Allergic Contact Dermatitis
medscape-Allergic Contact Dermatitis ,Background,History,Approach Considerations ,Medication Summary
Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity (allergy) resulting from cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity. This allergic reaction causes inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation.
The term contact dermatitis sometimes is used incorrectly as a synonym for allergic contact dermatitis. Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin (see Irritant Contact Dermatitis) and by specific sensitivity in the case of allergic contact dermatitis.
Jadassohn first described allergic contact dermatitis in 1895. He developed the patch test to identify the chemicals to which the patient was allergic. Sulzberger popularized patch testing in the United States in the 1930s. The Finn chamber method for patch testing was designed in the 1970s; these chambers consist of small metal cups, typically attached to strips of tape, filled with allergens dispersed in either petrolatum or water. The thin-layer rapid use epicutaneous (TRUE) test for patch testing became available in the United States in the 1990s.
The importance of specific substances as causes of allergic contact dermatitis varies with the prevalence of that substance in the environment. Mercury compounds once were significant causes of allergic contact dermatitis but rarely are used as topical medications and, currently, are uncommon as a cause of allergic contact dermatitis. Ethylenediamine, which was present in the original Mycolog cream, declined as a primary cause of allergic contact dermatitis once Mycolog cream was reformulated to no longer contain this allergen.
A detailed history, both before and after patch testing, is crucial in evaluating individuals with allergic contact dermatitis. Before patch testing, the history identifies potential causes of allergic contact dermatitis and the materials to which individuals are exposed that should be included in patch testing. After patch testing, the history determines the clinical significance of the findings. (See Clinical.)
Topical corticosteroids are the mainstay of treatment, while a variety of symptomatic treatments can provide short-term relief of pruritus. However, the definitive treatment of allergic contact dermatitis is the identification and removal of any potential causal agents; otherwise, the patient is at increased risk for chronic or recurrent dermatitis
Individuals with stasis dermatitis are at high risk for developing allergic contact dermatitis to materials and agents applied to the areas of stasis dermatitis and leg ulcers. Neomycin is an important cause of allergic contact dermatitis in these individuals because it is used frequently despite the lack of documentation of its efficacy in the treatment of stasis ulcers.
Individuals with otitis externa frequently are allergic to topical neomycin and topical corticosteroids.
Individuals with pruritus ani and pruritus vulvae may become sensitized to benzocaine and other medications applied to chronic pruritic processes.
Women with lichen sclerosus et atrophicus frequently develop allergic contact dermatitis, complicating the severe chronic vulvar dermatosis. Patch testing these patients may provide important information that can help in the management of recalcitrant and difficult-to-manage dermatosis.
Patients with a history of atopic dermatitis are at increased risk for developing nonspecific hand dermatitis and irritant contact dermatitis. However, they do not appear to be at an increased risk for allergic contact dermatitis, despite the wide range of topical medications and moisturizers used by individuals with chronic atopic dermatitis. They are at lower risk of allergic contact dermatitis to poison ivy. Some European studies indicate that patients with atopic dermatitis may have increased incidence of allergic contact dermatitis to nickel.
Onset of symptoms
Individuals with allergic contact dermatitis typically develop dermatitis, within a few days of exposure, in areas that were exposed directly to the allergen. Certain allergens (eg, neomycin) penetrate intact skin poorly, and the onset of dermatitis may be delayed up to a week following exposure.
A minimum of 10 days is required for individuals to develop specific sensitivity to a new contactant. For example, an individual who never has been sensitized to poison ivy may develop only a mild dermatitis 2 weeks following the initial exposure but typically develops severe dermatitis within 1-2 days of the second and subsequent exposures.
Remember that removing the poison ivy allergen from the skin is difficult, and unless an individual washes exposed skin within 30 minutes of exposure, allergic contact dermatitis will develop. The hallmark of the diagnosis of poison ivy is linear dermatitic lesions. The possibility of an external cause of dermatitis always must be considered if the dermatitis is linear or sharply defined.
The immediate onset of dermatitis following initial exposure to material suggests either a cross-sensitization reaction, prior forgotten exposure to the substance, or nonspecific irritant contact dermatitis provoked by the agent in question.
Individuals may develop dermatitis on eyelids and other exposed skin following exposure to airborne allergens or allergens transferred to that site by the fingers. Contact dermatitis may also result from allergy to eyelid makeup.
Immediate reactions, ie, visible lesions developing less than 30 minutes after exposure, indicate contact urticaria (not allergic contact dermatitis). This is particularly true if the lesions are urticarial in appearance and if the skin reaction is associated with other symptoms, such as distant urticaria, wheezing, ophthalmedema, rhinorrhea, or anaphylaxis.
Rubber latex currently is the most important source of allergic contact urticaria (see Latex Allergy). The term hypoallergenic may refer to gloves that do not contain sensitizing chemicals added to rubber latex but may not indicate whether the gloves are rubber latex free.
Some individuals may have delayed specific contact sensitivity to rubber latex, but contact urticaria to rubber latex is much more common than allergic contact dermatitis to latex. Individuals with hand dermatitis, hospital workers, children with spina bifida, and atopic individuals are at increased risk of developing contact urticaria to rubber latex. Individuals may have allergic contact dermatitis to chemicals added to rubber gloves and have contact urticaria to latex. Individuals wearing rubber gloves should be evaluated carefully for both possibilities.
Rare reports exist of immediate anaphylactic reactions to topical antibiotics (eg, bacitracin).
Contact dermatitis is 1 of the 10 leading occupational illnesses. It may prevent individuals from working. The hands are the sites exposed most intensely to contact allergens and irritants, both at work and at home. Allergic contact dermatitis in response to workplace materials may improve initially on weekends and during holidays, but individuals with chronic dermatitis may not demonstrate the classic history of weekend and holiday improvement.
Irritant contact dermatitis is more likely if multiple workers are affected in the workplace. Most allergens rarely sensitize a high percentage of the population.
Hobbies may be the source of allergic contact dermatitis. Examples include woodworking with exotic tropical woods or processing film using color-developing chemicals that may provoke cutaneous lesions of lichen planus from direct skin exposure.
Medications (both self-prescribed and physician-prescribed) are important causes of allergic contact dermatitis. The workplace nurse may dispense ineffective and sensitizing topical preparations, such as thimerosal (Merthiolate), which may change a simple abrasion into a severe case of allergic contact dermatitis. Individuals may develop allergy to preservatives in medications and/or to the active ingredients in topical medications, especially neomycin and topical corticosteroids.[11, 12]
Patients with dermatitis that did not clear with topical corticosteroid treatment should be considered for patch testing with a corticosteroid series and the commercial preparations of corticosteroids and their vehicles.
Topical corticosteroids are the mainstay of treatment, while a variety of symptomatic treatments can provide short-term relief of pruritus. However, the definitive treatment of allergic contact dermatitis is the identification and removal of any potential causal agents; otherwise, the patient is at increased risk for chronic or recurrent dermatitis. Online resources allow the physician to create a list of products free of allergens to which the patient is allergic.
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.