AUTHOR AND EDITOR INFORMATION

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 ACD. ACD 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 ACD 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 US in the 1990s.

The causes of ACD evolve over time. Mercury compounds once were important causes of ACD but rarely are used as topical medications and, currently, are less common as a cause of ACD. Ethylenediamine, which was present in the original Mycolog cream, declined as a primary cause of ACD once Mycolog cream was reformulated to no longer contain this allergen.

Pathophysiology

Most chemicals able to provoke ACD have small molecules (<500 d). Approximately 3000 chemicals are well documented as specific causes of ACD. The small chemical molecules responsible for ACD 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.

Cytokines also play an important role in ACD because they regulate accessory-adhesion molecules, such as intercellular adhesion molecule 1. Interleukin 8 may be a cytokine indicating ACD, 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, ACD develops within hours to several days of exposure.

CD4⁺ CCR10⁺ memory T cells persist in the dermis after ACD clinically resolves.

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 ACD, and 2.3% presented for irritant contact dermatitis.

International

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

Mortality/Morbidity

Death from ACD is rare in the US. ACD 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 ACD.

Race

No racial predilection exists for ACD.

Sex

ACD 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

ACD may occur in neonates. In elderly individuals, the development of ACD may be delayed somewhat, but the dermatitis may be more persistent once developed.

CLINICAL

Section 3 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

A detailed history, both before and after patch testing, is crucial in evaluating individuals with ACD. Potential causes of ACD and the materials to which individuals are exposed should be patch tested. Patients with ACD 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 ACD to materials and agents applied to the areas of stasis dermatitis and leg ulcers. Neomycin is an important cause of ACD 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 ACD, 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 ACD, 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 ACD to poison ivy.
  • Some European studies indicate that patients with atopic dermatitis may have increased incidence of ACD to nickel.
• Onset of symptoms
• • Individuals with ACD 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, ACD 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 ACD), 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 ACD 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 ACD 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. ACD 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 ACD, 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 ACD. The workplace nurse may dispense ineffective and sensitizing topical preparations, such as Merthiolate, which may change a simple abrasion into a severe case of ACD. Individuals may develop allergy to preservatives in medications and/or to the active ingredients in topical medications, especially neomycin and topical corticosteroids. 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 ACD may produce severe morbidity. Individuals with ACD 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 ACD is characterized by pruritic papules and vesicles on an erythematous base. Lichenified pruritic plaques may manifest chronic ACD. Occasionally, ACD may affect the entire integument (ie, erythroderma, exfoliative dermatitis). The initial site of dermatitis often provides the best clue regarding the potential cause of ACD.

• Hands: Hands are an important site of ACD, particularly in the workplace. Common causes of allergic dermatitis on the hands include the chemicals in rubber gloves.
• Perianal: ACD 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 ACD in cases of otitis externa.
• Airborne ACD: Chemicals in the air may produce airborne ACD. 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 ACD 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 ACD 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.¹
• 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 ACD resulting from exposure to poison ivy,² tropical woods, nickel, and hair dye (see Media File 2).

Causes

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

• Poison ivy is the classic example of acute ACD in North America. ACD 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 ACD in the world. ACD 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.
• 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. ACD 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).
• 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 ACD 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 ACD, since most allergens decrease in concentration in clothing following repeated washings.
• Preservative chemicals added to cosmetics, moisturizers, and topical medications are major causes of ACD (see Media File 4). The most widely used preservatives include parabens, which are not a frequent cause of ACD despite their wide use. The risk of ACD appears to be highest to quaternium-15, followed by ACD to isothiazolinones (Kathon CG).
• Formaldehyde is a major cause of ACD (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]).
• 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 ACD to fragrances found in topical medications. Deodorants may be the most common cause of ACD 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 ACD 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).¹ 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.
• Occasionally, individuals develop photo ACD. ACD 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).

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
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• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Mycosis fungoides

WORKUP

Section 5 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

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

Procedures

• Patch testing
• • 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 ACD. Patch testing is most cost effective and reduces the cost of therapy in patients with severe ACD.
  • 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 ACD 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 ACD. 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 per day 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 ACD
    • • 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 ACD
      • 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 ACD and photo-accentuated ACD from photo ACD. 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.

Histologic Findings

Histology of ACD 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. ACD is provokes atypical T-cell infiltrates, simulating mycosis fungoides.

TREATMENT

Section 6 of 11  

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• Differentials
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

The cause of 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, because of the apparently high risk of iatrogenic ACD 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 ACD 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 ACD of intertriginous areas.
  • Acute severe ACD, such as acute severe ACD 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 ACD when they offer safety advantages over topical corticosteroids. TIMs do not cause cutaneous atrophy or glaucoma or cataracts when applied near the eye. Pimecrolimus (Elidel cream) is a topical treatment often helpful for ACD of the face. Tacrolimus (Protopic 0.1% ointment) appears to be the most helpful TIM for ACD of the hands.
• Psoralen plus UV-A: Individuals with chronic ACD 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)³ or cyclosporine (Neoral), are used in recalcitrant cases of severe chronic widespread ACD 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 ACD may be incapacitated temporarily and unable to work. Most individuals with ACD 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 ACD or development of irritant contact dermatitis of ceramide cream (eg, Impruv).

MEDICATION

Section 7 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

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 ACD (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, ACD 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 ACD.

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

Drug Category: Topical immunomodulators

These agents modify immune processes that promote inflammation.

Drug Name	Tacrolimus (Protopic 1%)
Description	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%.
Adult Dose	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 Dose	<2 years: Not established 2-15 years: Apply 0.03% ointment bid to affected area(s) >15 years: Administer as adults
Contraindications	Documented hypersensitivity
Interactions	None reported
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	Patients may experience burning sensation during first few days of application; skin can become photosensitive and patients should be cautioned about exposure to direct or artificial sunlight and to use sunscreen; safety and efficacy in infected atopic dermatitis not known; application under occlusion, which may promote systemic exposure, has not been evaluated (do not use with occlusive dressings); absorption following topical applications is minimal (relative to systemic administration), but tacrolimus is excreted in human milk and, thus, a decision should be made whether to discontinue nursing or to discontinue drug, taking into account importance of drug to mother (potential for serious adverse reactions in nursing infants from tacrolimus should also be a concern)

Drug Category: 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.

Drug Name	Hydrocortisone (Valerate, Westcort)
Description	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.
Adult Dose	Apply sparingly to affected areas bid
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity; viral, fungal, and bacterial skin infections
Interactions	None reported
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

Drug Name	Prednisone (Deltasone, Meticorten, Orasone)
Description	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.
Adult Dose	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 Dose	4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2-3 wk, as symptoms resolve
Contraindications	Documented hypersensitivity; viral infection, peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections
Interactions	Coadministration with estrogens may decrease prednisone clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; abrupt discontinuation may cause adrenal crisis

Drug Name	Triamcinolone (Aristocort, Amcort, Aristospan Intra-articular)
Description	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.
Adult Dose	40-60 mg IM, may repeat in 4-6 wk 3-10 mg/mL intralesional
Pediatric Dose	<6 years: Not established 6-12 years: 0.03-0.2 mg/kg IM >12 years: Administer as in adults
Contraindications	Documented hypersensitivity; fungal, viral, and bacterial skin infections
Interactions	Coadministration with barbiturates, phenytoin, and rifampin decreases effects of triamcinolone
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, osteonecrosis, 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

Drug Category: 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 ACD beyond possibly decreasing pruritus via sedating effects.

Drug Category: 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 ACD.

Drug Category: 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.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Inpatient care rarely is required for ACD unless the dermatitis is so severe that patients cannot care for themselves. Examples may include severe ACD with marked eyelid swelling that impairs vision or severe ACD 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 ACD, 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 ACD, 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.⁴ Needless cases of ACD 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, ACD 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 ACD. Occasionally, they may develop depigmentation at sites of ACD to certain chemicals.

Prognosis

• Individuals with ACD 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 ACD, 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 ACD.
• 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 ACD 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

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• ACD 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.⁵
• ACD may be a direct trigger for skin ulceration in patients with venous insufficiency. Early diagnosis of ACD may prevent the development of venous ulcers.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.
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Media file 2:  Erythema multiformelike reaction that developed acutely following hair dying.
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Media file 3:  Allergic contact dermatitis to nickel in a necklace.
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Media type:  Photo

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

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

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Guin JD, Phillips D. Erythroderma from systemic contact dermatitis: a complication of systemic gentamicin in a patient with contact allergy to neomycin. Cutis. Jun 1989;43(6):564-7. [Medline].
2. Cohen LM, Cohen JL. Erythema multiforme associated with contact dermatitis to poison ivy: three cases and a review of the literature. Cutis. Sep 1998;62(3):139-42. [Medline].
3. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. Jan-Feb 2006;72(1):24-7. [Medline].
4. Shaffer MP, Belsito DV. Allergic contact dermatitis from glutaraldehyde in health-care workers. Contact Dermatitis. Sep 2000;43(3):150-6. [Medline].
5. Hougeir FG, Yiannias JA, Hinni ML, Hentz JG, el-Azhary RA. Oral metal contact allergy: a pilot study on the cause of oral squamous cell carcinoma. Int J Dermatol. Mar 2006;45(3):265-71. [Medline].
6. Assier-Bonnet H, Revuz J. [Topical neomycin: risks and benefits. Plea for withdrawal]. Ann Dermatol Venereol. 1997;124(10):721-5. [Medline].
7. Cohen DE, Brancaccio R, Andersen D, Belsito DV. Utility of a standard allergen series alone in the evaluation of allergic contact dermatitis: a retrospective study of 732 patients. J Am Acad Dermatol. Jun 1997;36(6 Pt 1):914-8. [Medline].
8. Diepgen TL, Coenraads PJ. The epidemiology of occupational contact dermatitis. Int Arch Occup Environ Health. Nov 1999;72(8):496-506. [Medline].
9. Gönül M, Gül U. Detection of contact hypersensitivity to corticosteroids in allergic contact dermatitis patients who do not respond to topical corticosteroids. Contact Dermatitis. Aug 2005;53(2):67-70. [Medline].
10. Hogan DJ. The prognosis of occupational contact dermatitis. Occup Med. Jan-Mar 1994;9(1):53-8. [Medline].
11. Jacobs JJ, Lehé CL, Hasegawa H, Elliott GR, Das PK. Skin irritants and contact sensitizers induce Langerhans cell migration and maturation at irritant concentration. Exp Dermatol. Jun 2006;15(6):432-40. [Medline].
12. Katagiri K, Arakawa S, Hatano Y, Fujiwara S. Fexofenadine, an H1-receptor antagonist, partially but rapidly inhibits the itch of contact dermatitis induced by diphenylcyclopropenone in patients with alopecia areata. J Dermatol. Feb 2006;33(2):75-9. [Medline].
13. Kist JM, el-Azhary RA, Hentz JG, Yiannias JA. The contact allergen replacement database and treatment of allergic contact dermatitis. Arch Dermatol. Dec 2004;140(12):1448-50. [Medline].
14. Kligman AM. The identification of contact allergens by human assay. 3. The maximization test: a procedure for screening and rating contact sensitizers. J Invest Dermatol. Nov 1966;47(5):393-409. [Medline].
15. Larkin A, Rietschel RL. The utility of patch tests using larger screening series of allergens. Am J Contact Dermat. Sep 1998;9(3):142-5. [Medline].
16. Lawley TJ, Kubota Y. Cell adhesion molecules and cutaneous inflammation. Semin Dermatol. Sep 1991;10(3):256-9. [Medline].
17. Marks JG, Belsito DV, DeLeo VA, Fowler JF Jr, Fransway AF, Maibach HI, et al. North American Contact Dermatitis Group patch test results for the detection of delayed-type hypersensitivity to topical allergens. J Am Acad Dermatol. Jun 1998;38(6 Pt 1):911-8. [Medline].
18. Rajagopalan R, Anderson RT, Sarma S, Kallal J, Retchin C, Jones J, et al. An economic evaluation of patch testing in the diagnosis and management of allergic contact dermatitis. Am J Contact Dermat. Sep 1998;9(3):149-54. [Medline].
19. Rietschel RL, Fowler JR Jr. Fisher's Contact Dermatitis. 5^th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2001.
20. Shah M, Lewis FM, Gawkrodger DJ. Nickel as an occupational allergen. A survey of 368 nickel-sensitive subjects. Arch Dermatol. Oct 1998;134(10):1231-6. [Medline].
21. Shai A, Halevy S. Direct triggers for ulceration in patients with venous insufficiency. Int J Dermatol. Dec 2005;44(12):1006-9. [Medline].
22. Tadd C, Feldman S, Thompson S. Only 33% of Visits for Skin Disease in the US in 1995 Were to Dermatologists: Is Decreasing the Number of Dermatologists the Appropriate Response?. Dermatology Online [serial online]. 1998;4:Available at http://dermatology.cdlib.org/DOJvol4num1/original/thompson.html.
23. Templet JT, Hall S, Belsito DV. Etiology of hand dermatitis among patients referred for patch testing. Dermatitis. Mar 2004;15(1):25-32. [Medline].
24. Thompson T, Belsito DV. Allergic contact dermatitis from a diisocyanate in wool processing. Contact Dermatitis. Nov 1997;37(5):239. [Medline].

Article Last Updated: Mar 7, 2007