Vesicular Palmoplantar Eczema Medication

  • Author: Wingfield Rehmus, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Nov 30, 2010
 

Medication Summary

The goals of pharmacotherapy for vesicular palmoplantar eczema are to reduce morbidity and to prevent complications.

The dyshidrotic eczema severity index (DASI), a standardized severity scale for palmoplantar eczema, has made it easier to compare the efficacy of various therapies in controlled clinical trials.[29]

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Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the immune response of the body to diverse stimuli.

Betamethasone topical (Diprolene)

 

For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.

Clobetasol (Temovate)

 

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Prednisone (Deltasone)

 

Immunosuppressant to treat autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

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Systemic immunosuppressives

Class Summary

These agents are used for severe acute episodes and as steroid-sparing agents in the chronic forms of the disease.

Azathioprine (Imuran)

 

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, resulting in low autoimmune activity. Used in transplant recipients and some autoimmune conditions.

Cyclosporine (Neoral, Sandimmune)

 

Calcineurin inhibitor. Potent immunosuppressant; nonmyelotoxic but markedly nephrotoxic. Widely used in organ and tissue transplantation and skin diseases (eg, psoriasis, atopic dermatitis).

Methotrexate (Rheumatrex)

 

Antimetabolite; inhibits enzyme dihydrofolate reductase, which is essential for purine and pyrimidine synthesis. Unknown mechanism of anti-inflammatory action. Folinic acid after MTX administration helps prevent MTX-induced mucositis or myelosuppression.

Mycophenolate (CellCept)

 

Immunosuppressant to prevent acute rejection of renal or cardiac transplants. Inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, inhibiting their proliferation. Inhibits antibody production.

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Retinoids

Class Summary

Beta-carotene derivatives have marked effects on keratinizing epithelia. Etretinate often helps control hyperkeratosis in hyperkeratotic palmar eczema. Therapy may have to be continued indefinitely. The incidence of adverse effects tends to be high.

Acitretin (Soriatane)

 

Retinoic acid analog, like etretinate and isotretinoin. Etretinate is main metabolite and has clinical effects similar to those of etretinate. Mechanism of action unknown.

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Nickel-chelating agents

Class Summary

These drugs split into 2 molecules of sodium diethyldithiocarbamate after absorption, which, in turn, chelates divalent metal ions (eg, Ni++) and results in the increased urinary excretion of nickel. Effective in the treatment of vesicular palmoplantar dermatitis in nickel-hypersensitive patients whose eczema is aggravated by oral challenge with nickel.

Disulfiram (Antabuse)

 

Thiuram derivative that interferes with aldehyde dehydrogenase. Chelating effect helpful in reducing the nickel burden in patients allergic to nickel.

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Phototherapy

Class Summary

PUVA therapy is used to treat many skin conditions, including psoriasis, eczema, urticaria, mycosis fungoides, vitiligo, and palmoplantar pustular dermatoses.

The drug 8-methoxypsoralen (8-MOP) is taken 2 h before exposure to UVA irradiation. The initial UVA irradiation dose of 2.5 J/cm2 is usually increased by 0.5 J/cm2 for approximately 6 treatments, then by 1 J/cm2 per treatment for a total of 25-35 treatments.

Local bath-PUVA therapy has been successful in treating palmoplantar eczema and psoriasis. Compared with systemic PUVA, local-bath therapy has several advantages, particularly the absence of phototoxicity, severe hyperpigmentation, and protracted photosensitivity. The drug 8-MOP in a 0.15% alcoholic solution is added to tap water (37°C) at a concentration of 1 mg 8-MOP/L (0.0001%). After a 15-minute bath, the palms or soles are exposed to UVA radiation.

Methoxsalen (Oxsoralen, Meladinine, Basotherm)

 

Inhibits mitosis by covalently binding to pyrimidine bases in DNA when photoactivated by UV-A.

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Topical immunosuppressives

Class Summary

Topical immunosuppressive agents, such as tacrolimus, have been successfully used to decrease the severity of chronic palmar eczema. These drugs may be used as steroid-sparing agents.

Tacrolimus topical (Protopic)

 

Reduces itching and inflammation by suppressing release of cytokines from T cells; inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha (all involved in early T-cell activation).

May inhibit release of preformed mediators from skin mast cells and basophils; may down-regulate FCeRI expression on Langerhans cells. Can be used in patients as young as 2 y. Drugs of this class more expensive than topical corticosteroids.

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Contributor Information and Disclosures
Author

Wingfield Rehmus, MD, MPH  Dermatologist, BC Children's Hospital, Vancouver, British Columbia

Wingfield Rehmus, MD, MPH is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Carol E Cheng  Boston University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

James J Nordlund, MD  Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

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.

Jeffrey J Miller, MD  Associate Professor of Dermatology, Penn State University College of Medicine; Staff Dermatologist, Penn 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, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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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