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Protein Contact Dermatitis Medication

  • Author: Cheryl Levin, MD; Chief Editor: Dirk M Elston, MD  more...
Updated: Jul 11, 2013

Medication Summary

Short-term treatment may include high-potency topical corticosteroids, such as clobetasol propionate, to decrease inflammation. Topical tacrolimus 1% ointment may be a good long-term choice. Oral antihistamines may be administered if severe pruritus ensues.[11]


Corticosteroids, Topical

Class Summary

Corticosteroids are immunosuppressives with anti-inflammatory properties that modify the body's immune response to diverse stimuli. Other actions include vasoconstriction and antiproliferation. These agents have limited use in the treatment of protein contact dermatitis.

Clobetasol propionate (Temovate, Clobex, Cormax)


A class I superpotent topical steroid, clobetasol suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. This agent decreases inflammation by stabilizing lysosomal membranes, inhibiting polymorphonuclear leukocyte and mast cell degranulation.


Immunomodulators, Topical

Class Summary

These agents modify immune processes that promote inflammation.

Tacrolimus (Protopic, Prograf)


The mechanism of action of tacrolimus in atopic dermatitis not known. Reduces itching and inflammation by suppressing release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin (IL)–3, IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha, all of which are involved in early stages of T-cell activation.

Additionally, tacrolimus may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of high-affinity IgE receptor (FCeRI) on Langerhans cells.

Tacrolimus can be used in patients as young as 2 years. It is more expensive than topical corticosteroids. This agent is available as an ointment in concentrations of 0.03% and 0.1%. It is indicated only after other treatment options have failed.



Class Summary

Antihistamines act by competitive inhibition of histamine at the H1 receptor. They may control itching by blocking effects of endogenously released histamine.

Hydroxyzine hydrochloride (Vistaril)


This agent antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the central nervous system.

Contributor Information and Disclosures

Cheryl Levin, MD Resident Physician, Department of Dermatology, University of Minnesota Medical School

Cheryl Levin, MD is a member of the following medical societies: American Academy of Dermatology, Women's Dermatologic Society, Medical Dermatology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

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

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: XOMA; Biogen/IDEC; Novartis; Janssen Biotech, Abbvie, CSL pharma<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 dividends from trust accounts, but I do not control these accounts, and 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; for: Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


Erin M Warshaw, MD, MS Associate Professor, Clinical Scholar Track and Co-Director of Contact Dermatitis Clinic, Department of Dermatology, University of Minnesota Medical School; Chief of Dermatology, Division of Dermatology, Minneapolis Veterans Affairs Medical Center

Erin M Warshaw, MD, MS is a member of the following medical societies: American Contact Dermatitis Society and Women's Dermatologic Society

Disclosure: Nothing to disclose.

  1. Hjorth N, Roed-Petersen J. Occupational protein contact dermatitis in food handlers. Contact Dermatitis. 1976 Feb. 2(1):28-42. [Medline].

  2. Veien NK, Hattel T, Justesen O, Nørholm A. Causes of eczema in the food industry. Derm Beruf Umwelt. 1983. 31(3):84-6. [Medline].

  3. Jones HE, Reinhardt JH, Rinaldi MG. Immunologic susceptibility to chronic dermatophytosis. Arch Dermatol. 1974 Aug. 110(2):213-20. [Medline].

  4. Wang LF, Lin JY, Hsieh KH, Lin RH. Epicutaneous exposure of protein antigen induces a predominant TH2-like response with high IgE production in mice. Journal of Immunology. 1996. 156:4079-82.

  5. Lehto M, Koivuluhta M, Wang G, Amghaiab I, Majuri ML, Savolainen K. Epicutaneous natural rubber latex sensitization induces T helper 2-type dermatitis and strong prohevein-specific IgE response. J Invest Dermatol. 2003 Apr. 120(4):633-40. [Medline].

  6. Janssens V, Morren M, Dooms-Goossens A, Degreef H. Protein contact dermatitis: myth or reality?. Br J Dermatol. 1995 Jan. 132(1):1-6. [Medline].

  7. Levin C, Warshaw E. Protein contact dermatitis: allergens, pathogenesis, and management. Dermatitis. 2008 Sep-Oct. 19(5):241-51. [Medline].

  8. Hannuksela M. Protein Contact Dermatitis. Frosch PJ, Torkil M, Lepoittevin J-P. Contact Dermatitis. 4th. Berlin: Springer; 2006. 345-348.

  9. Hansen KS, Petersen HO. Protein contact dermatitis in slaughterhouse workers. Contact Dermatitis. 1989 Oct. 21(4):221-4. [Medline].

  10. Warshaw E, Lee G, Storrs FJ. Hand dermatitis: a review of clinical features therapeutic options, and long-term outcomes. American Journal of Contact Dermatitis. 2003. 14:119-37.

  11. Mercader P, de la Cuadra-Oyanguren J, Rodriguez-Serna M, Pitarch-Bort G, Fortea-Baixauli JM. Treatment of protein contact dermatitis with topical tacrolimus. Acta Derm Venereol. 2005. 85(6):555-6. [Medline].

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