Dermatitis Herpetiformis Treatment & Management

  • Author: Jami L Miller, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 13, 2011
 

Medical Care

Treatment of dermatitis herpetiformis (DH) include avoidance of gluten by consuming a gluten-free diet and pharmacotherapy.

A gluten-free diet is a lifelong commitment, and adherence to a strict diet is difficult to achieve. Improvement of skin disease with a gluten free diet takes several months. Gluten is present in various foods that are consumed on an everyday basis, most importantly wheat, barley, and rye. Concern has surrounded oats containing gluten, but studies have shown that consumption of a moderate amount of oats does not worsen dermatitis herpetiformis or celiac disease.[35, 36] Contamination of gluten-free products with gluten remains a potential problem.[37] Nutritional supplementation with multivitamins and iron may be prudent in patients on a strict gluten-free diet.[38]

Dapsone (diaminodiphenyl sulfone) and sulfapyridine are the primary medications used to treat dermatitis herpetiformis. The exact mechanism of action is unknown but is thought to be related to inhibition of neutrophil migration and function. Patients report a symptomatic improvement within hours after initiation of dapsone therapy. Patients should be monitored for the adverse effects of dapsone, primarily hemolytic anemia, methemoglobinemia, agranulocytosis, and neuropathy. For patients unable to tolerate dapsone, particularly those who develop hemolysis, sulfapyridine may be substituted. New lesion formation is suppressed for up to 2 days after a dose of dapsone; however, dapsone does not improve GI mucosal pathology.

A retrospective study has shown remission, defined as 2 years with no symptoms, in 12% of patients.[39] When dermatitis herpetiformis is well-controlled, attempts can be made to taper off dapsone and perhaps attempt a diet with gluten.

Other, less effective treatments for dermatitis herpetiformis include colchicine, cyclosporine, azathioprine, and prednisone.[31] Ultraviolet light may provide some symptomatic relief. Cyclosporine should be used with caution in patients with dermatitis herpetiformis because of a potential increase in the risk of developing intestinal lymphomas.

One case report described resolution of dermatitis herpetiformis after initiation of the Atkins diet.[40]

Nonsteroidal anti-inflammatory drugs may exacerbate dermatitis herpetiformis; however, ibuprofen appears to be safe.[41]

Iodides may elicit or exacerbate dermatitis herpetiformis.

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Consultations

  • Consider consultation with a gastroenterologist for evaluation and for recommendations regarding gluten-sensitive enteropathy (GSE).
  • Consult with a dietitian regarding patients who are modifying dietary intake to avoid gluten or who are instituting an elemental diet.
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Diet

Dietary intake of gluten causes the disease, and elimination of gluten from the diet improves it.

  • A position statement by the American Gastroenterological Association (AGA) Institute advises that treatment for patients with dermatitis herpetiformis, like that of all patients with celiac disease, requires a strict, lifelong adherence to a gluten-free diet. The AGA stresses the importance of patient education, motivation, and support in maintaining adherence, and recommends consultation with an experienced dietician, referral to a support group, and clinical follow up for compliance, as well as treatment of nutritional deficiency states.[42] See the guideline summary, AGA Institute medical position statement on the diagnosis and management of celiac disease.
  • Most patients (as many as 80%) who can maintain a gluten-free diet respond with control of their skin disease. Some patients are able to discontinue dapsone therapy. Compliance with a gluten-free diet is difficult and requires a motivated patient, and the best treatment response occurs with absolute gluten restriction in the diet.
  • Strict dietary vigilance may be required for 5-12 months before the dapsone dose can be reduced.
  • Maintaining a gluten-free diet is the only sustainable method of eliminating the disease, not only from the skin, but also from the GI mucosa.
  • Patients on a gluten-reduced diet may experience a decrease in symptoms; therefore, such a diet can reduce the dosage of dapsone required for disease control.
  • Neither IgA deposition nor circulating antibodies correlate with gluten intake in short-duration studies; however, some studies have suggested a correlation with complement deposition. Avoidance of dietary gluten for 10 years or more has resulted in loss of cutaneous IgA deposits, which then return upon reinstitution of gluten in the diet.
  • Elemental diets may improve the disease within weeks.[43, 44] These diets consist of free amino acids, small amounts of triglycerides, and short-chain polysaccharides; they are marketed by pharmaceutical companies. One report has suggested that this improvement may be independent of gluten ingestion; however, this finding has not been confirmed.[44]
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Contributor Information and Disclosures
Author

Jami L Miller, MD  Assistant Professor, Division of Dermatology, Department of Internal Medicine, Vanderbilt University Medical School; Director of Phototherapy Unit, Vanderbilt University Medical Center; Consulting Attending Physician, Nashville Veterans Affairs Medical Center

Jami L Miller, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Shehnaz Aysha K Zaman, MD  Resident Physician, Department of Dermatology, Vanderbilt Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Disclosure: Genetech Grant/research funds Principle Investigator; Centecor Grant/research funds Principle Investigator

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Julia R Nunley, MD  Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center

Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, and Women's Dermatologic Society

Disclosure: Novartis Grant/research funds Consulting; Biolex Grant/research funds sub-investigator

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

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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Light micrograph shows neutrophils in the dermal papillae, with fibrin deposition, neutrophil fragments, and edema (hematoxylin and eosin stain).
Papillary microabscesses form and progress to subepidermal vacuolization and vesicle formation in the lamina lucida, the weakest portion of the dermoepidermal junction (hematoxylin and eosin stain).
Classic vesicles of dermatitis herpetiformis.
Immunofluorescence showing immunoglobulin A at the dermoepidermal junction (direct immunofluorescence stain).
Polymorphic lesions on extensor surface of arm.
 
 
 
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