1. Moennich, Jessica
  2. Hanna, Diane M.
  3. Jacob, Sharon E.

Article Content


A 10-year-old girl presented with pink scaly plaques on her antecubital and popliteal fossae (Figure 1). In addition, she had swelling of the medial canthi of her eyelids. She reported that the dermatitis started a couple of years ago and that it was worsening despite use of over-the-counter hydrocortisone creams (which she used the most frequently), Desonate and Protopic.

Figure 1 - Click to enlarge in new windowFIGURE 1. Plaques of allergic contact dermatitis in the antecubital fossae of a 10-year-old girl.

Patch testing to our pediatric standard (Jacob, Burk, & Connelly, 2008) revealed a clinically relevant positive reaction to compositae mix.



The differential diagnosis is as follows:


1. atopic dermatitis (AD),


2. irritant contact dermatitis, and


3. allergic contact dermatitis (ACD).




Once thought to be rare in the pediatric population, ACD is now recognized as a significant problem. The incidence of ACD in children is rising perhaps due to increased exposure to sensitizing agents (Beattie, Green, Lowe, & Lewis-Jones, 2007). Several studies have demonstrated that 13%-24% of asymptomatic children will have positive patch test reactions (Barros, Baptista, Correia, & Azevedo, 1991; Bruckner, Weston, & Morelli, 2000; Mortz, Lauritsen, Bindslev-Jensen, & Andersen, 2002; Weston et al., 1986). In symptomatic children referred for testing due to suspected contact dermatitis, the incidence of positive reactions rises to approximately 41%-67% (Jacob, Brod, & Crawford, 2008). Although the relationship between AD and ACD remains controversial, it is well known that these two clinical entities can and do occur together (Klas, Corey, Storrs, Chan, & Hanifin, 1996). In fact, AD may be a predisposing risk factor to sensitization (Segurado Rodriguez, Ortiz de Frutos, & Guerra Tapia, 2004). One hypothesis to explain this association is that children with AD are more susceptible to sensitization because they have decreased skin barrier function. Loss-of-function mutations in the filaggrin gene, which predispose to AD, result in this skin barrier disruption and have also been shown to be associated with predisposition to irritant contact dermatitis (de Jongh et al., 2008). Another explanation for why children with AD could also contract ACD is that they can have prolonged exposure on damaged skin to sensitizing agents present in their emollients or steroid creams. Our clinical case illustrates this point as our atopic patient demonstrated a clinically relevant reaction to chamomile extract (compositae mix), an ingredient in the vehicle of her over-the-counter hydrocortisone and shampoo and conditioner. Notably, by instituting avoidance (of these products and this allergen) and barrier repair measures with emollients, our patient's atopic distribution and eyelid dermatitis resolved.


Because an undiagnosed ACD in an atopic child will often result in a chronic dermatitis that is recalcitrant to standard therapies, it is important to also consider a concomitant diagnosis of ACD. Some clinical clues that suggest that a child with AD also has ACD are a new-onset, deteriorating, or recalcitrant dermatitis (Jacob et al., 2008). Furthermore, ACD should also be suspected in children with involvement of atypical areas such as their face, hands, eyelids, or neck folds or with the presentation of dyshidrosis (Beattie et al., 2007; Jacob et al., 2008). An excellent example of these principles is illustrated in a case report recently published in Contact Dermatitis (Jacob & Stechschulte, 2008). This case describes a 4-year-old atopic girl with worsening flexural dermatitis and eyelid dermatitis. Patch testing revealed that the child was allergic to tosylamide-formaldehyde resin 10% in petrolatum, a chemical present in her nail polish. After avoidance of the allergen, she experienced a significant improvement in her dermatitis.


If ACD is suspected, it is important to refer the child for patch testing. Patch test evaluation includes not only administration of patch testing but also a careful intake history to assess the most likely allergens present in their environment (Jacob et al., 2008). Once the offending allergen is identified and strictly avoided, the children usually experience significant improvement in their dermatitis (Jacob et al., 2008). Furthermore, they may be able to discontinue the use of corticosteroids and immunosuppressive agents and experience an improvement in not only their dermatitis but also their and their family's quality of life.




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Beattie, P. E., Green, C., Lowe, G., & Lewis-Jones, M. S. (2007). Which children should we patch test? Clinical and Experimental Dermatology, 32, 6-11. [Context Link]


Bruckner, A. L., Weston, W. L., & Morelli, J. G. (2000). Does sensitization to contact allergens begin in infancy? Pediatrics, 105, e3. [Context Link]


de Jongh, C. M., Khrenova, L., Verberk, M. M., Calkoen, F., van Dijk, F. J., Voss, H., et al. (2008). Loss-of-function polymorphisms in the filaggrin gene are associated with an increased susceptibility to chronic irritant contact dermatitis: A case-control study. British Journal of Dermatology, 159, 621-627 [Context Link]


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Mortz, C. G., Lauritsen, J. M., Bindslev-Jensen, C., & Andersen, K. E. (2002). Contact allergy and allergic contact dermatitis in adolescents: Prevalence measures and associations. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis (TOACS). Acta Dermato-Venereologica, 82, 352-358. [Context Link]


Segurado Rodriguez, M. A., Ortiz de Frutos, F. J., & Guerra Tapia, A. (2004). Allergic contact dermatitis. Anales de Pediatria, 60, 599-601. [Context Link]


Weston, W. L., Weston, J. A., Kinoshita, J., Kloepfer, S., Carreon, L., Toth, S., et al. (1986). Prevalence of positive epicutaneous tests among infants, children, and adolescents. Pediatrics, 78, 1070-1074. [Context Link]