Atopic Dermatitis
The most common form of eczema is a chronic skin disorder, which can be stimulated by factors such as environmental triggers, genetics and immune mechanisms.
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1 in 10 Americans have atopic dermatitis
African/ Asian Americans are more likely to develop Atopic Dermatitis than white children [1]
Affects 11-20% of children and 5-15% of adults in the United Kingdom [2,3]
The prevalence of atopic dermatitis affects up to 20% of children and 10% of adults
The burden of disease ranks 15th worldwide for non-fatal diseases
Ranked number 1 in skin diseases measured in Disability Adjusted Life Years [3]
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Irritants such as soaps, detergents, washing liquids, bubble bath
Environmental factors such as cold/ dry weather, mould, dust and fur
Food allergies
Certain materials like wool and synthetic fabrics
Skin infections
Insect bites
Hormonal changes eg. before periods or during pregnancy [7]
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Medical Student
Epidermal dysfunction
The interleukins 4,13,31 and 33 reduce the production of epidermal barrier proteins.
This includes filaggrin protein, keratins and other molecules.
The effects of this epithelial skin dysfunction reduced skin hydration, increases skin pH, increases penetration of allergens, increased pro-inflammatory cytokines and reduced inflammatory threshold levels. [4]
Neuroimmunological mechanisms
The damage to neuro-immune systems plays an important role in the pathophysiology of Atopic Dermatitis.
Sensory nerve endings also release neuro-mediators into the skin- this stimulates the triage of inflammation, barrier defects and puritis [5]
Immune dysregulation
T-cell–mediated delayed-type hypersensitivity and includes a Th2-dominant component in the skin.
Immune cytokines like Interleukin 4 and 13 contribute to chemokine production, skin barrier dysfunction, allergic inflammation and the suppression of antimicrobial peptides.
The increased penetration of skin irritants and allergens also results in a Th2-dominant inflammation, which also drives IgE production and predisposes to immediate-type hypersensitivities. [4,6]
Genetics
The filaggrin gene which encodes the filaggrin protein, is a major component in structuring the outer layer of the epidermis (stratum corneum).
A mutation in this gene causes degradation products and contributes to impaired skin barrier functions (increasing the risk of Atopic Dermatitis)
The T helper type 2 signalling pathway is altered; causing an up-regulation of interleukins 4 and 13. Reducing gene expression, which leads to skin barrier defects. Contributing to the development of Atopic Dermatitis. [6]
Patients
Genetics
The existence of genetic mutation in a gene specific to the skin barrier is defective
Increases the risk of severe atopic dermatitis and higher IgE levels
Environmental factors
Irritants, tobacco smoke, pollen, dust mites, pet fur, mould, and certain materials like wool and synthetic fabrics
Defective skin barriers
Genetic mutations cause skin irritation and the development of dry skin and membranes
Mechanisms of the Immune System
Atopic dermatitis is a cell-controlled reaction which increases the risk of developing bacterial and viral skin infections.
The increase in environmental factors also stimulated specific protein production and immune response. [6,7]
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Weakened immune system
Family/personal history of hay fever or asthma
Dry skin
Filaggrin gene mutations
Stress
Female sex
Damp hands and feet
Environmental exposure to irritants [8]
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Redness and blisters
Weeping or crusted skin
Over time can become less red and thickened
Greyish/white patches on darker skin
Cracking of the skin
Can be found on the flexor aspects of the body, as well as the hands, eyes or neck.
In patients of African descent, perifollicular (around the follicle) and extensor areas are more commonly affected.
After an inflammatory episode, hypo/hyper-pigmentation is more likely to occur in skin of colour than white skin. [6]
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Severity grading:
Clear – Normal skin
Mild – Dry skin, infrequent itching, slight redness/purple/dark-red
Moderate – Dry skin, frequent itching, more marked redness
Scoring tools:
Visual analogue scales (0–10): severity, itch, and sleep loss over the past 3 days/nights
POEM (Patient-Oriented Eczema Measure)
Assess psychological impact – screen for reduced quality of life and distress
Identify allergens or irritants specific to the patient
Referal to a dermatologist may be needed
Patch test
Potentially triggering substances are attached to an area of the body using tape
Can be attached to places like the upper arm, the back or the forearm.
2 days later, the patches are removed and assessed to note any reactions.
Can be accessed 2 days post initial investigation as atopic dermatitis reactions can appear later. [7]
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Seborrheic dermatitis
Contact dermatitis
Lichen simplex
Psoriasis
Scabies
Impetigo
Zinc deficiency
Hyper IgE syndrome
Candidiasis [9]
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Medical Students
Grade severity:
Clear: Normal skin
Mild: Dry skin, infrequent itch
Moderate: Frequent itch, red/purple areas
Use Visual Analogue Scale (0–10) and POEM score
Assess psychological impact (QoL, distress)
Mild AD
Emollients
Mild steroid: Hydrocortisone 1% (after 48h of flare control)
Educate on self-care & flare prevention
Refer to dermatology or psychology if needed
Moderate AD
Identify triggers or infection
Emollients
Moderate steroids:
Betamethasone 0.025%
Clobetasone 0.05%
Use Hydrocortisone on delicate areas
Add non-sedating antihistamines for itch (e.g. cetirizine)
Consider calcineurin inhibitors (e.g. tacrolimus)
Refer if uncontrolled or psychological distress
Refer to specialists if food allergy suspected
Severe AD
Consider admission if eczema herpeticum
Potent steroids (e.g. Betamethasone 0.1%)
Moderate steroids on delicate skin
Use sedating antihistamines if sleep is affected
Short course of oral steroids in severe distress
Urgent referral if not improved in 1 week
Address psychological and allergy concerns
Patients
Mild AD
Use moisturisers (emollients) regularly
Apply mild steroid cream (e.g. Hydrocortisone) only as advised
Learn how to avoid triggers and care for your skin
Moderate AD
Moisturise often
Use stronger creams as prescribed (e.g. Betamethasone or Clobetasone)
Avoid known triggers (e.g. soaps, allergens)
You may be given allergy tablets (antihistamines) to reduce itching
See your doctor if symptoms continue or affect your wellbeing
May be referred if a food allergy is suspected
Severe AD
Seek help urgently if skin is badly infected or painful
Strong steroid creams may be needed (but used with care)
Allergy or sleep tablets may help with itching
You may be offered a short course of oral steroids
You should be referred to a skin doctor (dermatologist) if it's not improving
Support from a psychologist may help if it affects mental health
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Bacterial skin infections
Viral skin infections (herpes simplex virus)
Eczema herpeticum
Psychological effects such as bullying, problems sleeping, self-image/ confidence [7]
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Only children get eczema
Itchy skin isn’t a red flag
It will self resolve
Treatment will cure/eradicate eczema
Lifestyle changes won’t singularly help eczema
Atopic dermatitis is contagious
Atopic dermatitis is caused by stress [11,12]
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What can I do to manage my symptoms?
Are there any products that can make my eczema worse?
Are there ways I can treat my skin to reduce my chances of another flare-up?
What should I do if the medication doesn’t work?
When should I apply/use my medication?
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The British Association of Dermatologists
The National Eczema Society
Eczema Care Online
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[1] https://www.aad.org/public/diseases/eczema/types/atopic-dermatitis
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573657/#:~:text=The
[3] https://www.eczemacouncil.org/assets/docs/global-report-on-atopic-dermatitis-2022.pd
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6399565/
[5] https://www.sciencedirect.com/science/article/pii/S0091674922003803
[7] https://www.nhs.uk/conditions/atopic-eczema/causes/#:~:text=environmental
[8] https://atopicdermatitis.net/eczema-risk-factors
[10] https://cks.nice.org.uk/topics/eczema-atopic/management/severe-eczema/
[11] https://www.everydayhealth.com/eczema/eczema-myths-debunked/
[12]https://www.dermatologynwhouston.com/5-common-myths-about-eczema/
Source: DermNetNZ.org
Atopic Dermatitis
Damaged skin seen in short term (acute) eczema on the extensor aspects of the knees
Source: DermNetNZ.org
Atopic Dermatitis
Lichenification (process when skin becomes hard and leathery) and hyperpigmentation (increased pigmentation of the skin) on the knees in skin of colour due to atopic eczema
Source: DermNetNZ.org
Atopic Dermatitis
Patchy eczema on the arm
Source: DermNetNZ.org
Atopic Dermatitis
Chronic (long-term) changes of atopic eczema with inflammation, scaliness and lichenification
Source: DermNetNZ.org
Atopic Dermatitis
Facial and lid eczema in a toddler. Dennie Morgan folds seen on the bottom eye lid
Source: DermNetNZ
Atopic Dermatitis
Lichenification and scaly cheeks due to dermatitis
Source: Waikato District Health Board; DermNetNZ
Atopic Dermatitis
Lichenification and hyperpigmentation in chronic facial eczema
Source: DermNetNZ.org
Atopic Dermatitis
Eczema on the dorsal foot (top of foot)