Pemphigus, IgA Medication

  • Author: Lawrence S Chan, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 9, 2010
 

Medication Summary

In general, corticosteroids are the mainstay of treatment for IgA pemphigus. Dapsone, a medication with antineutrophilic effects, also may be helpful.

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Anti-inflammatory agents

Class Summary

IgA pemphigus is characterized histologically by inflammatory cell (neutrophil) infiltration in the upper epidermis. Anti-inflammatory agents theoretically block the inflammatory process and improve the disease conditions.[24, 25]

Prednisone (Deltasone)

 

Effective treatment for IgA pemphigus. Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production. Consult the pediatrician before prescribing medication in children.

Dapsone (Avlosulfon)

 

Bactericidal and bacteriostatic against mycobacteria; mechanism of action is similar to sulfonamides in which competitive antagonists of PABA prevent formation of folic acid, inhibiting bacterial growth. Used alone or in conjunction with other anti-inflammatory medications for treating IgA pemphigus. Consult the pediatrician before prescribing medication in children.

Acitretin (Soriatane)

 

Retinoic acid analog. Mechanism of action is unknown. Used effectively in several reported cases of IgA pemphigus.

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Contributor Information and Disclosures
Author

Lawrence S Chan, MD  Dr Orville J Stone Professor of Dermatology, Head, Department of Dermatology, University of Illinois College of Medicine

Lawrence S Chan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Dermatological Association, American Medical Association, Association of Professors of Dermatology, Chicago Dermatological Society, Dermatology Foundation, Illinois State Medical Society, Microcirculatory Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Takeji Nishikawa, MD  Emeritus Professor, Department of Dermatology, Keio University School of Medicine; Director, Samoncho Dermatology Clinic; Managing Director, The Waksman Foundation of Japan Inc

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Edward F Chan, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Department of Dermatology, Geisinger Medical Center

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Histopathologic examination of a blister lesion obtained from a patient with immunoglobulin A pemphigus shows a suprabasal blistering process, acantholysis, and an inflammatory cell infiltrate containing numerous neutrophils (hematoxylin and eosin, original magnification X50).
Indirect immunofluorescence microscopy performed on monkey esophagus substrate (with serum from a patient with immunoglobulin A pemphigus) detects the immunoglobulin A1 subclass of circulating autoantibodies that label the epithelial cell surfaces of the substrate.
 
 
 
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