Individuals with allergic contact dermatitis (see the image below) may have persistent or relapsing dermatitis, particularly if the material(s) to which they are allergic is not identified or if they practice inappropriate skin care. The longer an individual has severe dermatitis, the longer, it is believed, that the dermatitis will take to resolve once the cause is identified.
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Chronic stasis dermatitis with allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis produces areas....
See 5 Body Modifications and Piercing: Dermatologic Risks and Adverse Reactions, a Critical Images slideshow, to help recognize various body modifications and the related potential complications.
Signs and symptoms
Acute allergic contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base. Lichenified pruritic plaques may indicate a chronic form of the condition.
Individuals with allergic contact dermatitis typically develop the condition within a few days of exposure, in areas that were exposed directly to the allergen. Certain allergens (eg, neomycin), however, penetrate intact skin poorly; in such cases, the onset of dermatitis may be delayed for up to a week following exposure.
Individuals may develop widespread dermatitis from topical medications applied to leg ulcers or from cross-reacting systemic medications administered intravenously.
Intraoral metal contact allergy may result in mucositis that mimics lichen planus, which has an association with intraoral squamous cell carcinoma.
See Clinical Presentation for more detail.
Diagnosis
Diagnostic studies for allergic contact dermatitis include the following:
Potassium hydroxide preparation and/or fungal culture: To exclude tinea; these tests are often indicated for dermatitis of the hands and feet
Patch testing: To identify external chemicals to which the person is allergic
Repeat open application test (ROAT): To determine whether a reaction is significant in individuals who develop weak or 1+ positive reactions to a chemical
Dimethylgloxime test: To determine whether a metallic object contains enough nickel to provoke allergic dermatitis
Skin biopsy: May help to exclude other disorders, particularly tinea, psoriasis, and cutaneous lymphoma
See Workup for more detail.
Management
The definitive treatment for 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. Treatments also include the following:
Corticosteroids: Topical corticosteroids are the mainstay of treatment, although acute, severe allergic contact dermatitis, such as from poison ivy, often needs to be treated with a 2-week course of systemic corticosteroids
Topical immunomodulators (TIMs): Approved for atopic dermatitis, but they are also prescribed for cases of allergic contact dermatitis when they offer safety advantages over topical corticosteroids
Phototherapy: Administered to individuals with chronic allergic contact dermatitis that is not controlled well by topical corticosteroids; these patients may benefit from treatment with a combination of psoralen (a photosensitizer) and ultraviolet-A (PUVA)
Immunosuppressive agents: Chronic immunosuppressive agents are, in rare instances, used to treat recalcitrant cases of severe, chronic, widespread allergic contact dermatitis or severe hand dermatitis that prevents a patient from working or performing daily activities
Disulfiram: Occasionally, an individual who is highly allergic to nickel and has severe vesicular hand dermatitis will benefit from treatment with disulfiram (Antabuse); the drug has a chelating effect
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. (See Treatment.)
Go to Irritant Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
Approximately 3000 chemicals are well documented as specific causes of allergic contact dermatitis.
Compounds must be less than 500 d for efficient penetration through the stratum corneum barrier, which is the water-impermeable outer layer of the skin. Small organic molecules that are chemically reactive (chemical sensitizers) bind with self-proteins to generate immunogenic neoantigens through a process termed haptenization. Although haptens can penetrate through intact skin, patients with certain disease states that impair barrier function (eg, leg ulcers, perianal dermatitis) have an increased risk of sensitization to topically applied medications and their vehicle components.
Many patients with atopic dermatitis or allergic contact dermatitis to nickel harbor a defective form of the filaggrin gene.[1] Filaggrin helps aggregate cytoskeletal proteins that form the cornified cell envelope. In its absence, the barrier is defective.
Prehaptens are chemicals that are not activated by host proteins, but instead require chemical transformation by oxidative derivatization by ambient or air oxidation to form hydroperoxide. Examples include certain fragrance materials and dyes used in hair coloring, such as para-phenylenediamine.
Haptens activate Toll-like receptors (TLRs) and activate innate immunity. The importance of hapten-mediated activation of innate immunity is highlighted by the clinical observation that the irritancy of chemicals (ie, the ability of these chemicals to cause grossly visible skin inflammation upon primary exposure) correlates with their ability to act as contact sensitizers and to induce acute contact dermatitis.
Haptens or haptenated self-proteins are recognized by innate immune mechanisms in the skin, and this leads to the elaboration of a number of proinflammatory mediators, including interleukin (IL)–1β. As a result, skin-resident dendritic cells (DCs) become activated. There are several populations of DCs. Langerhans cells are the only DC subtype in the epidermis. Like all skin-resident DCs, Langerhans cells efficiently acquire antigen in the periphery and migrate to regional lymph nodes where they present antigen to naïve and memory T cells. These DCs, which may have been directly haptenated or could have acquired haptenated proteins from their surroundings, migrate to skin-draining lymph nodes where they present peptides from haptenated proteins to activate memory and naïve T cells.
In the final step, hapten-induced inflammation recruits activated effector T cells back to the initial site of antigen encounter in the skin. The effector T cells release proinflammatory cytokines, such as interferon-γ, and promote the killing of haptenated cells, resulting in the development of the classic inflammatory rash seen in allergic contact dermatitis.
Keratinocytes are crucial for the development of allergic contact dermatitis. They constitute the vast majority of cells in the epidermis and form the anatomic barrier of the skin. Keratinocytes express most TLRs, and this allows them to respond to TLR4-triggering haptens, such as nickel. Keratinocytes are also a source of IL-10, an immunosuppressive cytokine that limits the extent of contact hypersensitivity
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 following years of chronic low-grade exposure; for example, sensitivity to chromate in cement can eventually develop in individuals 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 clinical resolution of allergic contact dermatitis.
Approximately 25 chemicals appear to be responsible for as many as one half of all cases of allergic contact dermatitis. These include nickel, preservatives, dyes, and fragrances.
Poison ivy
Poison ivy (Toxicodendron radicans) 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
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 in young and middle-aged women.[2, 3]
Allergic contact dermatitis to nickel typically is manifested by dermatitis at the sites where earrings or necklaces (see the image below) containing nickel are worn or where metal objects (including the keypads of some cell phones[4] ) 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.
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Allergic contact dermatitis to nickel in a necklace.
Rubber gloves[5]
Allergy to 1 or more chemicals in rubber gloves is suggested in any individual with chronic hand dermatitis who wears 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).
Hair dye and temporary tattoos
p-Phenylenediamine (PPD) is a frequent component of and sensitizer in permanent hair dye products and temporary henna tattoos[6] ; 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. Epidemiologic data indicate that the median prevalence of positive patch test reactions to PPD among dermatitis patients is 4.3% (increasing) in Asia, 4% (plateau) in Europe, and 6.2% (decreasing) in North America.[7]
Textiles
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 suspected 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.
Preservatives
Preservative chemicals added to cosmetics, moisturizers, and topical medications are major causes of allergic contact dermatitis (see the image below). The risk of allergic contact dermatitis appears to be highest to quaternium-15, followed by allergic contact dermatitis to isothiazolinones. Methylisothiazolinone is used as an individual preservative and may be a significant allergen.[8] Kathon CG is methylchloroisothiazolinone in combination with methylisothiazolinone.
Although parabens are among the most widely used preservatives, they are not a frequent cause of allergic contact dermatitis.
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Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.
Schnuch et al estimated that preservatives found in leave-on topical products varied over 2 orders of magnitude in relative sensitization risk.[9]
Formaldehyde is a major cause of allergic contact dermatitis (see the image below). 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], and isothiazolinones[9] ). They are, in themselves, allergenic or may produce cross-sensitization to formaldehyde.
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Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.
Fragrances[10, 11]
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 in the United States, 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 that is often abraded by shaving in women.
Massage and physical therapists and geriatric nurses are at higher risk of occupational allergic contact dermatitis to fragrances.
Corticosteroids
In the last decade, it has become clear that some 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.
Neomycin
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 and venous ulcers 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).[12] Avoid these drugs both topically and systemically in individuals allergic to neomycin.
Benzocaine
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 lidocaine (Xylocaine), which does not cross-react with benzocaine.
Sunscreens
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 or may have nonspecific cutaneous irritation from these products.
Photoallergy
Occasionally, individuals develop photoallergic 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).
Acrylates and methacrylates[13, 14]
These agents are used in manufacturing, nail acrylics, and wound dressings, among other uses.
The National Health and Nutrition 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.
The TRUE test Web site can provide accurate basic information on common allergens. The Contact Allergen Management Program is provided as a service to the American Contact Dermatitis Society (ACDS) members and is particularly valuable for allergens found in topical skin care products. The Contact Allergen Management Program (CAMP) database contains more than 8100 known ingredients cataloged in more than 5500 commercial skincare products and is available as a Smartphone application.
International statistics
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.
Race, sex, and age-related demographics
No racial predilection exists for allergic contact dermatitis. Allergic contact dermatitis is more common in women than in men. This predominantly is a result of allergy to nickel, which is much more common in women than in men in most countries.
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.[15]
The prognosis depends on how well the affected individual can avoid the offending allergen.[16]
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 creams with ceramides or 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 chromates.
A particular problem is neurodermatitis (lichen simplex chronicus), in which individuals repeatedly rub or scratch an area initially affected by allergic contact dermatitis.
Mortality
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.
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, Smartphone applications, standard textbooks, and the TRUE test kit contain basic information about the chemicals.
Susceptible individuals need to read the list of ingredients before applying 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 patient education information, see the Skin, Hair, and Nails Center, as well as Contact Dermatitis.
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 included in patch testing. Evaluation of allergic contact dermatitis requires a much more detailed history than 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 and bacitracin are important causes of allergic contact dermatitis in these individuals because they are used frequently despite the lack of documentation of their 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. They are at lower risk of allergic contact dermatitis to poison ivy. An inverse association was found between contact sensitization and severe atopic dermatitis. Inverse associations were found for all groups of allergenic chemicals and metals, except for sensitization to fragrances and topical drugs, for which positive associations were identified.
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.
Eyelid dermatitis
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.
Contact urticaria
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.
Latex
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. 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. 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
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.[17, 18]
Patients with dermatitis that does 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.
Acute allergic contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base. Lichenified pruritic plaques may indicate 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. Note the following.
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.
Topical medication sites
Allergic contact dermatitis is frequent in the perianal area as a result of the use of sensitizing medications and remedies (eg, topical benzocaine). Topical medications are also important causes of allergic contact dermatitis in cases of otitis externa. Allergy to chemicals in ophthalmologic preparations may provoke dermatitis around the eyes.
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.
Hair dyes
Hair dye—in particular, the component p-phenylenediamine (PPD)—may trigger allergic contact dermatitis. 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 the image below). 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.
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Chronic stasis dermatitis with allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis produces areas....
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,[19] tropical woods, nickel, and hair dye (see the image below).
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Erythema multiformelike reaction that developed acutely following hair dying.
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 and treatment of allergic contact dermatitis may prevent the development of venous ulcers.
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.
Occasionally, allergic contact dermatitis is complicated by secondary bacterial infection, which may be treated by the appropriate systemic antibiotic.
A guideline summary on allergy testing is available from the American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology (Allergy Diagnostic Testing: An Updated Practice Parameter).[21]
Go to Irritant Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
Potassium hydroxide preparation and/or fungal culture to exclude tinea are often indicated for dermatitis of the hands and feet. This will identify disorders such as tinea pedis.
Patch testing[22, 23, 24] 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 should be performed by healthcare providers trained in the proper technique. Most dermatologists can perform patch testing using the TRUE test, 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.
The patch testing procedure is as follows:
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 reactions 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 may occur. 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 are as follows:
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
Chemicals in plastics and glues
Chemicals found in rubber products not included in the TRUE test
Chemicals in shoes and clothing
Ultraviolet (UV) protective ingredients in sunscreens
Other chemicals producing photo allergic contact dermatitis
Miscellaneous allergens
The chemicals listed above are tested under Finn chambers, allergEAZE chambers, or the IQ Chamber patch test. In photopatch testing, the chemicals are applied in duplicate sets. One set receives 10 J/cm2 of UV-A (or 1 J/cm2 less than the minimum erythema dose, whichever is lowest) 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.
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.
Individuals with atopic dermatitis may have more positive patch-test reactions to ingredients in personal care products, to the topical steroids that they use, as well as to antibiotics.[25]
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 clinical dermatitis does not develop, the 1+ reaction likely was not meaningful. Conversely, if dermatitis develops after a few days of repeated application of the suspected product, then the weak patch test reaction is highly relevant.
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, cobalt, 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, however.
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.
Collections of Langerhans cells on skin biopsy can be an important clue to the diagnosis of allergic contact dermatitis. Although eosinophils are typically associated with allergic contact dermatitis, a 2016 study did not identify a difference in eosinophil count between patch test–positive and patch test–negative cases.[26]
The 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 may provoke atypical T-cell infiltrates, simulating mycosis fungoides.
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.
Go to Irritant Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
Topical soaks with cool tap water, Burow solution (1:40 dilution), saline (1 tsp/pint) can be soothing. 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.
Large vesicles may rarely benefit from therapeutic drainage (but not removing the vesicle tops).[27] Puncturing or incising vesicles may introduce bacteria and lead to infection. These lesions should then be covered with dressing soaked in Burow solution.
Emollients (eg, white petrolatum, Eucerin) may be beneficial in chronic cases.
Sedating oral antihistamines may help diminish pruritus via a central effect. Patients should avoid using topical antihistamines, including topical doxepin,[28] because of the apparently high risk of iatrogenic allergic contact dermatitis to these agents; additionally, sedation can occur if large amounts of doxepin cream are applied.
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 or the face.
Acute severe allergic contact dermatitis, such as from 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 corticosteroid use.
The systemic corticosteroids must be administered for 2 weeks, because shorter courses are notorious for allowing poison ivy dermatitis to relapse. Long-acting intramuscular triamcinolone acetonide (Kenalog) 40-60 mg may be used in place of oral prednisone.
Long-term use of systemic corticosteroids to treat allergic contact dermatitis may produce severe morbidity. Individuals with allergic contact dermatitis should not receive long-term systemic corticosteroids or immunosuppressives unless extensive patch testing and evaluation have failed to identify remedial causes of the severe dermatitis.
Long-term widespread use of potent topical corticosteroids may produce local skin atrophy and systemic adverse effects. In particular, use around the eyes may theoretically cause cataracts, glaucoma, corneal thinning/perforation, and loss of the eye.
Allergy to corticosteroid molecules without C16-methyl substitution in the D-ring (ie, groups A [eg, hydrocortisone, hydrocortisone-21-butyrate] and D2 [eg, hydrocortisone-17-butyrate] may be much more frequently observed than allergy to those corticosteroid molecules that are halogenated and have a methyl group at C16 (ie, groups D1 [eg, betamethasone dipropionate, clobetasol propionate, diflorasone diacetate, fluticasone propionate, mometasone furoate] and C [eg, desoximetasone, desoxymethasone]).[29] C16-methylated corticosteroids should be preferentially prescribed if topical corticosteroid treatment is indicated.
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.[30] Pimecrolimus (Elidel cream) is a topical treatment that may be helpful for mild allergic contact dermatitis of the face. Tacrolimus (Protopic 0.1% ointment) is the most helpful TIM for allergic contact dermatitis of the hands.[31]
Individuals with chronic allergic contact dermatitis that is not controlled well by topical corticosteroids may benefit from psoralen plus ultraviolet-A (PUVA) treatments. Psoralen is a photosensitizer that is ingested prior to light exposure. Narrow-band UVB phototherapy may be as effective. Light at 308 nm can also be delivered to limited chronic areas of dermatitis.
Rarely, chronic immunosuppressive agents, such as azathioprine (Imuran),[32] mycophenolate (CellCept), 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.
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.
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.
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.
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.
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.[33] 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).
Patients 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. Creams containing ceramides (eg, Impruv, Cerave) can help restore the epidermal barrier in persons with irritant contact dermatitis and atopic dermatitis.
Acute dermatitis that resolves with short-term treatment does not require further evaluation or specialist consultation. For example, 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.
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.
Individuals may develop new allergies. A patient who experiences a relapse or a worsening of allergic contact dermatitis may require further history and, possibly, further patch testing.
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. Systemic treatment with immunosuppressive therapy may be warranted in severe and refractory cases. Methotrexate, cyclosporine, and azathioprine have all been used for this purpose.[16]
Oral antihistamines may help diminish pruritus caused by allergic contact dermatitis.
Clinical Context:
Pimecrolimus is indicated for eczema and atopic dermatitis. It was the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Pimecrolimus is derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus.
This agent selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids.
Clinical Context:
Tacrolimus reduces itching and inflammation by suppressing release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin 3 (IL-3), IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha (TNF-alpha), all of which are involved in the early stages of T-cell activation.
Additionally, tacrolimus may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of high-affinity IgE receptor (FCeRI) on Langerhans cells.
Tacrolimus is approved for moderate-to-severe atopic dermatitis and can be used in patients as young as 2 years. It is more expensive than topical corticosteroids. This agent is available as ointment in concentrations of 0.03 and 0.1%.
Clinical Context:
A class I superpotent topical steroid, clobetasol suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Use 0.05% cream or ointment.
Clinical Context:
Hydrocortisone is an adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity. Use 0.2% cream or ointment.
Clinical Context:
Prednisone is an immunosuppressant for treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.
Clinical Context:
Triamcinolone is indicated for inflammatory dermatosis responsive to steroids; it decreases inflammation by suppressing migration of PMNs and reversing capillary permeability. Intramuscular injection may be used for widespread skin disorder or intralesional injections may be used for localized skin disorder.
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.
Clinical Context:
Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the central nervous system.
Antihistamines act by competitive inhibition of histamine at the H1 receptor. They may control itching by blocking effects of endogenously released histamine. These agents have no role in treating allergic contact dermatitis beyond possibly decreasing pruritus via sedating effects.
Clinical Context:
Doxepin inhibits histamine and acetylcholine activity and has proven useful in the treatment of allergic dermatologic disorders. The oral form is marketed as an antidepressant but is used also for its antihistaminic/antipruritic effects. The dosage is 10-25 mg at night in adults; if necessary, this can be gradually increased to a maximum dose of 75 mg/d for dermatoses. The topical form is approved for pruritus in adults with atopic dermatitis or lichen simplex chronicus.
The tricyclic antidepressant doxepin is used in contact dermatitis for its sedative and antihistaminic properties. Oral doxepin may be considered if oral antihistamines are not helpful. Topical doxepin should be avoided because of the risk of iatrogenic allergic contact dermatitis.
Clinical Context:
Disulfiram is a thiuram derivative that interferes with aldehyde dehydrogenase. In patients highly allergic to nickel with severe vesicular hand dermatitis, the chelating effect of disulfiram is helpful in reducing the body's nickel burden in the individual allergic to nickel. Do not administer if patient has ingested alcohol within last 12 hours.
Although marketed as a treatment for alcoholism, disulfiram chelates nickel, which then is excreted in the urine. Lowering systemic levels of nickel has been reported to benefit individuals with pompholyx (dyshidrosis) and demonstrated hypersensitivity to the metal. Consider this therapy only for severe disabling dyshidrosis refractory to all other treatment in a patient proven allergic to nickel who does not drink alcohol and who consents to regular blood tests to identify liver toxicity from the medication.
How is the course of allergic contact dermatitis characterized?What are the signs and symptoms of allergic contact dermatitis?What are the diagnostic studies for allergic contact dermatitis?What is the treatment for allergic contact dermatitis?What is allergic contact dermatitis?What testing is available for allergic contact dermatitis?What determines the importance of specific substances as causes of allergic contact dermatitis?What is the role of patient history in the evaluation of allergic contact dermatitis?What is the main treatment for allergic contact dermatitis?What is the pathogenesis of allergic contact dermatitis?What are prehaptens associated with allergic contact dermatitis?What is the role of haptens in the pathophysiology of allergic contact dermatitis?What is the role of keratinocytes in the development of allergic contact dermatitis?How does the initial sensitization occur in the pathophysiology of allergic contact dermatitis?Which types of cells persist in the dermis after clinical resolution of allergic contact dermatitis?How is allergic contact dermatitis caused by poison ivy characterized?How is allergic contact dermatitis caused by nickel characterized?What causes allergic contact dermatitis?How is allergic contact dermatitis caused by rubber gloves characterized?How is allergic contact dermatitis caused by hair dye and temporary henna tattoos characterized?How is allergic contact dermatitis caused by textiles characterized?Which preservative chemicals are most likely to cause allergic contact dermatitis?What is the role of fragrances in the etiology of allergic contact dermatitis?What is the role of corticosteroids in the etiology of allergic contact dermatitis?What is the role of neomycin in the etiology of allergic contact dermatitis?Does benzocaine cause allergic contact dermatitis?Do sunscreens cause allergic contact dermatitis?What is the role of ultraviolet (UV) light in the development of allergic contact dermatitis?What kinds of plastics products are associated with allergic contact dermatitis?How common is allergic contact dermatitis in the US?What is the international prevalence of allergic contact dermatitis?What are the race, sex, and age-related demographics of allergic contact dermatitis?What is the prognosis of allergic contact dermatitis?What is the mortality associated with allergic contact dermatitis?What can patients with allergic contact dermatitis do to have the best prognosis?What does the patient education for allergic contact dermatitis consist of?What is the role of patient history in the evaluation of allergic contact dermatitis?Which skin conditions are associated with allergic contact dermatitis?Why is a history of atopic dermatitis (eczema) relevant in the evaluation of allergic contact dermatitis?How is the onset of symptoms characterized in allergic contact dermatitis?How is eyelid dermatitis associated with allergic contact dermatitis?How is contact urticaria distinguished from allergic contact dermatitis?What is the role of latex in allergic contact dermatitis?What is the role of occupational exposure to allergens in allergic contact dermatitis?Which kinds of hobbies are associated with allergic contact dermatitis?Which types of medications are associated with allergic contact dermatitis?What are the clinical findings of allergic contact dermatitis caused by hair dyes?What are the clinical findings of severe cutaneous reactions associated with allergic contact dermatitis?How is acute allergic contact dermatitis characterized?What are the clinical findings of allergic contact dermatitis on the hands?What are the clinical findings of allergic contact dermatitis associated with topical medications?What are the clinical findings of airborne allergic contact dermatitis?What are the clinical findings of allergic contact dermatitis associated with stasis dermatitis and stasis ulcers?What are the complications associated with allergic contact dermatitis?What are diagnostic considerations in allergic contact dermatitis?What are the differential diagnoses for Allergic Contact Dermatitis?Which lab studies are indicated in the workup of allergic contact dermatitis?What is the role of patch testing in the workup of allergic contact dermatitis?How is patch testing performed in the workup of allergic contact dermatitis?When is additional patch testing indicated in the workup of allergic contact dermatitis?What approach to patch testing provides the most accurate results in the diagnosis of allergic contact dermatitis?Which factors can affect the accuracy of patch testing results in the workup of allergic contact dermatitis?What adverse reaction is associated with patch testing for allergic contact dermatitis?What secondary patch test series or sets are available for the workup for allergic contact dermatitis?What are common causes of allergic contact dermatitis not included in the TRUE test and how are they tested?Is patch testing for allergic contact dermatitis safe in pregnancy?What is the role of the repeat open application test (ROAT) in the workup of allergic contact dermatitis?How are chemical tests used to identify allergens in allergic contact dermatitis?What is the role of skin biopsy in the workup of allergic contact dermatitis?How are the histologic findings characterized in allergic contact dermatitis?What is the treatment for allergic contact dermatitis?What treatment helps relieve symptoms of allergic contact dermatitis?How are corticosteroids used in the treatment of allergic contact dermatitis?What are the side effects of long-term use of corticosteroids in the treatment of allergic contact dermatitis?What is the role of topical immunomodulators (TIMs) in the treatment of allergic contact dermatitis?What is the role of phototherapy/PUVA for the treatment of allergic contact dermatitis?What is the role of immunosuppressive agents in the treatment of allergic contact dermatitis?What is the role of disulfiram in the treatment of allergic contact dermatitis?How are dietary recommendations used in the treatment of allergic contact dermatitis?When is hospital admission indicated in the treatment of allergic contact dermatitis?What activity restrictions are indicated in the treatment of allergic contact dermatitis?How can the recurrence of allergic contact dermatitis be prevented?How can the recurrence of allergic contact dermatitis associated with chemicals be prevented?How can allergic contact dermatitis be prevented in the occupational setting?What can patients do to prevent the recurrence of allergic contact dermatitis?When are consultations indicated in the treatment of allergic contact dermatitis?What does long-term monitoring of allergic contact dermatitis consist of?How is drug treatment used in the treatment of allergic contact dermatitis?Which medications are used in the treatment of severe acute allergic contact dermatitis?Which medications are used in the treatment of refractory cases of allergic contact dermatitis?Which medication is used to treat pruritus caused by allergic contact dermatitis?Which medications in the drug class Topical Immunomodulators are used in the treatment of Allergic Contact Dermatitis?Which medications in the drug class Corticosteroids are used in the treatment of Allergic Contact Dermatitis?Which medications in the drug class Antihistamines are used in the treatment of Allergic Contact Dermatitis?Which medications in the drug class Tricyclic Antidepressants are used in the treatment of Allergic Contact Dermatitis?Which medications in the drug class Chelation Agents are used in the treatment of Allergic Contact Dermatitis?
Thomas N Helm, MD, Clinical Professor of Dermatology and Pathology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Director, Buffalo Medical Group Dermatopathology Laboratory
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center
Disclosure: Nothing to disclose.
Acknowledgements
Donald Belsito, MD Professor of Clinical Dermatology, Department of Dermatology, Columbia University Medical Center
Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, New York County Medical Society, New York Dermatological Society, Noah Worcester Dermatological Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences,and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.
Mark Louden, MD Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department of Medicine, University of Miami, Leonard M Miller School of Medicine
Mark Louden, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.
R Scott Lowery, MD Associate Professor of Ophthalmology, Department of Pediatric Ophthalmology and Strabismus, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital
R Scott Lowery, MD is a member of the following medical societies: American Academy of Ophthalmology and Arkansas Medical Society
Disclosure: Nothing to disclose.
Joshua May, MD Bend Dermatology Clinic
Disclosure: Nothing to disclose.
John A Michael, MD
Disclosure: Nothing to disclose.
Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Institute
Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, and International Society of Refractive Surgery
Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other; Bausch & Lomb Honoraria Speaking and teaching; Merck Consulting fee Consulting; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching
Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
David Todd Schwartz, MD Associate Professor of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center and New York University Medical Center
David Todd Schwartz, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.
Bradley D Shy, MD Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center, New York University School of Medicine
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Jack L Wilson, PhD Distinguished Professor, Department of Anatomy and Neurobiology, University of Tennessee Health Science Center College of Medicine
Jack L Wilson, PhD is a member of the following medical societies: American Association of Anatomists, American Association of Clinical Anatomists, and American Heart Association
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.
Allergic contact dermatitis to nickel in a necklace.
Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.
Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.
Chronic stasis dermatitis with allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis produces areas of erythema in areas of atrophie blanche and varicose veins.
Erythema multiformelike reaction that developed acutely following hair dying.
Chronic stasis dermatitis with allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis produces areas of erythema in areas of atrophie blanche and varicose veins.
Erythema multiformelike reaction that developed acutely following hair dying.
Allergic contact dermatitis to nickel in a necklace.
Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.
Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.
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