eMedicine Specialties > Dermatology > Allergy & Immunology

Contact Dermatitis, Allergic

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

Updated: Jul 31, 2009

Introduction

Background

The term contact dermatitis sometimes is used incorrectly as a synonym for allergic contact dermatitis (ACD). Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin (see Contact Dermatitis, Irritant) and by specific sensitivity in the case of allergic contact dermatitis. Allergic contact dermatitis is inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation. It 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.

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 US in the 1930s. The Finn chamber was designed in the 1970s; this is the standard method for patch testing individuals to chemicals not found in the thin-layer rapid use epicutaneous (TRUE) test, which became available in the United States in the 1990s.

The causes of allergic contact dermatitis evolve over time. Mercury compounds once were important causes of allergic contact dermatitis but rarely are used as topical medications and, currently, are less common 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.

Pathophysiology

Most chemicals able to provoke allergic contact dermatitis have small molecules (<500 d). Approximately 3000 chemicals are well documented as specific causes of allergic contact dermatitis. The small chemical molecules responsible for allergic contact dermatitis must bind to carrier proteins on Langerhans cells, which are situated within the suprabasilar layer of the epidermis. Langerhans cells are the antigen-presenting cells within the skin. Langerhans cells interact with CD4⁺ T cells (helper T cells). Skin irritation by both nonallergenic and allergenic compounds induces Langerhans cell migration and maturation. In contrast, only allergenic compounds induce CD1a⁺ CD83⁺ Langerhans cell migration with partial maturation at subtoxic concentration.¹

Cytokines also play an important role in allergic contact dermatitis because they regulate accessory-adhesion molecules, such as intercellular adhesion molecule 1. Interleukin 8 may be a cytokine indicating allergic contact dermatitis, not irritant contact dermatitis. Langerhans cells can migrate from the epidermis to the regional draining lymph nodes. Sensitization to a chemical requires intact lymphatic pathways. The initial sensitization typically takes 10-14 days from initial exposure to a strong contact allergen such as poison ivy. Some individuals develop specific sensitivity to allergens (eg, chromate in cement) following years of chronic low-grade exposure associated with chronic irritant contact dermatitis resulting from the alkaline nature of cement. Once an individual is sensitized to a chemical, allergic contact dermatitis develops within hours to several days of exposure.

CD4⁺ CCR10⁺ memory T cells persist in the dermis after allergic contact dermatitis clinically resolves.

Filaggrin barrier defects that predispose individuals to atopic dermatitis might also predispose them to allergic contact dermatitis by allowing greater penetration of chemical haptens.²

Frequency

United States

The National Health and Nutritional Examination Survey (NHANES) estimated the prevalence of contact dermatitis to be 13.6 cases per 1000 population using physical examinations by dermatologists of a selected sample of patients. NHANES underreported the prevalence compared with the physical examination findings. The National Ambulatory Medical Care Survey conducted in 1995 estimated 8.4 million outpatient visits to American physicians for contact dermatitis. This was the second most frequent dermatologic diagnosis. Of office visits to dermatologists, 9% are for dermatitis. At a student health center dermatology clinic, 3.1% of patients presented for allergic contact dermatitis, and 2.3% presented for irritant contact dermatitis.

International

A Swedish study found that prevalence of allergic contact dermatitis of the hands was 2.7 cases per 1000 population. A Dutch study found that prevalence of allergic contact dermatitis of the hands was 12 cases per 1000 population.

Mortality/Morbidity

Death from allergic contact dermatitis is rare in the United States. Allergic contact dermatitis to the weed wild feverfew caused deaths in India when the seeds contaminated wheat shipments to India. This plant then became widespread and a primary cause of severe airborne allergic contact dermatitis.

Race

No racial predilection exists for allergic contact dermatitis.

Sex

Allergic contact dermatitis is more common in women than in men. This predominately is a result of allergy to nickel, which is much more common in women than in men in most countries.

Age

Allergic contact dermatitis may occur in neonates. In elderly individuals, the development of allergic contact dermatitis may be delayed somewhat, but the dermatitis may be more persistent once developed. Contact allergy to topical medicaments is more common in persons older than 70 years.³

Clinical

History

A detailed history, both before and after patch testing, is crucial in evaluating individuals with allergic contact dermatitis. Potential causes of allergic contact dermatitis and the materials to which individuals are exposed should be patch tested. Patients with allergic contact dermatitis require a much more detailed history compared to those with most other dermatologic disorders.

History is equally important after patch testing. Only history and questioning can determine whether the materials to which a patient is allergic are partly or wholly responsible for the current dermatitis. A positive patch reaction may indicate only a sensitivity and not the cause of current dermatitis.

• Preexisting skin diseases
  • 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.
• Atopic dermatitis
  • Patients with a history of atopic dermatitis are at increased risk for developing nonspecific hand dermatitis and irritant contact dermatitis.
  • Patients with a history of atopic dermatitis 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.
  • Patients with atopic dermatitis 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.
    • 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.
• Eyelid dermatitis: Individuals may develop dermatitis on eyelids and other exposed skin following exposure to airborne allergens.
• Contact urticaria
  • Immediate reactions, ie, visible lesions developing less than 30 minutes after exposure, indicate contact urticaria (not allergic contact dermatitis), particularly if urticarial in appearance and if 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).
• Occupational dermatitis: 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. The hands are crucial for performing many work-related tasks. 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: Hobbies may be the source of allergic contact dermatitis, eg, 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: Self-prescribed and physician-prescribed medications are important causes of allergic contact dermatitis. The workplace nurse may dispense ineffective and sensitizing topical preparations, such as 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.^4,5 Dermatitis patients who 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.
• Iatrogenic adverse effects: Chronic use of systemic corticosteroids to treat allergic contact dermatitis may produce severe morbidity. Individuals with allergic contact dermatitis should not receive chronic systemic corticosteroids or immunosuppressives, unless extensive patch testing and evaluation have failed to identify remedial causes of the severe dermatitis. Chronic widespread use of potent topical corticosteroids may produce local skin atrophy and systemic adverse effects.

Physical

Acute allergic contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base. Lichenified pruritic plaques may manifest chronic allergic contact dermatitis. Occasionally, allergic contact dermatitis may affect the entire integument (ie, erythroderma, exfoliative dermatitis). The initial site of dermatitis often provides the best clue regarding the potential cause of allergic contact dermatitis.

• Hands: Hands are an important site of allergic contact dermatitis, particularly in the workplace. Common causes of allergic dermatitis on the hands include the chemicals in rubber gloves.
• Perianal: Allergic contact dermatitis is frequent in the perianal area as a result of the use of sensitizing medications and remedies (eg, topical benzocaine).
• Otitis externa: Topical medications are important causes of allergic contact dermatitis in cases of otitis externa.
• Airborne allergic contact dermatitis: Chemicals in the air may produce airborne allergic contact dermatitis. This dermatitis usually occurs maximally on the eyelids, but it may affect other areas exposed to chemicals in the air, particularly the head and the neck.
• Ophthalmologic: Allergy to chemicals in ophthalmologic preparations may provoke dermatitis around the eyes.
• Hair dyes: Individuals allergic to hair dyes typically develop the most severe dermatitis on the ears and adjoining face rather than on the scalp.
• Stasis dermatitis and stasis ulcers: Individuals with stasis dermatitis and stasis ulcers are at high risk for developing allergic contact dermatitis to topical medications applied to inflamed or ulcerated skin (see Media File 1). The chronicity of this condition and the frequent occlusion of applied medications contribute to the high risk of allergic contact dermatitis to medicament (eg, neomycin) in these patients. Individuals may develop widespread dermatitis from topical medications applied to leg ulcers or from cross-reacting systemic medications administered intravenously. For example, a patient allergic to neomycin may develop systemic contact dermatitis if treated with intravenous gentamicin.

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 multiforme: Erythema multiforme (EM) is a severe cutaneous reaction with targetoid lesions that occurs primarily after exposure to certain medications or is triggered by infection, most commonly by herpes simplex virus. Rare cases of EM have been reported after allergic contact dermatitis resulting from exposure to poison ivy,⁶ tropical woods, nickel, and hair dye (see Media File 2).

Erythema multiformelike reaction that developed acutely following hair dying.

Causes

Approximately 25 chemicals appear to be responsible for as many as one half of all cases of allergic contact dermatitis.

• Poison ivy is the classic example of acute allergic contact dermatitis in North America. Allergic contact dermatitis from poison ivy is characterized by linear streaks of acute dermatitis that develop where plant parts have been in direct contact with the skin.
• Nickel is the leading cause of allergic contact dermatitis in the world. The incidence of nickel allergic contact dermatitis in North America is increasing; in contrast, new regulations in Europe have resulted in a decreasing prevalence of nickel allergy.⁷ Allergic contact dermatitis to nickel typically is manifested by dermatitis at the sites where earrings or necklaces (see Media File 3) containing nickel are worn or where metal objects containing nickel are in contact with the skin. Nickel may be considered a possible occupational allergen. Workers in whom nickel may be an occupational allergen primarily include hairdressers, retail clerks, caterers, domestic cleaners, and metalworkers. Individuals allergic to nickel occasionally may develop vesicles on the sides of the fingers (dyshidrotic hand eczema or pompholyx) from nickel in the diet.

Allergic contact dermatitis to nickel in a necklace.

• Allergy to 1 or more chemicals in rubber gloves is suggested in any individual with chronic hand dermatitis who is wearing them, unless patch testing demonstrates otherwise. Allergic contact dermatitis to chemicals in rubber gloves typically occurs maximally on the dorsal aspects of the hand. Usually, a cutoff of dermatitis occurs on the forearms where skin is no longer in contact with the gloves. Individuals allergic to chemicals in rubber gloves may develop dermatitis from other exposures to the chemicals (eg, under elastic waistbands).
• p-Phenylenediamine (PPD) is a frequent component of and sensitizer in permanent hair dye products and temporary henna tattoos⁸ ; exposure in to it in hair dye products may cause acute dermatitis with severe facial edema. Severe local reactions from PPD may occur in black henna tattoos in adults and children. The median prevalence of positive patch test reactions to PPD among dermatitis patients was 4.3% (increasing) in Asia, 4% (plateau) in Europe, and 6.2% (decreasing) in North America.⁹
• Individuals allergic to dyes and permanent press and wash-and-wear chemicals added to textiles typically develop dermatitis on the trunk, which occurs maximally on the lateral sides of the trunk but spares the vault of the axillae. Primary lesions may be small follicular papules or may be extensive plaques. Individuals in whom this allergic contact dermatitis is suggested should be tested with a series of textile chemicals, particularly if routine patch testing reveals no allergy to formaldehyde. New clothing is most likely to provoke allergic contact dermatitis, since most allergens decrease in concentration in clothing following repeated washings.
• Preservative chemicals added to cosmetics, moisturizers, and topical medications are major causes of allergic contact dermatitis (see Media File 4). The most widely used preservatives include parabens, which are not a frequent cause of allergic contact dermatitis despite their wide use. The risk of allergic contact dermatitis appears to be highest to quaternium-15, followed by allergic contact dermatitis to isothiazolinones (Kathon CG).

Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.

• Formaldehyde is a major cause of allergic contact dermatitis (see Media File 5). Certain preservative chemicals widely used in shampoos, lotions, other moisturizers, and cosmetics are termed formaldehyde releasers (ie, quaternium-15 [Dowicil 200], imidazolidinyl urea [Germall 115]).

Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.

• Individuals may develop allergy to fragrances. Fragrances are found not only in perfumes, colognes, aftershaves, deodorants, and soaps, but also in numerous other products, often as a mask to camouflage an unpleasant odor. Unscented products may contain fragrance chemicals used as a component of the product and not labeled as fragrance. Individuals allergic to fragrances should use fragrance-free products. Unfortunately, the exact chemicals responsible for a fragrance in a product are not labeled. Four thousand different fragrance molecules are available to formulate perfumes. The fragrance industry is not required to release the names of ingredients used to compose a fragrance, even when individuals develop allergic contact dermatitis to fragrances found in topical medications. Deodorants may be the most common cause of allergic contact dermatitis to fragrances because they are applied to occlude skin. They often abrade in American women.
• Massage and physical therapists and geriatric nurses are at higher risk of occupational allergic contact dermatitis to fragrances.
• In the last decade, it has become clear that many individuals with chronic dermatitis develop allergy to topical corticosteroids. Most affected individuals can be treated with some topical corticosteroids, but an individual can be allergic to all topical and systemic corticosteroids. Budesonide and tixocortol pivalate are useful patch test corticosteroids for identifying individuals allergic to topical corticosteroids.
• The risk of allergy to neomycin is related directly to the extent of its use in a population. The risk of allergy to neomycin is much higher when it is used to treat chronic stasis dermatitis than when it is used as a topical antibiotic on cuts and abrasions in children. Assume that individuals allergic to neomycin are allergic to chemically related aminoglycoside antibiotics (eg, gentamicin, tobramycin).¹⁰ Avoid these drugs both topically and systemically in individuals allergic to neomycin.
• Avoid topical use of benzocaine. Benzocaine is included in most standard patch test trays. Individuals allergic to benzocaine may safely use or be injected with Xylocaine, which does not cross-react with benzocaine.
• Many individuals complain of adverse reactions to sunscreens, but many of these individuals are not allergic to the sunscreen materials. They may be allergic to preservatives in these products (see Media File 4) or may have nonspecific cutaneous irritation from these products.

Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.

• Occasionally, individuals develop photo allergic contact dermatitis. Allergic contact dermatitis may be accentuated by ultraviolet (UV) light, or patients may develop an allergic reaction only when a chemical is present on the skin and when the skin is exposed sufficiently to ultraviolet light A (UV-A; 320-400 nm).

Differential Diagnoses

Other Problems to Be Considered

Mycosis fungoides

Workup

Laboratory Studies

• Potassium hydroxide preparation and/or fungal culture to exclude tinea are often indicated for dermatitis of the hands and feet.

Procedures

• Patch testing^11,12,13
  • Patch testing is required to identify the external chemicals to which the person is allergic. The greatest quality-of-life benefits from patch testing occur in patients with recurrent or chronic allergic contact dermatitis (ACD). Patch testing is most cost effective and reduces the cost of therapy in patients with severe allergic contact dermatitis.
  • Patch testing must be performed by health care providers trained in the proper technique. Most dermatologists can perform patch testing using the TRUE test (consult the Physicians' Desk Reference), which can identify relevant allergies in as many as one half of affected patients. More extensive patch testing is indicated to identify allergies to chemicals not found in the TRUE test. Such testing typically is available only in a limited number of dermatology offices and clinics.
  • Patch testing procedure
    • Small amounts of appropriate labeled dilutions of chemicals are applied to the skin and occluded for 2 days.
    • Patch tests may be left on for 3 days before removal.
    • For reasons of scheduling, a chemical must remain under a skin patch for a minimum of 1 day to produce a positive patch test reaction 2-7 days following initial application.
    • The patch test must be read not only at 48 hours, when the patch tests customarily are removed, but again between 72 hours and 1 week following initial application.
  • Individuals with suspected allergic contact dermatitis without positive reactions on the TRUE test or with chronic dermatitis or relapsing dermatitis, despite avoiding chemicals to which they are allergic (identified on TRUE test), need additional patch testing. Many individuals have more than 1 contact allergy and may be allergic to 1 or more chemicals found on the TRUE test and on special allergen trays or series. Testing to more allergens increases accuracy of the diagnosis of allergic contact dermatitis. Selection of allergens for testing requires consideration of the patient's history and access to appropriate environmental contactants.
  • Certain chemicals (eg, neomycin) typically produce delayed positive patch test reactions at 4 days or later following initial application. A tendency exists for elderly patients to manifest positive patch test reactions later than younger patients. Do not perform patch testing on patients taking more than 15 mg/d of prednisone. Oral antihistamines may be used during the patch test period if required.
  • Angry back syndrome or excited skin syndrome: If a patient has a large number of positive patch test reactions, retesting the patient sequentially to a small series of these allergens may be necessary to exclude nonspecific false-positive reactions. The syndrome most likely occurs in individuals who have active dermatitis at the time of patch testing or who have a strong positive patch test reaction, both of which may induce local skin hyperreactivity in the area where patches were applied.
  • Additional patch test series or sets include the following:
    • Corticosteroids, particularly tixocortol pivalate and budesonide
    • Ingredients in cosmetics not found in the TRUE test
    • Chemicals used in dentistry that may produce mucosal and lip dermatitis in dental clients or that may produce chronic dermatitis of the hands in dentists and dental team members
    • Chemicals used in hairdressing that may produce facial, ear, and neck dermatitis in clients or chronic hand dermatitis or eyelid dermatitis in hairdressers
    • Fragrances found in cosmetics and a wide range of consumer products
    • Important allergens not found in the TRUE test that are frequent causes of allergic contact dermatitis
      • Bacitracin
      • Acrylates used in dentistry, artificial nails, and printing
      • Chemicals used in baking
      • Pesticides (many cases of dermatitis attributed to pesticides result from other causes, particularly from plants such as poison ivy)
      • Chemicals used in machining, eg, cutting oils and fluids
      • Photographic chemicals used by photographers and photographic developers
      • Plants excluding poison ivy
      • Chemicals in plastics and glues
      • Chemicals found in rubber products not included in the TRUE test
      • Chemicals in shoes and clothing
      • UV protective ingredients in sunscreens
      • Other chemicals producing photo allergic contact dermatitis
      • Miscellaneous allergens
    • The chemicals listed above are tested under Finn chambers or IQ patch test. In photopatch testing, the chemicals are applied in duplicate sets. One set receives 10 J/cm² (or 1 J/cm² less than minimum erythema dose to UV-A, whichever is lowest) of UV-A 24 hours after application of the allergens. The other series is protected from UV exposure to differentiate allergic contact dermatitis and photo-accentuated allergic contact dermatitis from photo allergic contact dermatitis. Both sets are read at 48 hours after application, as well as at an additional time point as in routine patch testing.
• Repeat open application test: For individuals who develop weak or 1+ positive reactions to a chemical, the repeat open application test (ROAT) is useful in determining whether the reaction is significant. ROAT is most useful when an individual has a 1+ reaction to a chemical found in a leave-on consumer product. For example, an individual with a weak reaction to a preservative found in a moisturizer may apply the moisturizer twice a day for a week to the side of the neck or behind an ear. If the individual applies it twice a day for a week without developing clinical dermatitis, the 1+ reaction likely was not meaningful. Conversely, if the individual develops dermatitis following a few days of repeated application of the suspected product, then the weak patch test reaction is highly relevant.
• Dimethylgloxime test: The dimethylgloxime test is a useful and practical way to identify metallic objects that contain enough nickel to provoke allergic dermatitis in individuals allergic to nickel. Dermatology staff may test suspected metal products in the office, or the individual may purchase a test kit and test objects at home or at work, particularly jewelry or metallic surfaces. Other chemical tests are available for other suspected allergens (eg, formaldehyde, chromate). Occasionally, chemical analyses may be necessary to determine whether a material contains a suspected allergen or to identify new unknown allergens.
• Skin biopsy may help exclude other disorders, particularly tinea, psoriasis, and cutaneous lymphoma. Skin biopsy of skin lesions of the palms and soles has several potential pitfalls, which include the following:
  • The stratum corneum and epidermis are particularly thick on the palms and soles. This makes the histologic diagnosis of psoriasis more difficult and increases the possibility that the biopsy specimen will lack sufficient dermis for optimal diagnosis.
  • An overly deep skin biopsy of the thenar area can cut the motor nerve, which is the recurrent branch of the median nerve.
  • A biopsy from the sole may leave a chronic painful scar on which the patient must walk.
• Guideline summaries
  • American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology - Allergy diagnostic testing: an updated practice parameter. Part 1¹⁴
  • American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology - Allergy diagnostic testing: an updated practice parameter. Part 2¹⁵

Histologic Findings

Histology of allergic contact dermatitis is similar to that found in other forms of eczematous dermatitis. A pattern of subacute chronic dermatitis or acute dermatitis may be seen. The inflammatory infiltrate in the dermis predominately contains lymphocytes and other mononuclear cells. Epidermal edema (ie, spongiosis and microvesicle formation) may be seen, but these changes may be absent in long-standing dermatitis in which thickening of the epidermis (acanthosis) with hyperkeratosis and parakeratosis may be seen in the epidermis and stratum corneum. Allergic contact dermatitis is provokes atypical T-cell infiltrates, simulating mycosis fungoides.

Treatment

Medical Care

The cause of allergic contact dermatitis (ACD) must be identified; otherwise, the patient is at increased risk for chronic or recurrent dermatitis. The Contact Allergan Replacement Database of the American Contact Dermatitis Society allows the physician to create a list of products free of allergens to which the patient is allergic.

• Symptomatic treatment
  • Cool compresses with saline or aluminum acetate solution are helpful for acute vesicular dermatitis (eg, poison ivy).
  • Some individuals with widespread vesicular dermatitis may obtain relief from lukewarm oatmeal baths.
  • Sedating oral antihistamines may help diminish pruritus.
  • Patients should avoid using topical antihistamines, including topical doxepin,¹⁶ because of the apparently high risk of iatrogenic allergic contact dermatitis to these agents.
• Corticosteroids
  • Topical corticosteroids are the mainstay of treatment, with the strength of the topical corticosteroid appropriate to the body site. For severe allergic contact dermatitis of the hands, 3-week courses of class I topical corticosteroids are required, while class 6 or class 7 topical corticosteroids typically are used for allergic contact dermatitis of intertriginous areas.
  • Acute severe allergic contact dermatitis, such as acute severe allergic contact dermatitis to poison ivy, often needs to be treated with a 2-week course of systemic corticosteroids. Most adults require an initial dose of 40-60 mg. The oral corticosteroid is tapered over a 2-week period, but a complicated tapering regimen probably is not necessary given the short duration of systemic corticosteroids. The systemic corticosteroids must be administered for 2 weeks, because shorter courses are notorious for allowing poison ivy dermatitis to relapse. Long-acting triamcinolone acetonide (Kenalog) 40-60 mg may be used in place of oral prednisone in these cases.
• Topical immunomodulators: Topical immunomodulators (TIMs) are approved for atopic dermatitis and are prescribed for cases of allergic contact dermatitis when they offer safety advantages over topical corticosteroids. TIMs do not cause cutaneous atrophy, glaucoma, or cataracts when applied near the eye. Topical tacrolimus is an option in patients with allergic contact eyelid dermatitis not controlled by brief courses of class l or ll topical corticosteroids and allergen avoidance.¹⁷ Pimecrolimus (Elidel cream) is a topical treatment often helpful for allergic contact dermatitis of the face. Tacrolimus (Protopic 0.1% ointment) appears to be the most helpful TIM for allergic contact dermatitis of the hands.
• Psoralen plus UV-A: Individuals with chronic allergic contact dermatitis that is not controlled well by topical corticosteroids may benefit from psoralen plus UV-A (PUVA) treatments.
• Immunosuppressive agents: Rarely, chronic immunosuppressive agents, such as azathioprine (Imuran)¹⁸ or cyclosporine (Neoral), are used in recalcitrant cases of severe chronic widespread allergic contact dermatitis or severe hand dermatitis that prevents the individual from working or performing daily activities. Biologicals active on T cells may be helpful in the future.
• Disulfiram: Occasionally, an individual who is highly allergic to nickel with severe vesicular hand dermatitis benefits from treatment with disulfiram (Antabuse). The chelating effect of disulfiram is helpful in reducing the body's nickel burden. Alcohol ingestion may produce severe adverse reactions in patients taking disulfiram.

Consultations

Many primary care physicians treat individuals with typical poison ivy dermatitis who respond well to a 2-week treatment course using topical or systemic corticosteroids and subsequently avoid poison ivy and related plants. Acute dermatitis that resolves with short-term treatment does not require further evaluation. Individuals with chronic dermatitis, particularly if it possibly is related to work, require detailed history and patch testing to standard screening sets and additional allergens as indicated by history, occupation, hobbies, and results on initial patch testing.

Diet

Some chemicals tested by the TRUE test may be present in the diet. Individuals with severe dermatitis, particularly if it is a disabling vesicular dermatitis of the hands, may be treated with diets low in minerals and chemicals to which the individual is allergic. A low-nickel diet is the most common, but published diets are available that are low in chromate, cobalt, or balsam of Peru. These diets may be attempted for the occasional allergic patient with severe chronic vesicular dermatitis.

Activity

Individuals with severe acute allergic contact dermatitis may be incapacitated temporarily and unable to work. Most individuals with allergic contact dermatitis may require light duties or restrictions of duties. They should avoid further contact with the chemicals to which they are allergic or chemicals that cross-react with these materials. Patients also should minimize exposure to irritant chemicals, particularly if the dermatitis is active or recently resolved. They should use mild cleansing agents on the skin, such as Aquanil, Cetaphil cleanser, or Oilatum-AD, and should apply bland protective emollients, such as SBR Lipocream, Cetaphil cream or Neutrogena hand cream, to help minimize relapse of allergic contact dermatitis or development of irritant contact dermatitis of ceramide cream (eg, Impruv).

Medication

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, rhus 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. PUVA can be helpful in these cases.

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

For details of some of these therapies, which are by no means all inclusive, see the drug tables below.

Topical immunomodulators

These agents modify immune processes that promote inflammation.

Pimecrolimus (Elidel cream)

Indicated for eczema and atopic dermatitis. First nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus. Selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. 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.

Dosing

Adult

Apply topically to affected areas bid

Pediatric

<2 years: Not established
>2 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Potential exacerbation of existing infection at site of application; may cause burning and irritation; product insert revised and contains boxed warning stating long-term safety of calcineurin inhibitors has not been established; although causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported

Tacrolimus (Protopic 1%)

Reduces itching and inflammation by suppressing release of cytokines from T cells. Also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of FCeRI on Langerhans cells. Can be used in patients as young as 2 y. More expensive than topical corticosteroids. Available as ointment in concentrations of 0.03 and 0.1%.

Dosing

Adult

Apply thin layer to affected skin areas bid and rub in gently and completely; continue treatment for 1 wk after clearing of signs and symptoms

Pediatric

<2 years: Not established
2-15 years: Apply 0.03% ointment bid to affected area(s)
>15 years: Administer as adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use with occlusive dressings; may be associated with an increased risk of folliculitis in adults; may cause local burning sensation, stinging, soreness, or pruritus (typically improve as lesions heal); for external use only; minimize exposure to natural or artificial sunlight (eg, tanning beds or UVA/B treatment); be sure skin is completely dry before application; product insert revised and contains boxed warning stating long-term safety of calcineurin inhibitors has not been established; although causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported; only 0.03% ointment indicated for use in children aged 2-15 y

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)

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.
Use 0.05% cream or ointment.

Dosing

Adult

Apply bid for up to 2 wk; not to exceed 50 g/wk

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; viral or fungal skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in widespread or prolonged therapy; superpotent topical steroid and, in general, should not be applied to face or intertriginous areas except under care and close supervision of experienced dermatologist; skin atrophy, striae, or other problems may result from inappropriate use

Hydrocortisone (Valerate, Westcort)

Adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.
Use 0.2% cream or ointment.

Dosing

Adult

Apply sparingly to affected areas bid

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prolonged use, applying over large surface areas, application of potent steroids, and occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria; ointment is more potent than cream and, in general, more caution should be exercised; should not be applied to face or intertriginous areas except under care and close supervision of experienced dermatologist; skin atrophy, striae, or other problems may result from inappropriate use

Prednisone (Deltasone, Meticorten, Orasone)

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production.

Dosing

Adult

40-60 mg/d PO qd or divided bid/qid; taper over 2-3 wk, as symptoms resolve; 0.5-2 mg/kg/d; taper as condition improves; single morning dose is safer for long-term use, but divided doses have more anti-inflammatory effect

Pediatric

4-5 mg/m²/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2-3 wk, as symptoms resolve

Interactions

Ketoconazole, erythromycin, clarithromycin, estrogens, and birth control pills increase levels; aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels
May increase levels of potassium-depleting diuretics (potentiates potassium loss and digitalis toxicity) and cyclosporine; May decrease levels of isoniazid, insulin (resistance is induced), and salicylates; monitor anticoagulant therapy and theophylline levels

Contraindications

Absolute: Systemic fungal infection; herpes simplex keratitis; hypersensitivity (usually with corticotropin, occasionally with IV preparations)
Relative: hypertension, active tuberculosis, congestive heart failure, prior psychosis, positive IPPD test result, glaucoma, severe depression, diabetes, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, pregnancy

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; use lower dose in hypothyroidism, liver disease, and obesity (decrease cortisol-binding globulin and increase free fraction of steroid); pregnancy, hyperthyroidism, and concurrent estrogen therapy may increase cortisol-binding globulin

Triamcinolone (Aristocort, Amcort, Aristospan Intra-articular)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Intramuscular injection may be used for widespread skin disorder or intralesional injections may be used for localized skin disorder.

Dosing

Adult

40-60 mg IM, may repeat in 4-6 wk
3-10 mg/mL intralesional

Pediatric

<6 years: Not established
6-12 years: 0.03-0.2 mg/kg IM
>12 years: Administer as in adults

Interactions

Coadministration with barbiturates, phenytoin, and rifampin decreases effects of triamcinolone

Contraindications

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Multiple complications (eg, severe infections, hyperglycemia, edema, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation of glucocorticoids may cause adrenal crisis; SC injection may cause skin atrophy that may be slow to recover

Antihistamines

Act by competitive inhibition of histamine at the H1 receptor. May control itching by blocking effects of endogenously released histamine. Have no effect in treating allergic contact dermatitis beyond possibly decreasing pruritus via sedating effects.

Hydroxyzine (Atarax, Vistaril)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

Dosing

Adult

10-25 mg PO tid/qid; 25-100 mg PO qd/qid

Pediatric

0.7 mg/kg PO tid; 0.6 mg/kg/dose PO q6h

Interactions

CNS depression may increase with alcohol or other CNS depressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for patients with porphyria); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness

Tricyclic antidepressants

Used in contact dermatitis for its sedative and antihistaminic properties. May consider oral doxepin (10-25 mg at night in adults if other oral antihistamines are not helpful). Maximum dose is 75 mg/d PO for dermatoses. This is achieved by increasing the initial dosage gradually. Topical doxepin should be avoided because of the risk of iatrogenic allergic contact dermatitis.¹⁶

Doxepin (Adapin, Sinequan)

Inhibits histamine and acetylcholine activity and has proven useful in the treatment of allergic dermatologic disorders.

Dosing

Adult

10-25 mg/d PO hs or divided bid/tid

Pediatric

<12 years: Not recommended
>12 years: 10-25 mg/d PO hs or bid/tid

Interactions

Decreases antihypertensive effects of clonidine but increases effects of sympathomimetics and benzodiazepines; effects of tricyclic antidepressants increase with phenytoin, carbamazepine, and barbiturates; plasma levels of doxepin and tricyclic antidepressants are increased significantly by drugs that inhibit liver's cytochrome-P450 system; discontinue MAOIs at least 2 wk prior to initiating therapy

Contraindications

Documented hypersensitivity; urinary retention; acute recovery phase following myocardial infarction; glaucoma

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism, and patients receiving thyroid replacement

Chelation agents

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 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)

Thiuram derivative that interferes with aldehyde dehydrogenase. For 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 h.

Dosing

Adult

Initial: 500 mg PO qd
Maintenance: 125-500 mg PO qd

Pediatric

Not established

Interactions

Increases effects of diazepam and chlordiazepoxide; metronidazole, isoniazid, and phenytoin may increase toxicity of disulfiram; coadministration with warfarin may increase PT time

Contraindications

Documented hypersensitivity; severe myocardial disease and coronary occlusion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypothyroidism, diabetes, hepatic cirrhosis or insufficiency, and seizure disorders

Follow-up

Further Inpatient Care

• Inpatient care rarely is required for allergic contact dermatitis (ACD) unless the dermatitis is so severe that patients cannot care for themselves. Examples may include severe allergic contact dermatitis with marked eyelid swelling that impairs vision or severe allergic contact dermatitis of the penis, which may impede urination. If patients develop chronic severe allergic reactions to their home or workplace, they may require a temporary change of environment until the cause of the dermatitis is identified.

Further Outpatient Care

• Individuals may develop new allergies. An individual who develops a relapse or a worsening of the dermatitis may require further history and, possibly, further patch testing.

Deterrence/Prevention

• To prevent recurrence of allergic contact dermatitis, instruct patients thoroughly concerning allergen(s) and the types of products likely to contain allergen(s).
  • For many patients with allergic reactions to fragrances, preservatives, vehicles, and medicaments, reading cosmetic labels and package inserts of topical/systemic medicaments may be sufficient to avoid allergens.
  • For patients allergic to nickel, the dimethylgloxime test can alert them the presence of the metal.
  • For many other patients with allergic reactions to chemicals that are unlikely to be labeled on consumer products (eg, rubber accelerators), suitable allergen alternatives (eg, gloves specifically known to be accelerator free) must be provided by the practitioner.
• Many cases of allergic contact dermatitis, especially of the hands, occur in the occupational setting. Proper worker education and hygiene may prevent allergic reactions. For example, glutaraldehyde is a known sensitizer with widespread use as a cold sterilizing agent in medicine and dentistry.¹⁹ Needless cases of allergic contact dermatitis to this biocide occur because of the lack of proper education regarding the appropriate use of gloves and other barriers to cutaneous contact.
• Advise patients to avoid identified chemicals to which they are allergic to minimize the risk of relapse, the risk of chronic contact dermatitis, and the risk of adverse effects from chronic use of nonspecific suppressive treatments (eg, topical and systemic corticosteroids, cyclosporine).

Complications

• Occasionally, allergic contact dermatitis is complicated by secondary bacterial infection, which may be treated by the appropriate systemic antibiotic.
• Darkly pigmented individuals may develop areas of hyperpigmentation or hypopigmentation from allergic contact dermatitis. Occasionally, they may develop depigmentation at sites of allergic contact dermatitis to certain chemicals.

Prognosis

• Individuals with allergic contact dermatitis may have persistent or relapsing dermatitis, particularly if the material(s) to which they are allergic is not identified or if they continue to practice skin care that is no longer appropriate (ie, they continue to use harsh chemicals to wash their skin, they do not apply bland emollients to protect their skin).
• The longer an individual has severe dermatitis, the longer it is believed it will take the dermatitis to resolve once the cause is identified.
• Some individuals have persistent dermatitis following allergic contact dermatitis, which appears to be true especially in individuals allergic to chrome.
• A particular problem is neurodermatitis (lichen simplex chronicus), in which individuals repeatedly rub or scratch an area initially affected by allergic contact dermatitis.
• The TRUE test can provide accurate basic information on common allergens (T.R.U.E. TEST). The Contact Allergan Replacement Database of the American Contact Dermatitis Society is particularly valuable for allergens to topical skin care products (database restricted to American Contact Dermatitis Society members).

Patient Education

• Patients have the best prognosis when they are able to remember the materials to which they are allergic and how to avoid further exposures.
• Provide patients with as much information as possible concerning the chemical to which they are allergic, including all known names of the chemical.
• Web sites, standard textbooks, and the TRUE test kit contain basic information about the chemicals.
• Susceptible individuals need to read the list of ingredients before applying American cosmetic products to their skin, since preservative chemicals are used widely in consumer, medical, and workplace products. The same chemical may have different names when used for consumer or industrial purposes.
• Provide pamphlets with color pictures of poison ivy to individuals allergic to the plant. The American Academy of Dermatology also has pamphlets on allergic contact dermatitis and hand eczema.
• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Contact Dermatitis.

Miscellaneous

Medicolegal Pitfalls

• Allergic contact dermatitis is a major occupational disease, and individuals may be temporarily unable to work. Many require modification of the workplace to continue working. Hopefully, a thorough history and patch testing minimize the risk of iatrogenic complications from systemic corticosteroids and other immunosuppressives.

Special Concerns

• The safety of patch testing in pregnancy has not been studied; however, the minute amounts of allergens applied appear unlikely to be absorbed in sufficient amounts to harm the fetus. Nonetheless, as with all treatments in pregnant women, the benefits of testing should be weighed against any potential, albeit undocumented, risk.
• Intraoral metal contact allergy may result in mucositis that mimics lichen planus, which has an association with intraoral squamous cell carcinoma. Intraoral squamous cell carcinoma adjacent to a dental restoration containing a metal to which the patient was allergic has been reported.²⁰
• Allergic contact dermatitis may be a direct trigger for skin ulceration in patients with venous insufficiency. Early diagnosis of allergic contact dermatitis may prevent the development of venous ulcers.

Multimedia

Media file 1: 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.

Media file 2: Erythema multiformelike reaction that developed acutely following hair dying.

Media file 3: Allergic contact dermatitis to nickel in a necklace.

Media file 4: Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.

Media file 5: Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.

References

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Keywords

contact dermatitis, allergic contact dermatitis, ACD, allergic dermatitis, skin allergy, contact hypersensitivity

Contributor Information and Disclosures

Author

Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; 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, and Canadian Dermatology Association
Disclosure: Nothing to disclose.

Medical Editor

Donald Belsito, MD, Clinical Professor, Department of Internal Medicine, Division of Dermatology, University of Missouri at Kansas City; Private Practice, American Dermatology Associates, LLC
Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, Kansas Medical Society, Noah Worcester Dermatological Society, Phi Beta Kappa, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University 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.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, 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; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Genetech Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Joshua May, BS, and previous Chief Editor, William D. James, MD, to the development and writing of this article.

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