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.

    • 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]

    • 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]

  • 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]

    • 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]

    • 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]

    • 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]

    • Seborrheic dermatitis

    • Contact dermatitis

    • Lichen simplex

    • Psoriasis

    • Scabies

    • Impetigo

    • Zinc deficiency

    • Hyper IgE syndrome

    • Candidiasis [9]

  • 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

    • Bacterial skin infections

    • Viral skin infections (herpes simplex virus)

    • Eczema herpeticum

    • Psychological effects such as bullying, problems sleeping, self-image/ confidence [7]

    • 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]

    • 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?

    • The British Association of Dermatologists

    • The National Eczema Society

    • Eczema Care Online

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)

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