Pediatric Annals

ISSUES IN TOPICAL THERAPY FOR CHILDREN 

Beyond Poison Ivy: Understanding Allergic Contact Dermatitis in Children

Anna L Bruckner, MD; William L Weston, MD

Abstract

The rash caused by poison ivy is a classic example of allergic contact dermatitis. Although many of us identify this vesicular eruption based on history or physical examination, we should be aware that a similar dermatitis may be caused by many substances that come in contact with children's skin. Considering that skin care products, cosmetics, toys, and clothing are specifically marketed to a younger audience, children are frequently exposed to many antigens that can cause allergic contact dermatitis. This article familiarizes the pediatrician with the pathogenesis, diagnosis, and treatment of allergic contact dermatitis.

PATHOGENESIS

Allergic contact dermatitis is an acquired, inflammatory reaction of the skin. It follows percutaneous absorption of an antigen (allergen) from the surface of the skin, with subsequent recruitment of previously sensitized, antigen-specific Tlymphocytes to the same area.1"4 Allergic contact dermatitis is a type IV delayed hypersensitivity reaction, so it requires an intact immune system. This reaction occurs in two phases, sensitization and elicitation.

Sensitization

Sensitization begins with the initial exposure to the allergen. Allergens that can sensitize by contact are usually substances with low molecular weights that readily penetrate the outer layer of the skin and are taken up by Langerhans' cells. Langerhans' cells process the antigen and then migrate to regional lymph nodes where they present the antigen to T-lymphocytes. After recognition of the antigen, specific T-lymphocytes undergo clonal expansion and circulate throughout the body. However, these T-lymphocytes now have the immune memory to recognize this antigen as foreign and will generate an immune response when rechallenged.

The strength 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, whereas weaker antigens require many exposures during weeks to years. Once sensitization occurs, however, it is long lived.13

Elicitation

On reexposure to the allergen, the sensitized Tlymphocytes proliferate and release inflammatory mediators, producing a localized dermatitis. This develops 12 to 24 hours after the reexposure. The resulting dermatitis may last up to 3 to 4 weeks if untreated.1"3

Table

INDICATIONS FOR PATCH TESTING

Occasionally, the etiology is not apparent. In this situation, epicutaneous patch testing may be indicated to help determine whether allergic contact dermatitis could be the culprit and what the allergen might be. Although we believe that this examination is simple, it should be performed by an experienced dermatologist. Patch testing involves the placement of antigens directly on the surface of the skin for 48 hours. The allergens are then removed and the skin is inspected for localized dermatitis, indicating sensitization to the antigen in the patch. In a recent commentary, Sherertz recommended the following guidelines for patch testing in children27:

1. Persistent or recurrent dermatitis requiring corticosteroids for control.

2. Atopic dermatitis not responding as expected to topical therapy.

3. Atopic dermatitis for which systemic treatment is being considered (eg, systemic steroids, immunosuppressives, and light therapy).

4. Other primary dermatologie conditions that are not improving with topical therapies or that are exacerbated by contactants.

TREATMENT

The mainstay of treatment for allergic contact dermatitis involves corticosteroids and avoidance of allergens. Acute eruptions are tamed with topical corticosteroids of moderate potency applied two times a day for 2 to 3 weeks. If the dermatitis involves more than 10% of the surface of the skin, however, systemic corticosteroids may be necessary. A single morning dose of prednisone (1 to 2 mg /kg) for 7 to 10 days followed by a taper during the next 7 to 10 days will clear the dermatitis. For both topical and systemic therapy, continuing treatment for a full 2 to 3 weeks is important because stopping…

The rash caused by poison ivy is a classic example of allergic contact dermatitis. Although many of us identify this vesicular eruption based on history or physical examination, we should be aware that a similar dermatitis may be caused by many substances that come in contact with children's skin. Considering that skin care products, cosmetics, toys, and clothing are specifically marketed to a younger audience, children are frequently exposed to many antigens that can cause allergic contact dermatitis. This article familiarizes the pediatrician with the pathogenesis, diagnosis, and treatment of allergic contact dermatitis.

PATHOGENESIS

Allergic contact dermatitis is an acquired, inflammatory reaction of the skin. It follows percutaneous absorption of an antigen (allergen) from the surface of the skin, with subsequent recruitment of previously sensitized, antigen-specific Tlymphocytes to the same area.1"4 Allergic contact dermatitis is a type IV delayed hypersensitivity reaction, so it requires an intact immune system. This reaction occurs in two phases, sensitization and elicitation.

Sensitization

Sensitization begins with the initial exposure to the allergen. Allergens that can sensitize by contact are usually substances with low molecular weights that readily penetrate the outer layer of the skin and are taken up by Langerhans' cells. Langerhans' cells process the antigen and then migrate to regional lymph nodes where they present the antigen to T-lymphocytes. After recognition of the antigen, specific T-lymphocytes undergo clonal expansion and circulate throughout the body. However, these T-lymphocytes now have the immune memory to recognize this antigen as foreign and will generate an immune response when rechallenged.

The strength 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, whereas weaker antigens require many exposures during weeks to years. Once sensitization occurs, however, it is long lived.13

Elicitation

On reexposure to the allergen, the sensitized Tlymphocytes proliferate and release inflammatory mediators, producing a localized dermatitis. This develops 12 to 24 hours after the reexposure. The resulting dermatitis may last up to 3 to 4 weeks if untreated.1"3

Table

TABLE 1Common Contact Allergens and Their Sources

TABLE 1

Common Contact Allergens and Their Sources

EPIDEMIOLOGY

For many reasons, the exact incidence and prevalence of allergic contact dermatitis in children is not known.5 Studies in the United States and Europe have estimated that allergic contact dermatitis represents at least 20% of all cases of childhood dermatitis.6 However, considering that nearly all individuals are eventually sensitized to poison ivy in endemic areas, this probably underestimates the true incidence. Furthermore, recent studies of children with dermatitis have shown that 15% to 66% are sensitized to contact allergens.720 Although these studies do not always explain the clinical relevance of sensitization, they suggest that allergic contact dermatitis is more common than previously estimated. Similarly, studies of asymptomatic children have shown that 13% to 25% are sensitized,21,22 with sensitization common as early as 6 months of age.23

It was previously believed that allergic contact dermatitis was rare in children due to infrequent exposure to allergens and a less mature immune system. However, it can occur in children of all ages. Fisher described the work of Strauss and Uhr, who induced sensitization to contact allergens in term and preterm infants.24 Case reports have also described allergic contact dermatitis in children as young as 1 week.25-26

Contact allergens can be man-made or found in nature. The most common contact allergen is urushiol, the sensitizing agent found in poison ivy, poison oak, and poison sumac. Other common childhood contact allergens and their sources (in decreasing order of frequency)21 include nickel, found in metals and common in jewelry and fasteners; neomycin, an antibiotic; potassium dichromate, a leather tanning agent; thimerosal, a preservative in eyedrops and vaccines; balsam of Peru, a fragrance; formaldehyde, a preservative; quaternium-15, a preservative; colophony, rosin from wood; p-tert-butylphenol formaldehyde resin, found in adhesives; and lanolin (wool alcohol), a cosmetic ingrethent. Table 1 lists the contact allergens routinely included in patch testing.

CLINICAL FEATURES

Allergic contact dermatitis presents as a pruritic dermatitis at the site of allergen contact. It can occur in both acute and chronic forms. Potent antigens such as poison ivy produce an acute dermatitis, characterized by erythema and edema with vesicles or bullae. These vesicles often rupture, leaving a crust. Less potent antigens produce a subacute or chronic dermatitis, characterized by lichenification, erythema, and scaling. Infrequently, a more generalized eczema can develop distal to the original site of contact. This is thought to be because of maximally activated T-lymphocytes that enter the circulation and then key in to other epidermal locations, causing disease there.

Table

TABLE 2When to Suspect Allergic Contact Dermatitis

TABLE 2

When to Suspect Allergic Contact Dermatitis

DIAGNOSIS

Because the dermatitis of allergic contact dermatitis is nonspecific, the key to its diagnosis is the history of exposure to allergens and the pattern of the eruption. For example, an acute eruption of linear vesicles on an exposed lower extremity after walking in the woods suggests poison ivy. Likewise, an erythematous, scaling rash on the earlobes of someone who wears earrings suggests nickel dermatitis. Patterns that suggest allergic contact dermatitis include any persistently localized dermatitis, unusually shaped dermatitis (eg, linear), or dermatitis in a distribution suggestive of contact (Table 2). Furthermore, the pattern of exposure can offer clues to the offending allergen. Table 3 lists examples of exposure patterns and their corresponding culprits.

DIFFERENTIAL DIAGNOSIS

The erythema and inflammation of an acute dermatitis can mimic cellulitis, but constitutional symptoms, such as fever, that are common in cellulitis are lacking in allergic contact dermatitis. The vesicles of an acute dermatitis can mimic viral infections such as herpes simplex or herpes zoster. Impetigo may also present as a vesicular or bullous eruption. Other forms of dermatitis (eg, irritant or atopic dermatitis) may be clinically identical to allergic contact dermatitis, especially when the latter is in the subacute or chronic form. A careful history of exposure to contact allergens will help differentiate these problems. Finally, a fixed drug eruption is also localized, but clinically appears as recurrent red or violet macules, bullae, or erosions. A history of recurrences associated with drug ingestion will help differentiate this condition from allergic contact dermatitis.

Table

TABLE 3Common Patterns of Allergic Contact Dermatitis and Corresponding Allergens

TABLE 3

Common Patterns of Allergic Contact Dermatitis and Corresponding Allergens

INDICATIONS FOR PATCH TESTING

Occasionally, the etiology is not apparent. In this situation, epicutaneous patch testing may be indicated to help determine whether allergic contact dermatitis could be the culprit and what the allergen might be. Although we believe that this examination is simple, it should be performed by an experienced dermatologist. Patch testing involves the placement of antigens directly on the surface of the skin for 48 hours. The allergens are then removed and the skin is inspected for localized dermatitis, indicating sensitization to the antigen in the patch. In a recent commentary, Sherertz recommended the following guidelines for patch testing in children27:

1. Persistent or recurrent dermatitis requiring corticosteroids for control.

2. Atopic dermatitis not responding as expected to topical therapy.

3. Atopic dermatitis for which systemic treatment is being considered (eg, systemic steroids, immunosuppressives, and light therapy).

4. Other primary dermatologie conditions that are not improving with topical therapies or that are exacerbated by contactants.

TREATMENT

The mainstay of treatment for allergic contact dermatitis involves corticosteroids and avoidance of allergens. Acute eruptions are tamed with topical corticosteroids of moderate potency applied two times a day for 2 to 3 weeks. If the dermatitis involves more than 10% of the surface of the skin, however, systemic corticosteroids may be necessary. A single morning dose of prednisone (1 to 2 mg /kg) for 7 to 10 days followed by a taper during the next 7 to 10 days will clear the dermatitis. For both topical and systemic therapy, continuing treatment for a full 2 to 3 weeks is important because stopping the corticosteroid too early may result in rebound of the dermatitis.

Identifying the offending allergen is important because avoidance is the best way to prevent future recurrences. This can often be done by history alone, but patch testing may be necessary to identify specific antigens. Printed information about allergens and their sources is available at many patch test centers. Avoidance of allergens may involve placing a barrier between the allergen and the skin (eg, wearing long pants while hiking, wearing socks with shoes, or using nail enamel to paint the exposed portions of metal fasteners). It may also be necessary for patients to read the ingrethents on product labels to choose products free of potential allergens.

CONCLUSION

Allergic contact dermatitis is an acquired, immune-mediated dermatitis that is common in children. Pediatricians should be familiar with common contact allergens in children, as well as patterns of dermatitis consistent with allergic contact dermatitis. Patch testing may be necessary to coririrm the diagnosis. The mainstay of therapy involves corticosteroids and preventing recurrences by avoiding the allergen.

REFERENCES

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2. Weston WL. Contact dermatitis in children. Curr Opin Pediatr. 1997;9:372-376.

3. Hogan PA, Weston WL. Allergic contact dermatitis in children. Pediatr Rei'. 1993;14:240-243.

4. McAlvany JP, Sherertz EF. Contact dermatitis in infants, children, and adolescents. Adv Dermatol. 1994;9:205-223.

5. Mortz CG, Andersen KE. Allergic contact dermatitis in children and adolescents. Contact Dermatitis. 1999;41: 121-130.

6. Weston WL, Weston JA. Allergic contact dermatitis in children. American Journal of Diseases in Childhood. 1984;138:932-936.

7. Roul S, Ducombs G, Taieb A. Usefulness of the European standard series for patch testing in children: a 3-year singlecentre study of 337 patients. Contact Dermatitis. 1999;40:232235.

8. Romaguera C, Vilaplana J. Contact dermatitis in children: 6 years experience (1992-1997). Contact Dermatitis. 1998^9: 277-280.

9. Manzini BM, Ferdani G, Simonetta' V, Donini M, Seidenari S. Contact sensitization in children. Pediatr Dermatol. 1998,15: 12-17.

10. Brasch J, Geier J. Patch test results in schoolchildren: results from the Information Network of Departments of Dermatology (IVDK) and the German Contact Dermatitis Research Group. Contact Dermatitis. 1997;37:286-293.

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14. Rudzki E, Rebandel P. Contact dermatitis in children. Contact Dermatitis. 1996;34:66-67.

15. Katsarou A, Koufou V, Armenaka M, KalogeromitiOS D, Papanayotou G, Vareltzidis A. Patch tests in children: a review of 14 years experience. Contact Dermatitis. 1996;34:70-71.

16. Wantke F, Hemmer W, Jarisch R, Götz M. Patch test reactions in children, adults, and the elderly: a comparative study in patients with suspected allergic contact dermatitis. Contact Dermatitis. 1996;34:316-319.

17. Sevila A, Romaguera C, Vilaplana J, Botella R. Contact dermatitis in children. Contact Dermatitis. 1994;30:292-294.

18. Concaio S, Goncalo M, Azenha A, et al. Allergic contact dermatitis in children: a multicenter study of the Portuguese Contact Dermatitis Group (GPEDC). Contact Dermatitis. 1992;26:112-115.

19. Rademaker M, Forsyth A. Contact dermatitis in children. Contact Dermatitis. 1989;20:104-107.

20. Baiato N, Lembo G, Patrono C, Ayala F. Patch testing in children. Contact Dermatitis. 1989;20:305-307.

21. Weston WL, Weston JA, Kinoshita J, et al. Prevalence of positive epicutaneous tests among infants, children, and adolescents. Pediatrics. 1986;78:1070-1074.

22. Barros MA, Baptista A, Correia TM, Azevedo F. Patch testing in children: a study of 562 schoolchildren. Contact Dermatitis. 1991;25:156-159.

23. Bruckner AL, Weston WL, Morelli JG. Does sensitization to contact allergens begin in infancy? Pediatrics. 2000;105:e3. Available at www.pediatrics.org/cgi/content/full/105/ l/e3.

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25. Fisher AA. Allergic contact dermatitis in early infancy. Cutis. 1994;54:300-302.

26. Seidenari S, Manzini BM, Motolese A Contact sensitization in infants: report of 3 cases. Contact Dermatitis. 1992;27319320.

27. Sherertz EF. Patch testing in children. Pediatr Dermatol. 1998;15:68-69.

TABLE 1

Common Contact Allergens and Their Sources

TABLE 2

When to Suspect Allergic Contact Dermatitis

TABLE 3

Common Patterns of Allergic Contact Dermatitis and Corresponding Allergens

10.3928/0090-4481-20010401-08

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