Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

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.

Next

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.

Previous
Next

Sulfonamides

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

 

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.

Previous
Next

Corticosteroids

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.

Previous
Next

Anti-inflammatory agents

Class Summary

These agents modulate events leading to inflammatory reactions.

Colchicine

 

Colchicine decreases leukocyte motility and phagocytosis in inflammatory responses.

Previous
Next

Antibiotics

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.

Previous
Next

Immunoglobulins

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.

Previous
 
 
Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Acknowledgements

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

Disclosure: Nothing to disclose.

References
  1. Zone JJ, Taylor TB, Meyer LJ, Petersen MJ. The 97 kDa linear IgA bullous disease antigen is identical to a portion of the extracellular domain of the 180 kDa bullous pemphigoid antigen, BPAg2. J Invest Dermatol. 1998 Mar. 110(3):207-10. [Medline].

  2. Zone JJ, Pazderka Smith E, Powell D, Taylor TB, Smith JB, Meyer LJ. Antigenic specificity of antibodies from patients with linear basement membrane deposition of IgA. Dermatology. 1994. 189 Suppl 1:64-6. [Medline].

  3. Sakaguchi M, Bito T, Oda Y, et al. Three cases of linear IgA/IgG bullous dermatosis showing IgA and IgG reactivity with multiple antigens, particularly laminin-332. JAMA Dermatol. 2013 Nov. 149(11):1308-13. [Medline].

  4. Zenke Y, Nakano T, Eto H, Koga H, Hashimoto T. A case of vancomycin-associated linear IgA bullous dermatosis and IgA antibodies to the a3 subunit of laminin-332. Br J Dermatol. 2014 Apr. 170(4):965-9. [Medline].

  5. Bernard P, Vaillant L, Labeille B, et al. Incidence and distribution of subepidermal autoimmune bullous skin diseases in three French regions. Bullous Diseases French Study Group. Arch Dermatol. 1995 Jan. 131(1):48-52. [Medline].

  6. Kharfi M, Khaled A, Karaa A, Zaraa I, Fazaa B, Kamoun MR. Linear IgA bullous dermatosis: the more frequent bullous dermatosis of children. Dermatol Online J. 2010 Jan 15. 16(1):2. [Medline].

  7. Chanal J, Ingen-Housz-Oro S, Ortonne N, et al. Linear IgA bullous dermatosis: comparison between the drug-induced and spontaneous forms. Br J Dermatol. 2013 Nov. 169(5):1041-8. [Medline].

  8. Wojnarowska F, Marsden RA, Bhogal B, Black MM. Chronic bullous disease of childhood, childhood cicatricial pemphigoid, and linear IgA disease of adults. A comparative study demonstrating clinical and immunopathologic overlap. J Am Acad Dermatol. 1988 Nov. 19(5 Pt 1):792-805. [Medline].

  9. Collier PM, Kelly SE, Wojnarowska F. Linear IgA disease and pregnancy. J Am Acad Dermatol. 1994 Mar. 30(3):407-11. [Medline].

  10. Billet SE, Kortuem KR, Gibson LE, El-Azhary R. A morbilliform variant of vancomycin-induced linear IgA bullous dermatosis. Arch Dermatol. 2008 Jun. 144(6):774-8. [Medline].

  11. Chan LS, Regezi JA, Cooper KD. Oral manifestations of linear IgA disease. J Am Acad Dermatol. 1990 Feb. 22(2 Pt 2):362-5. [Medline].

  12. Aultbrinker EA, Starr MB, Donnenfeld ED. Linear IgA disease. The ocular manifestations. Ophthalmology. 1988 Mar. 95(3):340-3. [Medline].

  13. Nousari HC, Kimyai-Asadi A, Caeiro JP, Anhalt GJ. Clinical, demographic, and immunohistologic features of vancomycin-induced linear IgA bullous disease of the skin. Report of 2 cases and review of the literature. Medicine (Baltimore). 1999 Jan. 78(1):1-8. [Medline].

  14. Alberta-Wszolek L, Mousette AM, Mahalingam M, Levin NA. Linear IgA bullous dermatosis following influenza vaccination. Dermatol Online J. 2009 Nov 15. 15(11):3. [Medline].

  15. Yhim HY, Kwon DH, Lee NR, Song EK, Yim CY, Kwak JY. Linear IgA bullous dermatosis following autologous PBSC transplantation in a patient with non-Hodgkin's lymphoma. Bone Marrow Transplant. 2010 Apr 12. [Medline].

  16. Godfrey K, Wojnarowska F, Leonard J. Linear IgA disease of adults: association with lymphoproliferative malignancy and possible role of other triggering factors. Br J Dermatol. 1990 Oct. 123(4):447-52. [Medline].

  17. Krejci-Manwaring J, West DA, Tonkovic-Capin V. If at first you don't succeed: a difficult case of Linear IgA. Dermatol Online J. 2009 Sep 15. 15(9):16. [Medline].

  18. Jablonska S, Chorzelski TP, Rosinska D, Maciejowska E. Linear IgA bullous dermatosis of childhood (chronic bullous dermatosis of childhood). Clin Dermatol. 1991 Jul-Sep. 9(3):393-401. [Medline].

  19. Klein PA, Callen JP. Drug-induced linear IgA bullous dermatosis after vancomycin discontinuance in a patient with renal insufficiency. J Am Acad Dermatol. 2000 Feb. 42(2 Pt 2):316-23. [Medline].

Previous
Next
 
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.