Pediatric Dermatology

A Practical Overview of Pediatric Atopic Dermatitis, Part 2: Triggers and Grading

Author and Disclosure Information

In part 2 of this 3-part series on atopic dermatitis (AD) in children, triggers for the appearance and flaring of AD are reviewed. The role of AD in the atopic march is explored. Furthermore, the usage of grading systems in the development of therapeutics and in clinical care is discussed. The natural history of AD has changed from improvement to 50% persistence and therefore it is important to council guardians and patients accordingly.

Practice Points

  • Atopic dermatitis (AD) can be triggered by viral infections, weather, and food allergens.
  • The scoring of AD is largely used experimentally and includes the eczema assessment and severity index; the SCORAD (SCORing Atopic Dermatitis); and the six area, six sign AD (SASSAD) scores.
  • There is a strong genetic contribution to the development of AD.
  • Children with AD may have persistent disease into adulthood in half of cases.


 

References

Atopic dermatitis (AD) may be triggered by viral infections, food allergens, weather, and other causes, and it may trigger an inflammatory progression known as the atopic march. This article reviews research on triggers of pediatric AD so that dermatologists may discuss trigger avoidance with patients and guardians. Other factors affecting AD development include genetics and hygiene. Grading of AD also is discussed.

The Atopic March

The persistence of AD in untreated skin can trigger an inflammatory progression called the atopic march in which food and environmental allergies as well as asthma may occur progressively due to ongoing inflammatory triggering.1 In a study of asthma and food allergy reporting and management in public schools in Chicago, Illinois, food allergies were seen in 9.3% of asthmatic students (n=18,000), and 40.1% of food allergic students (n=4000) had asthma.2 An observational study by Flohr et al3 in London, England, included 619 exclusively breastfed infants who were recruited at 3 months of age. The investigators determined that food sensitization was unrelated to the presence of filaggrin mutations, type of eczema (flexural vs nonflexural), and transepidermal water loss but was associated with AD severity as determined by SCORAD (SCORing Atopic Dermatitis), a composite score of AD that includes pruritus as a factor in severity. Other AD associations included 3 leading food allergens: eggs, milk, and peanuts. No association with cod, wheat, or sesame allergy was noted. The investigators concluded that AD and AD severity were the leading skin-related risk factors for food allergies and therefore food allergy development in breastfed infants was probably mediated by cutaneous antigen-presenting cells.3

The skin has been documented to react to contact with known food allergens4 and is known to be a route of allergic sensitization to allergens such as fragrance in patients with AD.5,6 Two phenotypes of eczema that have been associated with asthma development are severe AD disease and multiple environmental allergies, supporting the theory of the atopic march.7 There also is evidence that release of danger-associated proteins from an impaired barrier also may trigger asthma.8 An analysis of the 2007 National Survey of Children’s Health, a population-based study of91,642 children aged 0 to 17 years, showed that children with AD had a higher prevalence of comorbid asthma (25.1% vs 12.3%), hay fever (34.4% vs 14.3%), and food allergies (15.1% vs 3.6%) compared to children without AD.9 A recent article provided detailed information on how food and diet interplay with AD.10

Triggers of Disease Flares

Triggers are the leading source of AD flare initiation, and avoidance of triggers is an important mechanism by which patients can control disease activity. Despite the best skin care and trigger avoidance, disease flares occur, sometimes due to ongoing inflammation and other times due to inability to prevent flares such as heat and humidity. A survey of patients with AD in Spain identified the following triggers: cosmetic products, clothing, mites, detergents/soaps, and temperature changes.11 In childhood, wool also is a known trigger of AD.12 Viral infections including respiratory syncytial virus may trigger the first onset of AD.13 Patients with AD may become allergic to fragrance and metals causing disease exacerbation on exposure.14,15 Food allergens contribute to approximately 40% of cases of AD in infancy but are not the cause of AD. The best evidence for improvement of AD with food allergen avoidance exists for egg white allergy.16 Food avoidance programs should be developed in conjunction with an allergist, as it is no longer advised in many cases to completely withdraw foods; therefore, an allergist has to assess the level of allergic severity and the risk-benefit ratio of food avoidance or introduction.17 Emotional stressors, heat, and humidity, as well as indoor heating in the winter months, can cause AD flares.18

A study by Silverberg et al19 provided evidence of climate influences on the US prevalence of childhood eczema using a merged analysis of the 2007 National Survey of Children’s Health and the 2006-2007 National Climate Data Center and Weather Service. Results showed that eczema prevalence was significantly lower when associated with higher annual relative humidity (P=.01), UV index (P<.0001), and highest-quartile air temperature (P=.002).19 The Pediatric Eczema Elective Registry also showed that warm, humid, and high-sun-exposure climates are associated with poorly controlled eczema in affected patients.20 The association of eczema with latitude as well as its negative association with mean annual outdoor temperature has been described by Weiland et al21 in the ISAAC (International Study of Asthma and Allergies in Childhood) study. Long airplane flights in low humidity can trigger eczema in adults. Climate has been postulated to affect eczema through alterations in filaggrin and skin barrier function.22 Indoor temperature and humidity regulation may be used adjunctively for daily flare prevention.

Next Article:

A Practical Overview of Pediatric Atopic Dermatitis, Part 1: Epidemiology and Pathogenesis

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