image of silk fabric and dry skin

A. L. Bruckner, MD and W. L. Weston, MD

Department of Dermatology, University of Colorado Health Sciences Center, Aurora, Colorado, USA


Allergic contact dermatitis (ACD) may account for at least 20% of all childhood dermatitis. Clinically, its morphology is identical to other forms of dermatitis in acute, subacute and chronic forms. A persistent or unusual and localized pattern is often the key to diagnosis. Treatment has centered around the use of corticosteroids, with the adjunct of antihistamines, wet dressings, and emollients for alleviation of symptoms. The newer topical immunosuppressives, tacrolimus and pimecrolimus, may also hold promise as alternative therapies, although they have not been well-studied in this regard. Allergen identification, sometimes through patch testing, and allergen avoidance are the keys to preventing recurrences of this disease.

Key Words:
allergic contact dermatitis, allergen, childhood dermatitis

Allergic contact dermatitis (ACD) is an acquired, inflammatory reaction of the skin that requires absorption of an antigen from the skin surface and recruitment of previously sensitized, antigen-specific T lymphocytes into the skin. An intact immune system is required for the development of ACD, which occurs in two phases. The sensitization phase begins with initial exposure to the antigen. Contact antigens are usually low molecular weight substances that penetrate the outer layer of the skin and are taken up by Langerhans cells (LC). After processing the antigen and migrating to regional lymph nodes, LCs present the antigen to T lymphocytes. These antigen-specific T lymphocytes undergo clonal expansion, creating a pool of cells with immune memory that can generate an immune response upon re-exposure to the allergen. In this elicitation phase, the sensitized T lymphocytes proliferate and release inflammatory mediators, producing a localized dermatitis. The resulting dermatitis develops in 12-24 hours after allergen exposure, peaks in 3-5 days and may last 3-4 weeks, if untreated.1-3 The potency of the allergen determines the number of exposures necessary for this process to occur. A strong antigen such as poison ivy requires only one exposure, while weaker antigens require numerous exposures over weeks to years. Once sensitization occurs, however, it is thought to be long lived.1-3

The exact incidence and prevalence of ACD in children is not known.4 According to Weston,5 ACD may account for up to 20% of all cases of childhood dermatitis, but when considering that in endemic areas nearly all individuals are sensitized to poison ivy, this estimate may be higher. It was previously believed that ACD was rare in children, possibly due to a less mature immune system. Case reports, however, have described ACD in children as young as 1 week old,6,7 and recent studies of asymptomatic children have shown that 13-25% are sensitized to common contact allergens, with sensitization commonly beginning as early as 6 months of age.8-10

Contact allergens are found in both the natural and man-made environment, of which the most common is urushiol, a pentadecylcatechol found in plants of the Toxicodendron species, such as poison ivy, poison oak, and poison sumac. Other common childhood contact allergens include nickel, neomycin, chromates, thimerosal, Balsam of Peru, formaldehyde and related preservatives, colophony, p-Tertbutylphenol formaldehyde resin, lanolin, and several others.8-10

Clinical features

ACD presents as pruritic dermatitis, localized to the site of allergen contact. Acute ACD to potent allergens is characterized by erythema and edema with vesicles or bullae that often rupture, leaving a crust. More commonly, a subacute or chronic dermatitis, characterized by lichenification, erythema and scaling, is produced by less potent antigens. A more generalized dermatitis, termed autoeczematization, may develop distal to the original site of contact ≥1 week after the appearance of the initial, localized dermatitis.

Because the clinical morphology of ACD is identical to other forms of dermatitis, such as irritant or atopic dermatitis (AD), a history of allergen exposure and the pattern of the eruption are important keys in making the correct diagnosis. Patterns of dermatitis that are suggestive of ACD include persistent, localized dermatitis, dermatitis that has not responded as expected to therapy, and dermatitis in an unusual pattern or distribution. Its location is often a clue to the offending allergen.11

First lineSecond lineAdjunctPrevention
Acute ACDPrednisone (>10% BSA) Medium/medium-high potentcy topical CS (<10% BSA):

  • Fluocinolone 0.025%
  • Triamcinolone 0.1%
  • Mometasone 0.1%

  • Hydroxyzine
  • Diphenhydramine Wet dressings
Allergen avoidance
Subacute/Chronic ACDMedium potency topical CS (see above)Tacrolimus 0.03%, 0.1% Pimecrolimus 1%Antihistamines (see above) EmollientsAllergen avoidance

Table 1: Therapy of Childhood ACD


The treatment of ACD has not changed dramatically over the years and still involves two main principles: 1) the dermatitis must be treated; and 2) the allergen must be identified and avoided in order to prevent recurrence of the disease.

Acute ACD is best controlled with corticosteroids (CSs) (see Table 1). Through various mechanisms, CSs decrease the production of cytokines and halt lymphocyte proliferation, limiting the inflammatory response to contact allergens.12 If the dermatitis involves more than 10% of the skin surface, systemic steroids are indicated. A single morning dose of prednisone (1-2mg/kg) for 7-10 days, followed by a taper over the text 7-10 days is usually sufficient. Localized eruptions may be treated with steroid ointments of moderate potency applied twice daily for 2-3 weeks. For both topical and systemic therapy, continuing the treatment for 2-3 weeks is necessary, as stopping it too quickly may cause rebound dermatitis.

In addition to CSs, other treatments aimed at alleviating associated symptoms such as burning or pruritus may be beneficial. Sedating antihistamines such as diphenhydramine or hydroxyzine decrease itching and allow the patient to sleep through the night. As an alternative to standard dosing, we have found a single dose of hydroxyzine 1-2mg/kg given 30 minutes – 1 hour before bedtime to be effective in this regard. Wet dressings are also soothing and additionally help to debride crusts. Slightly dampened cotton garments are worn over the affected area and covered with a dry garment. The patient may use these dressings overnight or change them every 8 hours during the day.13

Subacute and chronic ACD is often the result of repeated exposures to modest or weak contact allergens, making treatment challenging. Systemic CSs are effective at suppressing chronic dermatitis, but their use should be avoided in this condition as their potential side-effects outweigh the benefits of the long course of therapy likely to be required.12 Depending on the part of the body affected, low or medium potency topical steroids applied twice daily are a more reasonable alternative. Appropriate long-term use of these medications does not cause hypothalamicpituitary- adrenal suppression in infants and children,14 although localized side-effects such as atrophy are possible.

Recently, two macrolide immunosuppressants have emerged as potential alternatives to CSs in the treatment of ACD. Tacrolimus is used systemically to prevent organ rejection after transplantation. It inhibits calcineurin, thereby halting the transcription of IL-2, decreasing the responsiveness of T lymphocytes to antigenic stimuli.15 As a topical ointment in 2 concentrations (Protopic® 0.03% and 0.1%, Fujisawa), it is approved for the treatment of AD, but only the 0.03% version is recommended for use in children aged 2 to 15 years. Topical tacrolimus can inhibit the inflammatory reaction in both pig and human models of ACD,16,17 but its efficacy as a treatment for ACD has not been well studied.

Pimecrolimus (SDZ ASM 981), an ascomycin analog, down-regulates the production of various cytokines that are released due to antigen-specific stimulation of immunememory T cells.18 A 1% cream (Elidel®, Norvartis) is approved in the US for the treatment of mild-to-moderate AD in children 2 years and older. In a recent report, 0.1% SDZ ASM 981 cream was as effective as topical clobetasol-17-proprionate in inhibiting the development of ACD in a pig model.19 Additionally, 0.6% SDZ ASM 981 cream was as effective as 0.1% betamethasone-17-valerate in the treatment of experimentally-produced nickel ACD in 66 volunteers.20

The T cell-specific mechanisms of action of tacrolimus and pimecrolimus are highly applicable to ACD. It is important to point out, however, that inhibiting the development of ACD in controlled situations does not necessarily correlate with effective treatment of clinically apparent disease. Further studies are needed to clarify the clinical efficacy of these medications for the treatment of ACD. We currently recommend that they be considered as alternatives to CS.

Identifying the offending allergen is important, as allergen avoidance is the key to prevention of recurrent disease. This may be done by history alone, but patch testing may be necessary to identify specific antigens.21 Once the allergen is known, the patient should be given educational information regarding potential sources. Avoidance may involve placing a barrier between the allergen and the skin. Examples include wearing long pants when out in the woods to prevent rhus dermatitis, and using nail enamel or a cloth patch to cover the exposed portions of metal fasteners in a person allergic to nickel.


ACD is an acquired, immune-mediated dermatitis that is common in children. Clinicians should be familiar with recognizing common patterns consistent with ACD. While CSs have been the mainstay of therapy, other topical immunosuppressives hold promise as alternative treatments. Allergen identification and avoidance is crucial in preventing future recurrences of the disease.


  1. Weston WL, Bruckner A. Allergic contact dermatitis. Ped Clin North Am 47(4):897-907 (2000).
  2. Weston WL. Contact dermatitis in children. Curr Opin Pediatr 9:372-6 (1997).
  3. Hogan PA, Weston, WL. Allergic contact dermatitis in children. Pediatr Rev 14(6):240-3 (1993).
  4. Mortz CG, Andersen KE. Allergic contact dermatitis in children and adolescents. Contact Dermatitis 41:121-30 (1999).
  5. Weston WL, Weston JA. Allergic contact dermatitis in children. Am J Dis Child 138:932-6 (1984 Oct).
  6. Fischer AA. Allergic contact dermatitis in early infancy. Cutis 54:300-2 (1994 Nov).
  7. Seidenari S, Manzini BM, Motolese A. Contact sensitization in infants: report of 3 cases. Contact Dermatitis 27:319-20 (1997).
  8. Weston WL, Weston JA, Kinoshita J, et al. Prevalence of positive epicutaneous test among infants, children and adolescents. Pediatrics 78(6):1070-4 (1986 Dec).
  9. Barros MA, Baptista A, Correia M, Azevedo F. Patch testing in children: a study of 562 schoolchildren. Contact Dermatitis 25:156-9 (1991).
  10. Bruckner AL, Weston WL, Morelli JG. Does sensitization to contact allergens begin in infancy? Pediatrics 105(1):e3 (2000 Jan).
  11. Belsito DV. The diagnostic evaluation, treatment, and prevention of allergic contact dermatitis in the new millennium. J Allergy Clin Immunol 105(3):409-20 (2000 Mar).
  12. Wolverton SE. Systemic corticosteroids. In: Wolverton SE, editor. Comprehensive dermatologic drug therapy. Philadelphia: W.B. Saunders Company p109-46 (2001).
  13. Weston WL, Lane AT, Morelli JG. Color textbook of pediatric dermatology. 3rd ed. St. Louis (MO): Mosby, Inc. (2002).
  14. Ellison JA, Patel L, Ray DW, David TJ, Clayton PE. Hypothalamicpituitary- adrenal function and glucocorticoid sensitivity in atopic dermatitis. Pediatrics 105(4 pt 1):794-9 (2000 Apr).
  15. Nasr IS. Topical tacrolimus in dermatology. Clin Exp Dermatol 25:250-4 (2000).
  16. Meingassner JG, Stutz A. Immunosuppressive macrolides of the type FK506: a novel class of topical agents for treatment of skin diseases? J Invest Dermatol 98:851-5 (1992).
  17. Lauerma AI, Maibach HI, Granlund H, Erkko P, Kartamaa M, Stubb S. Inhibition of contact allergy reactions by topical FK506. Lancet 340: 556 (1992 Aug).
  18. Grassberger M, Baumruker T, Enz A, et al. A novel anti-inflammatory drug, SDZ ASM 981, for the treatment of skin diseases: in vitro pharmacology. Br J Dermatol 141:264-73 (1999).
  19. Meingassner JG, Grassberger M, Fahrngruber H, Moore HD, Schuurman H, Stutz A. A novel anti-inflammatory drug, SDZ ASM 981, for the topical and oral treatment of skin diseases: in vivo pharmacology. Br J Dermatol 137: 568-76 (1997).
  20. Queille-Roussel C, Graiber M, Thurston M, et al. SDZ ASM 981 is the first non-steroid that suppresses established nickel contact dermatitis elicited by allergen challenge. Contact Dermatitis 42:349-50 (2000).
  21. Sherertz EF. Patch testing in children. Pediatr Dermatol 15:68-9 (1998).