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Linear IgA Dermatosis Medication

  • Author: Mark Tye Haeberle, MD; Chief Editor: William D James, MD  more...
Updated: Jun 18, 2015

Medication Summary

Large, randomized, placebo-controlled, double-blind studies have not been performed for the treatment of linear IgA dermatosis in children or adults. Most cases have been reported to respond to dapsone or sulfapyridine.[17] Some clinicians favor the use of sulfapyridine because of the lower incidence of adverse effects.[18] However, some patients' conditions may not respond to sulfapyridine but do respond to treatment with dapsone. A response may be seen in 48-72 hours. Other reportedly useful medications include prednisone, sulfamethoxypyridazine, colchicine, dicloxacillin, mycophenolate mofetil, and intravenous immunoglobulin.

Drug-induced disease may be treated merely by withdrawal of the offending agent. In cases of linear IgA dermatosis induced by vancomycin, new lesions stop forming within approximately 2 weeks of withdrawal.[19] Particularly severe cases of drug-induced linear IgA dermatosis respond to a short course of oral corticosteroids.


Leprostatic agents

Class Summary

These agents have been shown to be beneficial in the treatment of linear IgA dermatosis.

Dapsone (Avlosulfon)


Dapsone is bactericidal and bacteriostatic against mycobacteria; the mechanism of action is similar to that of sulfonamides where competitive antagonists of PABA prevent formation of folic acid, inhibiting bacterial growth.



Class Summary

These agents exert bacteriostatic action by competitive antagonism of para-aminobenzoic acid (PABA). Microorganisms that require exogenous folic acid and do not synthesize folic acid are not susceptible to the action of sulfonamides.



Sulfapyridine is a competitive antagonist of PABA. Its mechanism of action in linear IgA dermatosis is unknown. Sulfapyridine is currently not available in the United States.



Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Prednisone (Deltasone)


Prednisone is an immunosuppressant used for the treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.


Anti-inflammatory agents

Class Summary

These agents modulate events leading to inflammatory reactions.



Colchicine decreases leukocyte motility and phagocytosis in inflammatory responses.



Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Dicloxacillin (Dycill, Dynapen)


Dicloxacillin is used in the treatment of infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when staphylococcal infection is suspected.



Class Summary

These agents are used to improve the clinical and immunologic aspects of the disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.

Immune globulins intravenous (Carimune NF, Flebogamma, Gammagard Liquid, Gammagard S/D, Privigen)


Immune globulins neutralize circulating antibodies and down-regulate proinflammatory cytokines, including INF-gamma; They block Fc receptors on macrophages, suppress inducer T and B cells, augment suppressor T cells, and block the complement cascade.

Contributor Information and Disclosures

Mark Tye Haeberle, MD Resident Physician, Department of Medicine, Division of Dermatology, University of Louisville School of Medicine

Mark Tye Haeberle, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Student Association/Foundation, American Society of Dermatopathology

Disclosure: Nothing to disclose.


Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: Eli Lilly; XOMA; Biogen/IDEC; Novartis; Celgene<br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor and intermittent author; Received royalty from Elsevier for book author/editor; Received i do not control these accounts, but have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; .

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair Research Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Russell Hall, MD J Lamar Callaway Professor And Chair, Department of Dermatology, Duke University Medical Center, Duke University School of Medicine

Russell Hall, MD is a member of the following medical societies: American Academy of Dermatology, American Federation for Medical Research, American Society for Clinical Investigation, Society for Investigative Dermatology

Disclosure: Received consulting fee from Novan for consulting; Received consulting fee from Stieffel, a GSK company for consulting; Received salary from Society for Investigative Dermatology for board membership.


Peter A Klein, MD Associate Professor, Department of Dermatology, University Hospital, State University of New York at Stony Brook

Disclosure: Nothing to disclose.

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Annular lesions demonstrating the string of beads sign.
Bullous lesions on the genital area in a child with linear IgA dermatosis.
Persons with linear immunoglobulin A (IgA) dermatosis may present with prominent ocular signs and symptoms.
Neutrophilic microabscesses in linear immunoglobulin A (IgA) dermatosis.
Bullous lesions of the palmar surface in an elderly man with vancomycin-induced linear immunoglobulin A (IgA) dermatosis.
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