Development and Diagnosis of Atopic Dermatitis 

Effective management begins with diagnostic precision. This resource is structured to guide you through:

• Common definition, onset, presentation, and location of eczema
• Pathogenesis of the genetic, immunological, and environmental drivers of eczema
• The relationship between eczema and other allergic conditions within the Atopic March
• Consideration of other differential diagnoses that mimic eczema presentation
• Diagnosis based on established clinical criteria and tools to grade severity of eczema

What is Eczema? 

Eczema, atopic dermatitis, is a chronic skin condition clinically diagnosed by the presence of characteristic features such as pruritus, scaling, and lichenification that commonly relapses, with the onset of disease usually occurring before 1 year of age (1)

The prevalence of AD has been increasing, affecting on average 12.6% of children in the United States, and as high as 25%, disproportionately affecting black and hispanic populations (2, 3). 

While most cases of AD start before the age of 1, many children will outgrow the condition in the future (4). 

What can you tell caregivers?

• Eczema is common in children and often starts when they are babies. Many children get better or outgrow it as they get older.

Common Location of Eczema?

The distribution of eczema varies with age, with the most common location being the flexor regions, such as behind the knees and inner elbows. Infants often present with eczema on the cheeks, trunk, and extremities, whereas teenage children more commonly present with eczema of the hands and feet. 

What causes Eczema? 

The development of Atopic Dermatitis is multifactorial, including genetic predispositions, skin barrier disruption, environmental triggers and immune dysfunction (1). Further, AD is thought to be the first step in the Atopic March, in which defective skin barriers lead to immune sensitization to allergens, resulting in food allergies, asthma, and allergic rhinitis. AD and food allergies co-occur, with recent research showing that about 40% of children with AD develop FAs (5). 

Skin Barrier Dysfunction 

Reduced skin barrier integrity increases transepidermal water loss, leading to dry, micro-cracked, permeable skin.

Disruption of tight junctions allows for allergens and irritants to enter skin, leading to increased pro-inflammatory cytokine expression.

Loss of function from filaggrin mutations is strongly associated with early-onset, persistent, severe eczema.

Environmental Triggers

While environmental triggers don’t cause eczema, they exacerbate it by penetrating the impaired barrier and activating the innate and Th2 immune pathways.

Common irritants include: soaps, detergents, shampoos, hand sanitizers, alcohols, salvia, sweat, urine, feces, and rough fabrics.

Low temperatures, low humidity, and high pollution inhibit the Epidermal Differentiation Complex (EDC), leading to leaky skin barrier and increasing pro-inflammatory cytokines 

Cutaneous Allergen Sensitization

While early oral introduction of allergenic foods such as peanuts can promote immune tolerance, cutaneous exposure to food proteins—particularly through an impaired skin barrier—may promote IgE sensitization and the subsequent development of food allergy. 

Dual Exposure Hypothesis proposes that oral exposure promotes tolerance, whereas low-dose environmental exposure through the skin—especially inflamed or barrier-deficient skin—favors Th2-skewed immune responses and allergic sensitization. If a child experiences frequent environmental exposures through their skin, but avoids oral exposure to an allergenic food (e.g. peanuts), they may be more likely to develop an allergy, as the immune cells of the skin are more likely to cause sensitization to that food.

Peanut protein has been detected on high-touch household surfaces and in household dust after consumption, and on hands and in saliva following ingestion, highlighting multiple potential routes for environmental transfer and subsequent skin exposure (6-10).

Several studies have linked the presence of environmental peanut allergen to sensitization and food allergy to peanut. Although this association has been shown in those with healthy skin, eczema may increase the risk. Skin barrier dysfunction and inflammation may be components of eczema that specifically increase the risk of sensitization to environmental food exposure. Although the majority of studies have been on peanut, similar trends likely exist for other foods as well.

Handwashing and appropriate surface cleaning have been shown to significantly reduce detectable peanut allergen levels and may help mitigate environmental exposure (8-10).

What can you tell caregivers?

• Eczema happens because the skin’s protective barrier is weaker, so it loses moisture easily and lets in things that bother it.
• Dry skin leads to itchy skin. Scratching can damage the skin more and cause flares, which are periods of really bad eczema.
• Eczema is not contagious – it can’t spread from person to person.
• Everyday things like soaps, detergents, sweat, saliva, rough fabrics, cold weather, and pollution can make eczema worse.
• Some children with eczema are more likely to develop food allergies, especially when eczema is severe (very bad). Getting allergens on the skin over and over again increases this risk. In these cases, cleaning hands and surfaces after touching food allergens (like peanuts) is very important.
• Visit https://fampitfamily.org/understanding-eczema/ for more information.

Other Conditions To Consider:

Disorders that must be ruled out that commonly mimic eczema:

• Irritant or allergic contact dermatitis
• Psoriasis
• Seborrheic dermatitis
• Photodermatoses
• Primary immunodeficiency disorders
• Infestations
• Local and systemic infections (streptococcal, staphylococcal, fungal, syphilis)

Diagnosis of Eczema  

The American Academy of Dermatology recommends clinical diagnosis of atopic dermatitis based on historical features, morphology and distribution of skin lesions, and associated clinical signs, without requiring laboratory testing. 

Eczema Severity Scoring 

The following validated tools can be considered when practical.

1. EASI Score (Eczema Area and Severity Index) – objective clinician estimates of disease extent and severity. https://dermnetnz.org/topics/easi-score
   • Mild Eczema: 0.1-5
   • Moderate Eczema: 6-22
   • Severe Eczema: 23-72
2. SCORAD Index (Scoring Atopic Dermatitis) – objective measures and subjective patient assessment of itch and sleep loss. https://www.escorad.dermavalue.com/uploads/attachments/cla9qgirw00lb4of5u6iixu4s-scorad-en.pdf
   • Mild Eczema: 10-28
   • Moderate Eczema: 29-48
   • Severe Eczema: 49-103
3. POEM (Patient-Orientated Eczema Measure) – measures severity from the patient perspective using questions of symptom frequency. https://www.nottingham.ac.uk/research/groups/cebd/documents/methodological-resources/poem/30jan2025-poem-caregiver-uk-english.pdf
   • Mild Eczema: 3-7
   • Moderate Eczema: 8-16
   • Severe Eczema: 17-24 

Key takeaways 

• Eczema is a chronic, relapsing inflammatory skin disease with hallmark features of itchy, red, scaling skin. 
• Eczema disproportionately affects children, with most cases occurring before the age of one.
• Eczema is a multifactorial disease involving genetic predisposition, skin barrier dysfunction, environmental triggers and immune dysregulation.
• Atopic March, with 40% of children with AD developing food allergies. 

• Route of allergen exposure matters! While early oral exposure to allergenic food may decrease food allergy development, low-dose cutaneous exposure can increase the risk of food allergy development, supporting the dual-allergen exposure hypothesis.
• Impaired skin barrier, as seen in atopic dermatitis, increases the sensitization risk as increased permeability and inflammation facilitate allergen penetration.
• Hand washing is a great prevention method to spreading allergic food proteins, thus educating families on hand washing prior to handling their children. 
• Environmental triggers do not cause eczema, but exacerbate disease. 
• Cold temperatures, low humidity and pollution worsen skin barrier and increase inflammatory signaling. 
• Clinical diagnosis is based on patient history, lesion morphology and distribution and associated clinical symptoms. 
• The use of severity scoring tools may be practical to guide treatment regimes. 

Resources: 

1. Schoch, J., Anderson, K., Jones, A., Tollefson, M. (2025). Atopic dermatitis: update on skin-directed management: clinical report. American Academy of Pediatrics. https://doi.org/10.1542/peds.2025-071812
2. Choragudi, S., Yosipovitch, G. (2023). Trends in the prevalence of eczema along US children by age, sex, race, and ethnicity from 1997 to 2018. JAMA Dermatology. doi:10.1001/jamadermatol.2022.6647 
3. Monir, R., Schoch, J., Garven, C., Neu, J., Lemas, D. (2022). Association between atopic dermatitis and race from infancy to early childhood: a retrospective cohort study. International Journal of Dermatology. https://doi.org/10.1111/ijd.15805
4. Roduit, C., Frei, R., Depner M, et al. (2017). Phenotypes of atopic dermatitis depending on the timing of onset and progression in childhood. JAMA Pediatr. 10.1001/jamapediatrics.2017.0556
5. Tham, E., Leung, D. (2019). Mechanisms by which atopic dermatitis predisposes to food allergy and the atopic march. Allergy,Asthma, & Immunology Research. https://doi.org/10.4168/aair.2019.11.1.4
6. Brough HA, et al. (2020) Environmental peanut exposure and the risk of peanut sensitization and allergy. J Allergy Clin Immunol.145(2):633–643.
7. Smeekens JM, et al. (2021). Household food allergen exposure and sensitization in early life. Curr Allergy Asthma Rep.21:48.
8. Perry TT, et al. (2020) Distribution of peanut allergen in the environment and effectiveness of cleaning methods. J Allergy Clin Immunol. 145(2):667–669.
9. Greenhawt M, et al. (2021) Peanut allergen persistence on hands and the effect of handwashing. Ann Allergy Asthma Immunol.127(2):214–220.
10. Maloney JM, et al. (2020). Persistence of peanut protein in saliva after ingestion. J Allergy Clin Immunol. 146(4):889–891.
11. Turner PJ, Campbell DE, Boyle RJ, Levin ME. (2021). Primary prevention of food allergy: Translating evidence from clinical trials to population-based recommendations. J Allergy Clin Immunol. 147(6):2020–2029.
12. Leung DYM, Berdyshev E, Goleva E. (2020). Cutaneous barrier dysfunction in allergic diseases. J Allergy Clin Immunol. 145(6):1485–1497.
13. Lack G, et al. (2022). The dual-allergen exposure hypothesis: Revisited and updated. Allergy. 2022;77(1):7–16.
14. Brough HA, et al. (2020). Atopic dermatitis increases the effect of environmental peanut exposure on peanut sensitization. J Allergy Clin Immunol. 146(2):367–375.
15. Flohr C, et al. (2021). Atopic dermatitis and the risk of food allergy. Allergy. 76(3):748–761.
16. Strid J, Hourihane J, Kimber I, Callard R, Strobel S. (2022). Epicutaneous exposure to food allergens and the development of food allergy. Clin Exp Allergy. 52(4):465–477.
17. Leyva-Castillo JM, et al. (2023). Epithelial-derived cytokines in allergic skin inflammation and food allergy. Nat Rev Immunol. 23(4):233–247.
18. ​​Eichenfield, L., et al. (2014). Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. Journal of the American Academy of Dermatology, 70(2), 338–351. https://doi.org/10.1016/j.jaad.2013.10.010