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.

Epidemiology

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]

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

Pathophysiology

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]

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

Causes [7]
- 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
Risk factors [8]
- 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
Presentations [6]
- 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.

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

Investigations [7]
- 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.
Differential diagnosis [9]
- Seborrheic dermatitis
- Contact dermatitis
- Lichen simplex
- Psoriasis
- Scabies
- Impetigo
- Zinc deficiency
- Hyper IgE syndrome
- Candidiasis
Management [10]
- Assessing the severity of atopic dermatitis
  - Clear- Normal skin
  - Mild- Areas of dry skin and infrequent itching, can have a small amount of redness/ purple/dark-red
  - Moderate- Areas of dry skin, frequent itching and redness/ purple/dark-red
- Visual analogue scales (0–10) of the person's assessment of severity, itch, and sleep loss over the last 3 days and nights
- The Patient-Oriented Eczema Measure (POEM)
- Assessing the psychological impact of Atopic Dermatitis
Medical students
- Mild atopic dermatitis
  - Use of emollients
  - Use of mild topical corticosteroid (used after 48 hours after flare has been controlled)
    - Hydrocortisone 1%
  - Appropriate and useful information/ advice including advice on reducing the risk of flares, self-care, myth-busting and advice on what not to use
  - Refer to routine dermatology appointment if management is not controlling the condition
  - Refer to a clinical psychologist if the condition is causing a reduction in quality of life and psychological well-being.
- Moderate atopic dermatitis
  - Consider the possibility of trigger factors or infection
  - Use of emollients
  - Use of moderately potent topical corticosteroid (used after 48 hours after flare has been controlled)
    - Betamethasone valerate 0.025%
    - Clobetasone butyrate 0.05%
  - Delicate areas of skin (eg. flexures, the face) use a moderate potency corticosteroid
    - Hydrocortisone 1%
  - Occlusive dressings or dry bandages may be considered
  - If the itch is present- consider a trial of a non-sedating antihistamines
    - Cetirizine
    - Loratadine
    - Fexofenadine
  - Use of preventative treatment according to condition severity with topical corticosteroids
  - Secondary treatment may include topical calcineurin inhibitors- non-steroidal immunomodulatory agents
    - Tacrolimus
    - Pimecrolimus
  - Appropriate and useful information/ advice including advice on reducing the risk of flares, self-care, myth-busting and advice on what not to use
  - Refer to routine dermatology appointment if management is not controlling the condition
  - Refer to a clinical psychologist if the condition is causing a reduction in quality of life and psychological well-being.
  - Refer to immunology, dermatology, or paediatrics if a food allergy is suspected
- Severe atopic dermatitis
  - Consider admission or referral if indication of eczema herpeticum
  - Consider the possibility of trigger factors or infection
  - Use of emollients in generous amounts
  - Use of potent topical corticosteroid
    - Betamethasone valerate 0.1%
  - Delicate areas of skin (eg. flexures, the face) use a moderate potency corticosteroid
    - Betamethasone valerate 0.025%
    - Clobetasone butyrate 0.05%
  - Do not use potent corticosteroids in children under 12 months old or very potent corticosteroids in children of all ages.
  - If the itch is present- consider a trial of a non-sedating antihistamines
    - Cetirizine
    - Loratadine
    - Fexofenadine
  - If itch is present and affects sleep- consider trial of a sedating antihistamines
    - Chlorphenamine
  - If there is severe, extensive eczema causing psychological distress- consider prescribing a short course of an oral corticosteroid
  - Use of preventative treatment according to condition severity with topical corticosteroids
  - Appropriate and useful information/ advice including advice on reducing the risk of flares, self-care, myth-busting and advice on what not to use
  - Refer to routine dermatology appointment if management is not controlling the condition
  - Refer urgently (within 2 weeks) to dermatology if eczema is severe and has not responded to optimum topical treatment after 1 week.
  - Refer to a clinical psychologist if the condition is causing a reduction in quality of life and psychological well-being.
  - Refer to immunology, dermatology, or paediatrics if a food allergy is suspected
Patients
- Mild atopic dermatitis
  - Use of emollients
  - Use of mild topical corticosteroid (used after 48 hours after flare has been controlled)
  - Appropriate and useful information/ advice including advice on reducing the risk of flares, self-care, myth-busting and advice on what not to use
- Moderate atopic dermatitis
  - Consider the possibility of trigger factors or infection
  - Use of emollients
  - Use of moderately potent topical corticosteroid (used after 48 hours after flare has been controlled)
  - Delicate areas of skin (eg. flexures, the face) use a moderate potency corticosteroid
  - Occlusive dressings or dry bandages may be considered
  - If the itch is present- consider a trial of a non-sedating antihistamines
  - Use of preventative treatment according to condition severity with topical corticosteroids
  - Secondary treatment may include topical calcineurin inhibitors- non-steroidal immuno-modulatory agents
  - Appropriate and useful information/ advice including advice on reducing the risk of flares, self-care, myth-busting and advice on what not to use
  - Refer to routine dermatology appointment if management is not controlling the condition
  - Refer to a clinical psychologist if the condition is causing a reduction in quality of life and psychological well-being.
  - Refer to immunology, dermatology, or paediatrics if a food allergy is suspected
- Severe atopic dermatitis
  - Consider admission or referral if indication of eczema herpeticum
  - Consider the possibility of trigger factors or infection
  - Use of emollients in generous amounts
  - Use of potent topical corticosteroid
  - Delicate areas of skin (eg. flexures, the face) use a moderate potency corticosteroid
  - If the itch is present- consider a trial of a non-sedating antihistamines
  - If itch is present and affects sleep- consider trial of a sedating antihistamines
  - If there is severe, extensive eczema causing psychological distress- consider prescribing a short course of an oral corticosteroid
  - Use of preventative treatment according to condition severity with topical corticosteroids
  - Appropriate and useful information/ advice including advice on reducing the risk of flares, self-care, myth-busting and advice on what not to use
  - Refer to routine dermatology appointment if management is not controlling the condition
  - Refer urgently (within 2 weeks) to dermatology if eczema is severe and has not responded to optimum topical treatment after 1 week.
  - Refer to a clinical psychologist if the condition is causing a reduction in quality of life and psychological well-being.
  - Refer to immunology, dermatology, or paediatrics if a food allergy is suspected

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)

Complications [7]
- Bacterial skin infections
- Viral skin infections (herpes simplex virus)
- Eczema herpeticum
- Psychological effects such as bullying, problems sleeping, self-image/ confidence
Myths behind Atopic Dermatitis
- 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]

Questions you may want to ask your doctor
- 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?