Contact dermatitis is among the most common inflammatory skin conditions encountered by clinicians.
Contact dermatitis is among the most common inflammatory skin conditions encountered by clinicians.1 Its primary characteristics are red, usually very pruritic skin lesions that develop after contact with a foreign substance. This substance may be irritating to the contacted skin, leading to dermatitis (known as irritant contact dermatitis), or the reaction may be the result of an allergic reaction (allergic contact dermatitis). Allergic contact dermatitis is a delayed T-cell—mediated hypersensitivity reaction in which an allergen comes into contact with the skin and dermatitis occurs with re-exposure.1,2
Given the 2 distinct types of contact dermatitis, the number of allergens or skin irritants that may cause this condition is extremely high, although some substances are more commonly implicated in this condition (table3).3 Occupational, environmental, and other exposures can lead to contact dermatitis.2 Chemical irritants are a common occupational cause, and Toxicodendron (formerly Rhus) species exposure (eg, poison ivy, poison oak, and poison sumac) is a common environmental cause.3 Other common substances that cause contact dermatitis include nickel and neomycin.1 In patch testing studies, these agents caused contact dermatitis in 10% to 15% of patients. This is concerning because nickel is a component of many types of composite metals, including stainless steel, and is found in items as ubiquitous as scissors and cell phones. Fragrance ingredients that are potential contact allergens are found in numerous cosmetics, soaps, shampoos, and other products; therefore, it is difficult to pinpoint the inciting agent when examining a patient with contact dermatitis. Pharmacists should be particularly cognizant of neomycin’s ability to trigger contact dermatitis in susceptible patients given its over-the-counter use, as well as the possibility of contact dermatitis from transdermal patches (figure) or other topical dosage forms.4
Patients who present with potential acute contact dermatitis should have patch testing performed.5 Both the American Contact Dermatitis Society and the North American Contact Dermatitis Group recommend patch testing. One commonly used test, the thin layer rapid use epicutaneous patch test, also known as the T.R.U.E. Test, challenges patients with a negative control and 35 antigens that commonly cause contact dermatitis.3 However, it is important to consider the patient’s history to determine if more specific exposures, occupation, body location, or age dictate that other patch testing should be done.2 Before completing patch testing, it is important to reduce the dose of, or hold, medications that are immunosuppressive, such as topical calcineurin inhibitors, corticosteroids, or ultraviolet radiation, as these may decrease the allergic response to the test antigens.3 Test readings should be done 48 hours after the patch is removed, and again at 96 hours post removal. Repeated tests may also be done occasionally up to 7 days after patch removal when assessing delayed hypersensitivity reactions.6 After collecting potential exposure history and evaluating skin tests, the allergen can be considered as a definite, probable, or possible cause of the patient’s symptoms.
Patch tests before surgeries are only recommended for those with metal sensitivities. If a patient does test positive, the decision to proceed with implants should be a conversation among the surgeon, patient, and allergist, since there are no current guidelines available. While there is no consensus on which patients to target for patching, patch testing could have high positivity in patients who develop delayed hypersensitivity drug reactions, such as with Stevens-Johnson syndrome, a drug rash with eosinophilia and systemic symptoms, and maculopapular rashes. It is important to note that patch testing should not be completed for those with Toxicodendron (eg, poison ivy) exposure since large bullous reactions and sensitization may occur.3
The most recent guidelines give more in-depth statements regarding occupational contact dermatitis, which is among the most frequently seen occupational illnesses reported in the United States. Occupational contact dermatitis is most often seen on the hands, but can also be found on the arms, face, and wrists.3 The Mathias criteria, the validity of which was confirmed in a 2- to 5-year prospective study, are used to determine if a patient’s contact dermatitis is caused and worsened by occupational exposures. This criteria considers the timing of symptom onset and resolution, potential occupational and nonoccupational exposures, and location of disease.3,7
The most effective treatment of contact dermatitis is to avoid the known irritant or allergen altogether. It is important to educate patients on potential cross-reactivity or contamination by potential allergens. To aid in compliance, and perhaps improve quality of life, patients should be given a list of possible alternative products to dermatitis precipitants; such lists can be found on the Contact Allergen Management Program database for the American Contact Dermatitis Society, and the SkinSAFE Database created by the Mayo Clinic.8,9 Counsel patients to not assume that products labeled as “natural” mean they are definitely safe. Further recommendations should be made for skin protection, such as goggles and gloves with cotton liners when applicable, to assist patients in avoiding direct contact with the allergen. Furthermore, maintaining the barrier function of the skin through lipid-rich moisturizers can also be potentially beneficial.3
Avoidance of the allergen might not always be feasible or might not completely resolve the dermatitis. Topical corticosteroids (TCS) are generally acknowledged as first-line treatment for both acute and chronic dermatitis. If the dermatitis is localized, TCS should be an adequate treatment. However, if patients have dermatitis that is more extensive or severe, systemic corticosteroid therapy may be needed. For TCS, avoid using potent fluorinated or ointment dosage forms on areas of thin skin. This includes the face, eyelids, a child’s skin, and intertriginous locations. It is important to note that the use of steroids should not replace the process of determining an allergen and avoiding it; steroids should be used only for short-term durations. Sensitization to corticosteroids, the medication vehicle, or excipients should be considered if the dermatitis worsens.3
Other topical treatments to consider are topical T-cell selective inhibitors, such as topical tacrolimus and pimecrolimus. While the efficacy of these medications has not been determined for contact dermatitis, they have been effective in treating atopic dermatitis. If steroids are not effective, azathioprine, cyclosporine, and psoralen plus ultraviolet A have been used previously and may be considered as alternative treatment. When determining and discussing potential treatments, make sure to utilize clinical judgment when assessing risks and benefits, as well as the patient’s informed consent.3
Contact dermatitis is common, and patients with this condition regularly consult pharmacists. The primary mode of management is avoidance of triggers, and pharmacists can aid patients in assessing potential triggers. Topical routes of drug administration, particularly transdermal patches, can trigger contact dermatitis. Topical steroids are the agents of first choice in treating this condition, with severe cases requiring referral for consideration of other therapies, including systemic corticosteroids.
1. Mowad CM, Anderson B, Scheinman P, Pootongkam S, Nedorost S, Brod B. Allergic contact dermatitis: patient diagnosis and evaluation. J Am Acad Dermatol. 2016;74(6):1029-1040. doi: 10.1016/j.jaad.2015.02.1139.
2. Cashman MW, Reutemann PA, Ehrlich A. Contact dermatitis in the United States: epidemiology, economic impact, and workplace prevention. Dermatol Clin. 2012;30(1):87-98,viii. doi: 10.1016/j.det.2011.08.004.
3. Fonacier L, Bernstein DI, Pacheco K, et al; American Academy of Allergy, Asthma & Immunology; American College of Allergy, Asthma & Immunology; Joint Council of Allergy, Asthma & Immunology. Contact dermatitis: a practice parameter-update 2015. J Allergy Clin Immunol Pract. 2015;3(suppl 3):S1-S39. doi: 10.1016/j.jaip.2015.02.009.
4. Ale I, Lachapelle JM, Maibach HI. Skin tolerability associated with transdermal drug delivery systems: an overview. Adv Ther. 2009;26(10):920-935. doi: 10.1007/s12325-009-0075-9.
5. Ramirez F, Chren MM, Botto N. A review of the impact of patch testing on quality of life in allergic contact dermatitis. J Am Acad Dermatol. 2017;76(5):1000-1004. doi: 10.1016/j.jaad.2016.12.011.
6. Contact dermatitis. Cleveland Clinic website. https://my.clevelandclinic.org/ health/articles/contact-dermatitis. Updated January 5, 2015. Accessed June 16, 2017.
7. Ingber A, Merims S. The validity of the Mathias criteria for establishing occupational causation and aggravation of contact dermatitis. Contact Dermatitis. 2004;51(1):9-12. doi: 10.1111/j.0105-1873.2004.00273.x.
8. ACDS [American Contact Dermatitis Society] CAMP [Contact Allergen Management Program]. ACDS website. www.contactderm.org/i4a/pages/index. cfm?pageid=3489. Accessed June 20, 2017.
9. Learning center. SkinSAFE website. www.skinsafeproducts.com/learn. Accessed June 20, 2017.
Geoffrey C. Wall, PharmD, FCCP, BCPS, is a professor of Clinical Sciences at Drake University College of Pharmacy and Health Sciences in Des Moines, Iowa.Julianne Schlichting is a student pharmacist at Drake University College of Pharmacy and Health Sciences in Des Moines, Iowa.