Version May 2024
INTRODUCTION — Allergic contact dermatitis (ACD) is commonly encountered by the practicing clinician. The most common clinical expression is an eczematous dermatitis that can be mild to severe, acute and short lived or chronic. The management of ACD is based upon the identification of the offending allergen, avoidance of exposure, use of safe alternatives, and treatment of symptoms.
This topic will discuss the management of ACD. The basic mechanisms, clinical manifestations, and diagnosis of ACD; common allergens in ACD; and patch testing are discussed separately. Poison ivy dermatitis, eyelid dermatitis, hand eczema, and contact dermatitis in children are also discussed separately.
●(See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)
●(See "Clinical features and diagnosis of allergic contact dermatitis".)
●(See "Common allergens in allergic contact dermatitis".)
●(See "Patch testing".)
●(See "Poison ivy (Toxicodendron) dermatitis".)
●(See "Eyelid dermatitis (eczema)".)
●(See "Chronic hand eczema".)
●(See "Allergic contact dermatitis in children".)
GENERAL PRINCIPLES — The optimal management of ACD requires a multipronged approach [1]:
●Identification and avoidance of the offending allergen
●Alternatives to offending products
●Skin protection
●Treatment of skin inflammation
●Restoration of the skin barrier
The identification of the offending allergen is a key step in the management of ACD. Although the offending allergen is often identified through a detailed history, patch testing may be necessary to identify specific antigens. (See "Clinical features and diagnosis of allergic contact dermatitis", section on 'History' and "Patch testing".)
ALLERGEN AVOIDANCE — The education of patients on avoidance of offending substances and recommendations of alternative, allergen-free products are a critical part of the management of patients with ACD [2].
Patient education — It is helpful to provide patients with information to help them understand the complex nature of their dermatitis and implement appropriate allergen avoidance and skin protection measures. Information for patients can be found on the websites of most of the companies that manufacture the allergens used for patch testing or systems to detect allergens (eg, specific metals) in commonly used objects, including SmartPractice (www.truetest.com and www.allergeaze.com), Chemotechnique Diagnostics (www.chemotechnique.se), the Contact Dermatitis Institute (www.contactdermatitisinstitute.com), as well as the American Contact Dermatitis Society website.
Common contact allergens — Common contact allergens include plant allergens, metals, fragrances, acrylates, medicaments, and preservatives.
Plants — Many plant families that are ubiquitous throughout the world, including Anacardiaceae (eg, Toxicodendron [poison ivy], cashew nut tree, Indian marking nut tree, mango tree), Compositae (eg, ragweed, goldenrod, sunflowers, chamomile, chrysanthemums), Alliaceae (eg, garlic, onion), and Myrtaceae (eg, tea tree), contain resins and oils that can cause ACD in sensitized individuals [3,4]. Compositae and Anacardiaceae are also responsible for most cases of airborne ACD, due to exposure to pollen or other particles suspended in the air.
The avoidance measures for contact allergy to plants of the Toxicodendron genus (poison ivy, oak, and sumac) are discussed separately. (See "Poison ivy (Toxicodendron) dermatitis", section on 'Prevention'.)
Nickel — Nickel is found in alloys and plated objects, including jewelry, buttons, zippers, coins, keys, scissors, children's toys [5], cell phones [6], handheld computers [7], and metal tools. (See "Common allergens in allergic contact dermatitis".)
●Identifying nickel in common use objects – Providing patients who are nickel sensitive with a list of objects that may contain nickel may be helpful. A nickel test kit may also be useful for patients to identify nickel-releasing objects at home or at work. These kits, which use dimethylglyoxime, do not harm the object being tested. In one study, the nickel spot test had a sensitivity and specificity of 60 and 98 percent, respectively, in detecting nickel released in amounts >0.5 microg/cm2 per week by a set of earrings [8]. This is the threshold established by the European Union Nickel Directive for products intended to be in direct and prolonged contact with the skin.
●Avoiding nickel exposure – Since jewelry (including some yellow and white gold jewelry) and metal components of clothing are the most common sources of nickel that are in prolonged contact with the skin, several avoidance measures have been suggested to limit nickel exposure from these sources [9]:
•Coating a nickel object with a physical barrier may prevent the release of nickel ions. The application of a clear barrier (eg, Nickel Guard) or clear nail polish to the buttons and rivets of jeans may prevent nickel release through at least two wash and dry cycles [10].
•Iron-on patches may be applied on clothes to cover metal parts that come in contact with the skin.
•Duct tape can adhere to the inside of buttons or snaps; it is inexpensive, easy to apply, and widely available.
•Chemical barriers for nickel include chelating and nonchelating barrier creams. Barrier creams containing agents such as disodium ethylenediaminetetraacetate (EDTA) act by chelating the positive ionic charge and rendering the metal inactive [11,12]. Nonchelating creams may prevent the penetration of nickel through the skin.
Cosmetics and personal care products — Although cosmetics and personal care products contain a high number of chemical ingredients, only a few of them are responsible for most cases of ACD. These include [13-16] (see "Common allergens in allergic contact dermatitis", section on 'Preservatives' and "Common allergens in allergic contact dermatitis", section on 'Fragrances'):
●Fragrances and botanicals (limonene, linalool)
●Preservatives (eg, quaternium-15, methylisothiazolinone [MI] or the combination of methylchloroisothiazolinone [MCI]/MI [marketed as Kathon CG or Kathon WT], imidazolidinyl and diazolidinyl urea, and others)
●Excipients (eg, propylene glycol, lanolin, or colorants)
●Glues (eg, acrylates in nail products)
●Sunscreens
●Hair dyes (para-phenylenediamine and derivatives)
●Surfactants (cocamidopropyl betaine, decyl glucosides)
Learning to read the labels of cosmetic or personal care products is important for patients with ACD. Information on specific ingredients in personal care or household products commercialized in the United States can be found online at the Consumer Product Information Database.
Alternative products — Clinicians may obtain information on alternative products for patients with allergies from several sources. The Contact Allergen Management Program of the American Contact Dermatitis Society, which requires membership, allows the clinician to create an individualized list of products, including gloves that are free of specific allergens. SkinSAFE is another resource for alternative products [17].
The American Contact Alternatives Group provides an extensive list of alternatives for the allergens included in the 2018 American Contact Dermatitis Society core series [18]. Specific lists of alternatives for facial cosmetics and hair products containing few or none of the allergens included in the core allergen series of the American Contact Dermatitis Society are also available [19,20].
ALLERGEN AVOIDANCE AND ALLERGIC CONTACT DERMATITIS PREVENTION IN THE WORKPLACE
General measures — Avoidance in the workplace requires a more complex strategy. Several general measures may be adopted in the workplace to reduce exposure to chemicals, including:
●Substitution of safer alternatives for allergenic materials
●Automation
●Process enclosure
●Use of equipment for handling substances [21]
●Keeping a safe working distance
●Promptly washing any chemical exposures from the skin
●Using protective clothing and gloves
Occupational prevention measures include [22]:
●Workplace training programs focused on barrier repair, hazards of wet work
●Regular examinations for early disease recognition
●Capacity to manage more advanced disease
Protective gloves — Protective gloves can reduce or eliminate the exposure of the hands to hazardous substances. Gloves are ideally selected based on the glove permeation and degradation properties and the nature of the compounds that are manipulated [23].
Multilayer laminate gloves, which incorporate a hydrophilic/polar layer between two hydrophobic/nonpolar layers, usually provide a high level of protection against a wide range of chemicals. Manufacturers of protective gloves provide lists of applications, hazards, and chemicals for which their gloves have been tested (eg, www.bestglove.com or www.ansell.com).
However, gloves (particularly rubber gloves) contain allergens that may worsen hand dermatitis in some patients. Also, improperly chosen gloves may actually allow allergen penetration and then trap the allergen against the skin. Education on the proper way to put on and take off gloves is required to minimize exposures.
Skin protection — Irritant contact dermatitis is often associated with or precedes the development of ACD. Prework (barrier) creams and after work (emollient) creams appear to confer some degree of protection against irritant contact dermatitis, although evidence from randomized trials is limited [24]. The substitution of milder detergents for abrasive or irritating cleansers and the application of allergen-free emollients (eg, petrolatum-based emollients) after each hand washing may reduce the risk of hand dermatitis at the workplace [25].
The regular application of emollients to normal skin after repeated exposure to irritants may help to maintain the skin barrier function [26]. Emollients may be liberally used as an adjunct to corticosteroids in the treatment of ACD, particularly chronic, lichenified dermatitis.
PHARMACOLOGIC TREATMENT — Although avoidance of the offending allergen is the mainstay of management of ACD, pharmacologic treatment is required to achieve rapid control of symptoms in most cases. The treatment of ACD follows the general principles of eczema treatment and includes topical corticosteroids and topical calcineurin inhibitors, systemic immunosuppressors, and phototherapy. Emollients may be liberally used as an adjunct to corticosteroids in the treatment of ACD, particularly chronic, lichenified dermatitis.
The approach to treatment depends on the severity of ACD and the site(s) involved (algorithm 1) [16,25,27-32].
Acute, localized allergic contact dermatitis — Topical corticosteroids and topical tacrolimus are first-line treatments for acute, localized ACD. Emollients can be liberally used multiple times per day as an adjunctive treatment to topical therapy.
Hands, feet, and nonflexural areas — We suggest high-potency topical corticosteroids (groups 1 to 3 (table 1)) for treatment of ACD that does not involve the face or flexural areas (algorithm 1). Topical corticosteroids are applied once or twice daily for two to four weeks or until resolution of symptoms. If the dermatitis is acute and weeping, topical corticosteroids may be used in combination with drying agents (eg, aluminum acetate compresses, calamine lotion, colloidal oatmeal compresses or baths).
Potential adverse effects of topical corticosteroids include cutaneous atrophy, telangiectasias, and striae. They are more likely to occur with prolonged use of high-potency agents and especially on facial and intertriginous skin. (See "Topical corticosteroids: Use and adverse effects".)
The efficacy of topical corticosteroids for the treatment of ACD has been evaluated in a few small, randomized trials, some of which were performed in individuals with experimentally induced ACD [33-36]. However, their use is largely supported by evidence for efficacy in other forms of eczematous dermatitis [27,37].
Face and flexural areas — Our approach to the management of acute ACD involving the face and/or flexural areas is as follows (algorithm 1):
●We suggest medium- to low-potency topical corticosteroids (groups 4 to 6 (table 1)) as the initial treatment for mild to moderate ACD of the face and flexural areas. Topical corticosteroids are applied once or twice daily for one to two weeks. Thereafter, topical corticosteroids can be tapered (eg, with every other day application) over the following two weeks.
●Topical tacrolimus is an alternative to topical corticosteroids for patients who require prolonged, continuous treatment (beyond two weeks). Unlike topical corticosteroids, topical calcineurin inhibitors do not cause skin atrophy. Tacrolimus 0.1% ointment is applied twice daily until improvement is noted and then tapered. Local adverse effects of topical calcineurin inhibitors include burning and stinging at the site of application.
The efficacy of topical calcineurin inhibitors for ACD has been evaluated in a few small, randomized trials, some of which involving individuals with experimentally induced ACD [28,29,35,36,38]. In one study, tacrolimus 0.1% ointment applied twice daily was more effective than placebo in clearing the eruption over eight weeks of continued exposure to the allergen [28]. Pimecrolimus 1% cream does not seem to be effective for ACD [38].
There are no high-quality studies comparing topical calcineurin inhibitors with topical corticosteroids for the treatment of ACD. In a small trial that involved 30 patients with chronic hand ACD, tacrolimus 0.1% ointment was as effective as mometasone furoate 0.1% ointment in reducing erythema, infiltration, vesiculation, desquamation, and itching [36].
Extensive, severe, or disabling allergic contact dermatitis — We suggest systemic corticosteroids as the first-line treatment for acute extensive, severe, or disabling ACD (ie, involving >20 percent of the total body surface area or involving the face, hands, feet, or genitalia) (algorithm 1). Treatment is started with prednisone (or equivalent dose of other systemic corticosteroids (table 2)) at a dose of 0.5 to 1 mg/kg per day (maximum 60 mg/day) for seven days. The dose may be reduced by 50 percent over the next five to seven days and then tapered and discontinued over the following two weeks.
Systemic corticosteroids for ACD have not been studied in randomized trials. In clinical practice, they are frequently beneficial in the treatment of poison ivy dermatitis, a common form of ACD. (See "Poison ivy (Toxicodendron) dermatitis", section on 'Severe dermatitis'.)
Chronic allergic contact dermatitis — Breakdown of the skin barrier (atrophy) is a complicating factor in many cases of chronic ACD and is exacerbated by overuse of topical corticosteroids. Every effort should be made to minimize continuous use of these agents beyond two to four weeks.
Allergen-free emollients may be liberally used as an adjunct to active topical therapies in the treatment of ACD, particularly chronic, lichenified dermatitis (algorithm 1).
●Intermittent topical corticosteroids – We suggest intermittent high-potency topical corticosteroids (groups 1 to 3 (table 1)) for long-term control of chronic ACD involving the hands, feet, or nonflexural areas. Topical corticosteroids are applied once daily for 7 to 10 days initially, followed by every-other-day treatment. In case of recurrence, continuous treatment can be reinstated.
In a randomized trial, 120 patients with chronic hand eczema initially treated with mometasone furoate 0.1% fatty cream for up to nine weeks or until the dermatitis cleared were randomly assigned to a 30-week maintenance period with intermittent mometasone furoate (once daily on Sunday, Tuesday, and Thursday or on Saturday and Sunday) or vehicle. Mometasone furoate applied three times weekly was more effective than vehicle in preventing recurrence of dermatitis (83 versus 26 percent) [39].
●Topical tacrolimus – We suggest topical tacrolimus for the management of chronic ACD localized to the face or intertriginous areas and for chronic, localized ACD resistant to topical corticosteroids. Tacrolimus 0.1% ointment can be applied once or twice daily to affected areas until resolution. Treatment can be restarted if there is a recurrence.
●Second-line therapies – For patients with chronic ACD that is unresponsive to topical therapies, therapeutic options include:
•Phototherapy – Small, observational studies of patients with chronic hand eczema of various etiologies demonstrated clinical improvement with bath psoralen plus ultraviolet A (PUVA) photochemotherapy or narrowband ultraviolet B (NBUVB) [30-32,40]. NBUVB is more convenient for the patient and associated with fewer side effects than PUVA. (See "Chronic hand eczema" and "Psoralen plus ultraviolet A (PUVA) photochemotherapy" and "UVB phototherapy (broadband and narrowband)".)
•Systemic immunosuppressive agents – Methotrexate, azathioprine, mycophenolate mofetil, and cyclosporine are infrequently used for the management of chronic ACD [41]. Situations such as airborne plant contact dermatitis from Compositae (eg, parthenium, ragweed, aster, sunflower, chrysanthemum, artichoke) or photodermatitis, where allergen avoidance is impossible, are examples.
PROGNOSIS — There is no reliable method to desensitize patients to allergens. The prognosis for improvement hinges on the ability to avoid allergen(s) and, if applicable, their cross-reacting substances [2]. Allergens that are more ubiquitous in the environment, such as sesquiterpene lactones found in common outdoor plants or formaldehyde commonly found in the workplace and household products, tend to be associated with a less favorable prognosis. Outcomes related to occupational contact dermatitis depend on the ability to establish a workplace free of allergens.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Contact dermatitis".)
SUMMARY AND RECOMMENDATIONS
●Allergen avoidance – Allergen avoidance is the cornerstone of the management of allergic contact dermatitis (ACD). Educating patients about avoidance of offending substances and use of alternative, allergen-free products is a critical part of the management of ACD. Avoiding occupational exposures requires a complex strategy that may involve engineering control methods (eg, automation, process enclosure), personal hygiene measures (eg, promptly washing chemicals from the skin), and using personal protective equipment.
Information for patients can be found on the websites of most companies that manufacture allergens used for patch testing or systems to identify allergens in commonly used objects (eg, www.smartpractice.com, www.truetest.com, www.allergeaze.com, www.chemotechnique.se) as well as the American Contact Dermatitis Society website. (See 'Allergen avoidance' above and 'Allergen avoidance and allergic contact dermatitis prevention in the workplace' above.)
●Skin protection – Prework (barrier) creams and after work (emollient) creams appear to confer some degree of protection against contact dermatitis, although evidence from randomized trials is limited. Regular use of emollients may help to maintain the skin barrier function. (See 'Skin protection' above.)
●Pharmacologic treatment – The approach to treatment depends on the severity of ACD and the site(s) involved (algorithm 1). (See 'Pharmacologic treatment' above.)
•Acute, limited allergic contact dermatitis of the hands, feet, and nonintertriginous areas – We suggest high-potency topical corticosteroids (groups 1 to 3 (table 1)) for the treatment of ACD that involves <20 percent of the body surface area, does not involve the face or flexural areas, and is not disabling (Grade 2C). Topical corticosteroids are applied once or twice daily for two to four weeks or until resolution of symptoms. (See 'Hands, feet, and nonflexural areas' above.)
•Acute, localized allergic contact dermatitis of the face and intertriginous areas – We suggest medium- to low-potency topical corticosteroids (groups 4 to 6 (table 1)) rather than topical tacrolimus as initial therapy for mild to moderate ACD of the face and flexural areas (Grade 2C). Topical corticosteroids are applied once or twice daily for one to two weeks. Topical tacrolimus is a reasonable alternative for patients who require prolonged, continuous treatment (beyond two weeks). Topical tacrolimus 0.1% ointment is applied twice daily until resolution and then tapered. (See 'Face and flexural areas' above.)
•Extensive, severe, or disabling allergic contact dermatitis – We suggest systemic, rather than topical, corticosteroids as the first-line treatment for acute extensive, severe, or disabling ACD (ie, involving >20 percent of the total body surface area or involving the face, hands, feet, or genitalia) (Grade 2C). Treatment is started with prednisone (or equivalent dose of other systemic corticosteroids (table 2)) at a dose of 0.5 to 1 mg/kg per day (maximum 60 mg per day) for seven days. The dose may be reduced by 50 percent in the next five to seven days and then tapered and discontinued over the following two weeks. (See 'Extensive, severe, or disabling allergic contact dermatitis' above.)
•Chronic allergic contact dermatitis
-Hands, feet, nonflexural areas – For long-term control of chronic ACD involving the hands, feet, or nonflexural areas, we suggest intermittent high-potency topical corticosteroids (groups 1 to 3 (table 1)) rather than continuous treatment (Grade 2C). Topical corticosteroids are applied once daily three times per week on alternate days.
-Face and flexural areas – For chronic ACD of the face and flexural areas, we suggest topical tacrolimus over topical corticosteroids (Grade 2C). Topical tacrolimus 0.1% ointment is applied once or twice daily for as long as needed.
-Refractory, chronic allergic contact dermatitis – Phototherapy with psoralen plus ultraviolet A (PUVA) or narrowband ultraviolet B (NBUVB) or systemic immunosuppressive medications are therapeutic options in patients with chronic ACD that is unresponsive to topical or oral corticosteroids. (See 'Chronic allergic contact dermatitis' above.)
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