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Allergic Contact Dermatitis

Key Points

  • Contact dermatitis can have either an irritant or an allergic origin. Distinguishing between these entities can be informed by a careful history, including timing of onset of symptoms.
  • Allergic contact dermatitis is caused by a delayed-type hypersensitivity (DTH), or Type IV hypersensitivity, reaction to an allergen.
  • Treatment necessitates avoidance of the allergen, and often requires topical corticosteroids to reduce inflammation.
  • Identifying allergens underlying a contact dermatitis can be difficult. A careful history, including occupational and intermittent exposures (i.e., hobbies, cosmetic practices), is critical. Allergen testing, such as a “use” test or standardized patch testing, can be very helpful to identify potential contactants, but clinical correlation is necessary in the interpretation.

Introduction

Contact dermatitis is a common cutaneous condition, with an estimated incidence of 43 cases per 100,000 persons. It can have either an irritant or an allergic origin. Irritant reactions can present with similar features to contact dermatitis, but tend to appear less than 12 hours after exposure, and are strictly limited to exposed sites. Allergic reactions are delayed (12-72 hours, except for primary sensitization, where an induction phase of 7-10 days is typical), and exhibit a tendency to spread as the immunologic reaction reaches sites where less antigen was deposited initially.

Whereas irritant dermatitis may stem from non-specific inflammation mediated by the innate immune system, allergic contact dermatitis results from hapten-specific T cell mediated delayed-type hypersensitivity (DTH), or Type IV hypersensitivity, reaction to an allergen. Potential allergens arise from almost anything in the environment, ranging from plant-derived chemicals, preservatives, fragrances, or chemicals used in the processing of products and fabrics.

The top 10 contact allergens (North American Contact Dermatitis Group):

  • Metals:
    • nickel (nickel sulfate)
    • gold (sodium gold thiosulfate)
    • cobalt (cobalt chloride)
  • Preservatives:
    • formaldehyde
    • quaternium-15
    • thimerosal
  • Topical antibiotics:
    • neomycin sulfate
    • bacitracin
  • Fragrance elements
    • fragrance mix
    • balsam of peru (myroxylon perirae)

Identifying relevant contact allergens can be challenging. A careful history, including occupational and intermittent exposures due to hobbies or cosmetic practices, is critical. Allergen testing may occur by a “use” test or standardized patch testing. A “use” test involves putting a small amount of suspected allergen (such as a cosmetic product) occluded under a bandage for 48-72 hours and assessing the development of inflammation. Standardized patch testing typically involves the application of commercially available patches (such as TRUE test) impregnated with allergen onto the skin with clinical evaluation at 48, 72, and 96 hours for evidence of inflammation. Patch testing should be done on non-inflamed skin, such as on the back, and performed in the absence of systemic antihistamines or corticosteroids, when possible. Skin erythema, vesiculation, or eczematous changes indicates a positive result, and all positive results should be carefully considered for their clinical relevance.

Initial Evaluation

The presentation of allergic contact dermatitis may range from mild edema, erythema, or eczematous papules and plaques, to bright erythema with vesicles, bullae, and crusting; less erythema, and lichenification or fissuring may be noted in chronic cases. Patients almost always report associated pruritus. The area of inflammation may extend slightly beyond the area of contact with the allergen, but linear or geometric patterns of inflammation in the shapes of potential contactants are highly suggestive of an allergic contact dermatitis.

Morphology: Allergic contact dermatitis may range from mild reactions (erythema) to vesiculation or eczematous changes.

Exposure to airborne contactants may present in a diffuse eruption on the face, neck, V-neck chest.

Allergic contact dermatitis to rubber in swimming goggles.

Allergic contact dermatitis to metals (in earrings, belt buckle, bracelet, ring, eyeglasses).

Allergic contact dermatitis to urushiol (poison ivy, oak, sumac) is often suggested by linear streaks of skin inflammation, marking areas where the patient brushed up against leaves of the plant.

Allergic contact dermatitis to topical antibiotic applied to an ulcer.

Allergic contact dermatitis to an herbal medication applied with an adhesive patch (either the herbal medication or adhesive are potential allergens in this case).

Allergic contact dermatitis to cosmetics: Hair-dye, nail lacquer (typically presents on the eyelids due to transfer of allergen from touching the eyes).

Differential diagnosis

Atopic dermatitis: Pruritic, eczematous, or lichenified plaques.

Scabies: Intensely pruritic, eczematous or lichenified plaques.

Dermatophyte (tinea pedis): Erythema, hyperkeratosis, and vesiculation may mimic shoe dermatitis. Dermatophyte infection typically involves the interdigital web spaces, which are usually spared in shoe contact dermatitis.

Drug eruption: Generalized pruritic, erythematous macules and papules may be difficult to distinguish between a systemic contact dermatitis.

Treatment

First-line treatment: Limiting exposure to potential contactants is an essential first step. Topical measures to reduce inflammation are first-line treatment for limited disease, and systemic anti-inflammatory medications may be necessary in cases of widespread skin involvement.

Limited areas of involvement

  • Treat with cool compresses, using aluminum acetate (such as Domeboro tablets or packets, one tablet or packet dissolved in 1 cup of tap water). A clean washcloth or towel should be used and applied wet (but not soaking wet) to the rash for 15-20 minutes b.i.d.
  • Prescribe a potent topical steroid preparation such as fluocinonide (such as Lidex) in a drying vehicle (e.g., gel) to be applied b.i.d. to the rash.
  • For acute contact dermatitis on the face or intertriginous areas, a non-fluorinated, low to medium-potency topical steroid (e.g., desonide, such as Desonate, Desowen, LoKara, Verdeso) or hydrocortisone 2.5% cream (such as Hytone) is preferable. Alternative treatments for the face are pimecrolimus 1% cream (such as Elidel) or tacrolimus 0.03 or 0.1% ointment (such as Protopic). Note that use of topical calcineurin inhibitors such as pimecrolimus or tacrolimus is an off-label use of these medications with limited evidence.
  • For additional relief of pruritus, an astringent lotion, with or without additional ingredients such as menthol, camphor, and phenol in low concentration ( l%) (e.g., Sarna), can be applied as frequently as needed.
  • For pruritus, antihistamines should be prescribed, e.g., diphenhydramine (such as Benadryl) 25-50 mg at bedtime or hydroxyzine (such as Atarax or Vistaril) 10-50 mg.
  • During the day, a non-sedating antihistamine can be administered for pruritus: loratadine (such as Claritin) 10 mg, fexofenadine (such as Allegra) 180 mg, or cetirizine (such as Zyrtec) 10 mg.

Widespread involvement

  • Systemic steroids: Topical steroids are only minimally effective for acute contact dermatitis. Therefore, as disease becomes more generalized and/or involves face, genitalia, or other areas that compromise normal activity, a course of systemic steroids may be indicated. For re-exposure (as in recurrent episodes of poison ivy or poison oak), a 10-14-day tapering course of prednisone, beginning with 1 mg/kg/day, is indicated.
  • For patients with primary sensitization, where the course may extend up to 4-6 weeks, a more extended course of systemic prednisone may be necessary.
  • Cool baths with oilated colloidal oatmeal (such as Aveeno) can provide substantial, temporary relief for patients with extensive disease.
  • Secondary bacterial infection, although uncommon, may occur, and can be hard to clinically detect in the setting of extensive contact dermatitis. If there is high suspicion for infection, administer oral systemic antibiotics, such as cephalexin 500 mg t.i.d., erythromycin or dicloxacillin 1 g/day to patients. An alternative treatment for patients without clear evidence of systemic illness is to recommend bleach baths (1/4 cup of bleach in a full tub of lukewarm water, soaking 10-15 minutes) every other day.

Subsequent therapy

Search for the suspected irritant/allergen: In many cases of contact dermatitis, the cause is apparent, but some cases may require patch testing to pinpoint the culprit (e.g., in shoes, clothing, and deodorants many potential contactants are present together). Patch tests are best performed by physicians experienced in these procedures.

Pitfalls

  • Keep a high suspicion for inadvertent ongoing exposure. For example, rhus dermatitis (contact dermatitis to urushiol in poison ivy or poison oak) may occur through ongoing exposure with contaminated clothing, shoes, or sports equipment.
  • Irritant reactions are often confused with allergic dermatitis by both patients and physicians. Yet the distinction is important because irritant reactions are concentration dependent. Therefore, certain agents that are irritants in one bodily site may be safe to use in another site (e.g., aluminum chloride may be an irritant in occluded, intertriginous areas but nonreactive when used as an astringent on the palms, soles, or back).
  • Airborne contact dermatitis can be difficult to distinguish from photoallergy or phototoxicity. An important clue is extension of the rash to the neck, submental, and/or infranasal areas (e.g., photoprotected areas).

When to refer to a dermatologist

  • When the diagnosis is not clear. The common differential diagnosis includes atopic dermatitis, asteatotic dermatitis, mite infestation, dermatophyte infection, drug eruption.
  • When the allergen or irritant cannot be identified. Patch testing is best performed in the hands of a dermatologist experienced with this procedure.
  • For counseling on allergen avoidance, especially when there is a documented occupational exposure that may impact the safety of a worker in the workplace.

Clinical Cases

Case 1

  • 8-year-old healthy boy, develops pruritic peri-orbital rash
  • No new medications, soaps, lotions
  • Started swimming classes two weeks ago, uses new swim goggles with rubber padding. On further history, the child’s parents endorse a history of rashes of unknown cause, in which exposure to rubber products was suspected.
  • On exam, he has bilateral peri-orbital edema, erythema and mild eczematous changes
  • A diagnosis of allergic contact dermatitis is given

Treatment

  • Hydrocortisone 2.5% cream applied b.i.d. for several days, replace swim goggles with a pair with non-rubber padding
  • Educational materials on allergic contact dermatitis, rubber allergy is given
  • Follow-up in one week

One-week follow-up visit

  • Rash is resolved
  • Hydrocortisone is discontinued
  • Given history of possible recurrent allergic contact dermatitis, recommend limited patch testing to different types of rubber and chemicals utilized in rubber processing; this testing is done several weeks later, and a positive reaction to mercaptobenzothiazole (a chemical accelerant used in the processing of rubber) is confirmed

Case 2

  • 18-year-old healthy student with a intensely-pruritic rash present for 7 days on arms, legs
  • Went camping last week in a forested area known to have poison oak; no other known exposures; another member of the camping group has similar rash on legs
  • Exam: Bright erythema with overlying vesicles, several linear streaks of erythema and fine vesiculation noted on the arms; no mucosal or genital involvement
  • Diagnosis: Rhus dermatitis (allergic contact dermatitis to poison oak)
  • Treatment: triamcinolone 0.1% cream b.i.d., aluminum acetate compresses daily, hydroxyzine 25mg taken in the evening for pruritus
  • Follow-up in 2 weeks (resolved)

Case 3

  • 42-year-old woman who develops pruritic rash on lateral cheeks, neck, and shoulders ten days after dying her hair
  • No other new cosmetics, shampoos, conditioners, lotions, or medications
  • Exam: brightly erythematous, eczematous plaques on the lateral cheeks, lateral aspects of the neck, upper shoulders, V-neck chest
  • Diagnosis: allergic contact dermatitis to hair dye chemical
  • Treatment: desonide 0.05% cream applied b.i.d., aluminum acetate compresses b.id., hydroxyzine 25 mg at bedtime for nighttime pruritus
  • Follow-up in 3 weeks

Three-week follow-up evaluation

  • Clinically improved, but still with faintly erythematous, eczematous patches in the same distribution
  • Patient reports ongoing pruritus
  • Treatment: recommend ongoing topical treatment, with limited patch testing ordered to common hair cosmetic chemicals

Patch testing results

  • A limited patch testing series of common hair cosmetic chemicals is performed, revealing a reaction to paraphenylenediamine (PPDA)
  • Educational materials and counseling on products containing PPDA is given

References

Davis M (2009) Unusual patterns of contact dermatitis: medicaments, Dermatol Clinics 27:289-297.

Lee P, Elsaie M, Jacobs S (2009) Allergic contact dermatitis in children: common allergens and treatment: A review. Curr Opin Peds 21:491-498.

Milingou M, et al (2010) Patch testing in children. Ped Derm 27: 255-259.

Nicholson P, et al (2010) Evidence-based guidelines for the prevention, identification, and management of occupational contact dermatitis and urticaria. Contact Derm 63:177-186.

Nosbaum A, et al (2009) Allergic and irritant contact dermatitis. Eur J Dermatol 19:325-32.

Usatine RP and Riojas M (2010) Diagnosis and management of contact dermatitis. Am Fam Phys 82: 249-255.