Close
New

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

 

Allergic Contact Dermatitis Medication

  • Author: Daniel J Hogan, MD; Chief Editor: William D James, MD  more...
 
Updated: Apr 22, 2015
 

Medication Summary

The goal of pharmacotherapy is to reduce morbidity and to prevent complications. Topical glucocorticosteroids are the mainstay of therapy. Topical calcineurin inhibitors (immunomodulators) may be preferred for persistent facial particularly periocular dermatitis. When choosing a topical glucocorticosteroid, match the potency to the location of the dermatitis and the vehicle to the morphology (ointment for dry scaling lesions; lotion or cream for weeping areas of dermatitis).

For severe acute allergic contact dermatitis (eg, poison ivy dermatitis, erythroderma), systemic glucocorticosteroids or other immunosuppressive medications (eg, azathioprine) may be occasionally needed for widespread and severe chronic dermatitis, particularly to airborne allergens such as feverfew (Parthenium hysterophores).

In some cases, allergic contact dermatitis may prove persistent despite avoidance of the allergen. In some of these cases (eg, nickel), ingestion of minute amounts of the allergen is believed to drive the process, and chelation therapy with disulfiram can be beneficial. In other instances, the cause of persistence remains enigmatic; many allergens penetrate through rubber gloves. Psoralen–ultraviolet A (PUVA) therapy can be helpful in these cases.

Oral antihistamines may help diminish pruritus caused by allergic contact dermatitis.

Next

Topical Immunomodulators

Class Summary

These agents modify immune processes that promote inflammation.

Pimecrolimus (Elidel cream)

 

Pimecrolimus is indicated for eczema and atopic dermatitis. It was the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Pimecrolimus is derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus.

This agent selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids.

Tacrolimus ointment (Protopic) 0.1% or 0.03%

 

Tacrolimus reduces itching and inflammation by suppressing release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin 3 (IL-3), IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha (TNF-alpha), all of which are involved in the 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 is approved for moderate-to-severe atopic dermatitis and can be used in patients as young as 2 years. It is more expensive than topical corticosteroids. This agent is available as ointment in concentrations of 0.03 and 0.1%.

Previous
Next

Corticosteroids

Class Summary

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

Clobetasol (Temovate) 0.05% cream, ointment, or solution

 

A class I superpotent topical steroid, clobetasol suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Use 0.05% cream or ointment.

Hydrocortisone topical (Westcort, Dermarest)

 

Hydrocortisone is an adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity. Use 0.2% cream or ointment.

Prednisone

 

Prednisone is an immunosuppressant for treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Triamcinolone (Kenalog, Oralone, Triderm)

 

Triamcinolone is indicated for inflammatory dermatosis responsive to steroids; it decreases inflammation by suppressing migration of PMNs and reversing capillary permeability. Intramuscular injection may be used for widespread skin disorder or intralesional injections may be used for localized skin disorder.

Previous
Next

Antihistamines

Class Summary

Antihistamines act by competitive inhibition of histamine at the H1 receptor. They may control itching by blocking effects of endogenously released histamine. These agents have no role in treating allergic contact dermatitis beyond possibly decreasing pruritus via sedating effects.

Hydroxyzine (Vistaril)

 

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

Previous
Next

Tricyclic Antidepressants

Class Summary

The tricyclic antidepressant doxepin is used in contact dermatitis for its sedative and antihistaminic properties. Oral doxepin may be considered if oral antihistamines are not helpful. Topical doxepin should be avoided because of the risk of iatrogenic allergic contact dermatitis.[23]

Doxepin (Prudoxin, Zonalon)

 

Doxepin inhibits histamine and acetylcholine activity and has proven useful in the treatment of allergic dermatologic disorders. The oral form is marketed as an antidepressant but is used also for its antihistaminic/antipruritic effects. The dosage is 10-25 mg at night in adults; if necessary, this can be gradually increased to a maximum dose of 75 mg/d for dermatoses. The topical form is approved for pruritus in adults with atopic dermatitis or lichen simplex chronicus.

Previous
Next

Chelation Agents

Class Summary

Although marketed as a treatment for alcoholism, disulfiram chelates nickel, which then is excreted in the urine. Lowering systemic levels of nickel has been reported to benefit individuals with pompholyx (dyshidrosis) and demonstrated hypersensitivity to the metal. Consider this therapy only for severe disabling dyshidrosis refractory to all other treatment in a patient proven allergic to nickel who does not drink alcohol and who consents to regular blood tests to identify liver toxicity from the medication.

Disulfiram (Antabuse)

 

Disulfiram is a thiuram derivative that interferes with aldehyde dehydrogenase. In patients highly allergic to nickel with severe vesicular hand dermatitis, the chelating effect of disulfiram is helpful in reducing the body's nickel burden in the individual allergic to nickel. Do not administer if patient has ingested alcohol within last 12 hours.

Previous
 
Contributor Information and Disclosures
Author

Daniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Canadian Dermatology Association

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.

Acknowledgements

Donald Belsito, MD Professor of Clinical Dermatology, Department of Dermatology, Columbia University Medical Center

Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, New York County Medical Society, New York Dermatological Society, Noah Worcester Dermatological Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences,and Society for Academic Emergency Medicine

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, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Celgene Honoraria Safety Monitoring Committee

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Mark Louden, MD Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department of Medicine, University of Miami, Leonard M Miller School of Medicine

Mark Louden, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

R Scott Lowery, MD Associate Professor of Ophthalmology, Department of Pediatric Ophthalmology and Strabismus, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

R Scott Lowery, MD is a member of the following medical societies: American Academy of Ophthalmology and Arkansas Medical Society

Disclosure: Nothing to disclose.

Joshua May, MD Bend Dermatology Clinic

Disclosure: Nothing to disclose.

John A Michael, MD

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Institute

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, and International Society of Refractive Surgery

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other; Bausch & Lomb Honoraria Speaking and teaching; Merck Consulting fee Consulting; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

David Todd Schwartz, MD Associate Professor of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center and New York University Medical Center

David Todd Schwartz, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Bradley D Shy, MD Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center, New York University School of Medicine

Disclosure: Nothing to disclose.

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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Jack L Wilson, PhD Distinguished Professor, Department of Anatomy and Neurobiology, University of Tennessee Health Science Center College of Medicine

Jack L Wilson, PhD is a member of the following medical societies: American Association of Anatomists, American Association of Clinical Anatomists, and American Heart Association

Disclosure: Nothing to disclose.

References
  1. Novak N, Baurecht H, Schafer T, Rodriguez E, et al. Loss-of-function mutations in the filaggrin gene and allergic contact sensitization to nickel. J Invest Dermatol. 2008 Jun. 128(6):1430-5. [Medline].

  2. Lu LK, Warshaw EM, Dunnick CA. Prevention of nickel allergy: the case for regulation?. Dermatol Clin. 2009 Apr. 27(2):155-61, vi-vii. [Medline].

  3. Thyssen JP, Linneberg A, Menne T, Nielsen NH, Johansen JD. Contact allergy to allergens of the TRUE-test (panels 1 and 2) has decreased modestly in the general population. Br J Dermatol. 2009 Nov. 161(5):1124-9. [Medline].

  4. Moennich JN, Zirwas M, Jacob SE. Nickel-induced facial dermatitis: adolescents beware of the cell phone. Cutis. 2009 Oct. 84(4):199-200. [Medline].

  5. Ponten A, Hamnerius N, Bruze M, et al. Occupational allergic contact dermatitis caused by sterile non-latex protective gloves: clinical investigation and chemical analyses. Contact Dermatitis. 2013 Feb. 68(2):103-10. [Medline].

  6. Jacob SE, Zapolanski T, Chayavichitsilp P, Connelly EA, Eichenfield LF. p-Phenylenediamine in black henna tattoos: a practice in need of policy in children. Arch Pediatr Adolesc Med. 2008 Aug. 162(8):790-2. [Medline].

  7. Thyssen JP, White JM. Epidemiological data on consumer allergy to p-phenylenediamine. Contact Dermatitis. 2008 Dec. 59(6):327-43. [Medline].

  8. Lundov MD, Krongaard T, Menne TL, Johansen JD. Methylisothiazolinone contact allergy: a review. Br J Dermatol. 2011 Dec. 165(6):1178-82. [Medline].

  9. Schnuch A, Mildau G, Kratz EM, Uter W. Risk of sensitization to preservatives estimated on the basis of patch test data and exposure, according to a sample of 3541 leave-on products. Contact Dermatitis. 2011 Sep. 65(3):167-74. [Medline].

  10. Brared Christensson J, Andersen KE, Bruze M, et al. Air-oxidized linalool: a frequent cause of fragrance contact allergy. Contact Dermatitis. 2012 Nov. 67(5):247-59. [Medline].

  11. Niklasson IB, Delaine T, Islam MN, Karlsson R, Luthman K, Karlberg AT. Cinnamyl alcohol oxidizes rapidly upon air exposure. Contact Dermatitis. 2013 Mar. 68(3):129-38. [Medline].

  12. Guin JD, Phillips D. Erythroderma from systemic contact dermatitis: a complication of systemic gentamicin in a patient with contact allergy to neomycin. Cutis. 1989 Jun. 43(6):564-7. [Medline].

  13. Green CM, Holden CR, Gawkrodger DJ. Contact allergy to topical medicaments becomes more common with advancing age: an age-stratified study. Contact Dermatitis. 2007 Apr. 56(4):229-31. [Medline].

  14. Assier-Bonnet H, Revuz J. [Topical neomycin: risks and benefits. Plea for withdrawal]. Ann Dermatol Venereol. 1997. 124(10):721-5. [Medline].

  15. Gonul M, Gul U. Detection of contact hypersensitivity to corticosteroids in allergic contact dermatitis patients who do not respond to topical corticosteroids. Contact Dermatitis. 2005 Aug. 53(2):67-70. [Medline].

  16. Cohen LM, Cohen JL. Erythema multiforme associated with contact dermatitis to poison ivy: three cases and a review of the literature. Cutis. 1998 Sep. 62(3):139-42. [Medline].

  17. Cohen DE, Brancaccio R, Andersen D, Belsito DV. Utility of a standard allergen series alone in the evaluation of allergic contact dermatitis: a retrospective study of 732 patients. J Am Acad Dermatol. 1997 Jun. 36(6 Pt 1):914-8. [Medline].

  18. [Guideline] Bernstein IL, Li JT, Bernstein DI, et al. Allergy diagnostic testing: an updated practice parameter. Ann Allergy Asthma Immunol. 2008 Mar. 100(3 Suppl 3):S1-148. [Medline].

  19. Larkin A, Rietschel RL. The utility of patch tests using larger screening series of allergens. Am J Contact Dermat. 1998 Sep. 9(3):142-5. [Medline].

  20. Marks JG, Belsito DV, DeLeo VA, et al. North American Contact Dermatitis Group patch test results for the detection of delayed-type hypersensitivity to topical allergens. J Am Acad Dermatol. 1998 Jun. 38(6 Pt 1):911-8. [Medline].

  21. Rajagopalan R, Anderson RT, Sarma S, et al. An economic evaluation of patch testing in the diagnosis and management of allergic contact dermatitis. Am J Contact Dermat. 1998 Sep. 9(3):149-54. [Medline].

  22. Jacobs JJ, Lehe CL, Hasegawa H, Elliott GR, Das PK. Skin irritants and contact sensitizers induce Langerhans cell migration and maturation at irritant concentration. Exp Dermatol. 2006 Jun. 15(6):432-40. [Medline].

  23. Taylor JS, Praditsuwan P, Handel D, Kuffner G. Allergic contact dermatitis from doxepin cream. One-year patch test clinic experience. Arch Dermatol. 1996 May. 132(5):515-8. [Medline].

  24. Baeck M, Chemelle JA, Rasse C, Terreux R, Goossens A. C(16) -methyl corticosteroids are far less allergenic than the non-methylated molecules. Contact Dermatitis. 2011 Jun. 64(6):305-312. [Medline].

  25. Katsarou A, Armenaka M, Vosynioti V, Lagogianni E, Kalogeromitros D, Katsambas A. Tacrolimus ointment 0.1% in the treatment of allergic contact eyelid dermatitis. J Eur Acad Dermatol Venereol. 2009 Apr. 23(4):382-7. [Medline].

  26. Katsarou A, Makris M, Papagiannaki K, Lagogianni E, Tagka A, Kalogeromitros D. Tacrolimus 0.1% vs mometasone furoate topical treatment in allergic contact hand eczema: a prospective randomized clinical study. Eur J Dermatol. 2012 Mar-Apr. 22(2):192-6. [Medline].

  27. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006 Jan-Feb. 72(1):24-7. [Medline].

  28. Shaffer MP, Belsito DV. Allergic contact dermatitis from glutaraldehyde in health-care workers. Contact Dermatitis. 2000 Sep. 43(3):150-6. [Medline].

  29. Kaplan DH, Igyarto BZ, Gaspari AA. Early immune events in the induction of allergic contact dermatitis. Nat Rev Immunol. 2012 Jan 13. 12(2):114-24. [Medline]. [Full Text].

  30. Pot LM, Scheitza SM, Coenraads PJ, Blomeke B. Penetration and haptenation of p-phenylenediamine. Contact Dermatitis. 2013 Apr. 68(4):193-207. [Medline].

  31. Thyssen JP, Johansen JD, Linneberg A, Menne T, Engkilde K. The association between contact sensitization and atopic disease by linkage of a clinical database and a nationwide patient registry. Allergy. 2012 Sep. 67(9):1157-64. [Medline].

 
Previous
Next
 
Chronic stasis dermatitis with allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis produces areas of erythema in areas of atrophie blanche and varicose veins.
Erythema multiformelike reaction that developed acutely following hair dying.
Allergic contact dermatitis to nickel in a necklace.
Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.
Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.