008

Arch Dermatol

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“…These observations strongly indicate the pathogenic relevance of Dsg1/3-reactive IgG autoantibodies in pemphigus and provide a rationale for utilizing therapeutic approaches aimed at removing circulating autoantibodies in PV and PF. Several groups successfully performed plasmapheresis in cases of severe or recalcitrant pemphigus [9,10,11]. Since plasmapheresis nonspecifically removes plasma proteins including clotting factors, hormones and albumin, the method of immunoadsorption (IA) was introduced as a more specific approach eliminating immunoglobulins and circulating immune complexes [12].…”

Section: Introductionmentioning

confidence: 99%

Prolonged Clinical Remission of Patients with Severe Pemphigus upon Rapid Removal of Desmoglein-Reactive Autoantibodies by Immunoadsorption

et al. 2006

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Background: In pemphigus, loss of epidermal adhesion is induced by binding of circulating autoantibodies to the desmosomal cadherins desmoglein 3 (Dsg3) in pemphigus vulgaris (PV) and desmoglein 1 (Dsg1) in pemphigus foliaceus (PF), respectively. Therapeutic removal of Dsg-reactive autoantibodies by immunoadsorption (IA) has been demonstrated to exert clinical remission of the disease. Objectives: The aim of this intervention study was to evaluate the efficacy and safety of the peptide-based Globaffin^® adsorber system in the treatment of severe pemphigus cases. Patients and Methods: We applied IA in 4 PV and 2 PF patients with severe chronic disease resistant to conventional immunosuppressive therapy. IA was performed on 4 consecutive days, representing 1 treatment cycle, followed by a 4-week treatment-free interval. Serum samples for determining serum IgG and anti-Dsg1/Dsg3 IgG autoantibodies were drawn daily before and after IA, respectively. During follow-up, patients were examined carefully, and laboratory parameters were controlled monthly for up to 1 year. Results: IA led to excellent clinical responses. Skin and mucosal lesions cleared almost completely within weeks. One IA cycle reduced anti-Dsg1 and anti-Dsg3 autoantibodies by an average of 50–70% as determined by ELISA. Conclusions: Using the Globaffin adsorber system, IA represents an effective and safe treatment opportunity in severe and therapy-resistant pemphigus.

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“…Plasmapheresis (Cotterill et al, 1978;Blaszczyk et al, 1981;Swanson and Dahl, 1981;Roujeau et al, 1982;Bystryn, 1988;Roujeau, 1993;Turner et al, 2000) sometimes with cyclosporin (Ruocco, 1988) or cyclophosphamide (Kiel synchronization protocol) and extracorporeal photophoresis (Edelson, 1984) have also been reported to be of benefit.…”

Section: Plasmapheresismentioning

confidence: 99%

Pemphigus Vulgaris: Update on Etiopathogenesis, Oral Manifestations, and Management

Scully

Challacombe

2002

Critical Reviews in Oral Biology & Medicine

136

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ABSTRACT:Pemphigus is a group of potentially life-threatening diseases characterized by cutaneous and mucosal blistering. There is a fairly strong genetic background to pemphigus with linkage to HLA class II alleles. Certain ethnic groups, such as Ashkenazi Jews and those of Mediterranean origin, are especially liable to pemphigus. Pemphigus vulgaris (PV), the most common and important variant, is an autoimmune blistering disease characterized by circulating pathogenic IgG antibodies against desmoglein 3 (Dsg3), about half the patients also having Dsg1 autoantibodies. Oral lesions are initially vesiculobullous but readily rupture, new bullae developing as the older ones rupture and ulcerate. Biopsy of perilesional tissue, with histological and immunostaining examinations, is essential to the diagnosis. Serum autoantibodies to either Dsg1 or Dsg3 are best detected by both normal human skin and monkey esophagus or by enzyme-linked immunosorbent assay (ELISA). Before the introduction of corticosteroids, pemphigus vulgaris was typically fatal mainly from dehydration or secondary systemic infections. Current treatment is largely based on systemic immunosuppression using systemic corticosteroids, with azathioprine, dapsone, methotrexate, cyclophosphamide, and gold as adjuvants or alternatives, but mycophenolate mofetil and intravenous immunoglobulins also appear promising.

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Plasmapheresis therapy of pemphigus

Cited by 24 publications

References 0 publications

Improvement of Intravenous Immunoglobulin Therapy for Bullous Pemphigoid by Adding Immunosuppressive Agents

Improvement of Intravenous Immunoglobulin Therapy for Bullous Pemphigoid by Adding Immunosuppressive Agents

Prolonged Clinical Remission of Patients with Severe Pemphigus upon Rapid Removal of Desmoglein-Reactive Autoantibodies by Immunoadsorption

Pemphigus Vulgaris: Update on Etiopathogenesis, Oral Manifestations, and Management

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