eMedicine Specialties > Dermatology > Allergy & Immunology

Contact Dermatitis, Allergic

Author: Daniel J Hogan, MD, Director of Bay Pines Dermatology Residency Program, Bay Pines Veterans Affairs Healthcare System
Coauthor(s): Joshua May, BS, Department of Dermatology, Louisiana State University Health Sciences Center School of Medicine
Contributor Information and Disclosures

Updated: Mar 7, 2007

Introduction

Background

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

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).

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