Abstract

ACD is now recognized as a significant problem. The incidence of ACD in children is rising perhaps due to increased exposure to sensitizing agents Several studies have demonstrated that 13%-24% of asymptomatic children will have positive patch test reactions. If ACD is suspected, it is important to refer the child for patch testing.

 Case

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 hereyelids. 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.

What is differencial diagnosis:

The differential diagnosis is as follows:

1. Atopic dermatitis (AD),
2. Irritant contact dermatitis, and
3. Allergic contact dermatitis (ACD).

Discussion

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 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 associationis 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 improvementintheirdermatitis (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.

References

1. Barros, M. A., Baptista, A., Correia, T. M., & Azevedo, F. (1991). Patch testing in

children: A study of 562 schoolchildren. Contact Dermatitis, 25, 156-159.

2. Beattie, P. E., Green, C., Lowe, G., & Lewi

Jones, M. S. (2007). Which children should we patch test? Clinical and Experimental Dermatology, 32, 6-11.

3. Bruckner, A. L., Weston, W. L., & Morelli, J. G. (2000). Does sensitization to contact allergens begin in infancy? Pediatrics, 105, e3.
4. 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
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9. Mortz, C. G., Lauritsen, J. M., Bindslev-Jensen, C., & Andersen, K. E. (2002). Contact allergy and allergic contact dermatitis in adolescents: Prevalence measures   and    The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis (TOACS). Acta Dermato-Venereologica, 82, 352-358.
10. Segurado Rodriguez, M. A., Ortiz de Frutos, F. J., & Guerra Tapia, A. (2004). Allergic contact dermatitis. Anales de Pediatria, 60, 599-601.
11. 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.