Atopic Dermatitis Flashcards
What is dermatitis?
AKA eczema
Inflammation of the skin
What is atopic eczema?
The most common inflammatory skin disease (Dermatosis)
PC of atopic eczema in children?
Cardinal symptom is ITCHING (the itch-scratch cycle)
In >80% of people, it starts in early infancy:
• Often on the face and extensor surfaces; nappy area is often spared
• Cradle cap is common (seborrheic dermatitis)
In older children, it has a typical flexural pattern
Diagnostic criteria for atopic eczema?
Itching
+
3/more of: • Visible flexural rash • History of flexural rash • Personal Hx of atopy, or in a 1st-degree relative • Dry skin in past year • Onset <2 years of age
NOTE - in infants, the cheeks and extensor surfaces are affected, rather than a flexural rash
Signs of chronic eczema?
- Excoriations, i.e: scratch marks
- Lichenification (exaggeration of normal skin creases, due to chronic scratching and rubbing)
Other complications include scarring, pigmentary changes, habit scratching
NOTE - chronic scratching exposes epitopes, leading to sensitisation and the production of autoimmune antibodies
Explain the atopic ‘march’
Eczema begins in infancy
Asthma usually >2 years of age
Hayfever (AKA perennial rhinitis) from the age of 7
Effects of eczema on daily life?
Can reduce QoL and it often affects parents as well
Restriction of lifestyle, e.g: swimming, holiday, pets, clothing
Psychosocial impact, e.g: embarrassment, teasing, etc
Cause of atopic eczema?
Mixture of genetic and environmental factors; it is more common in:
• Westernised cultures
• Industrial areas
Genetic inheritance of atopic eczema?
Multi-gene inheritance
Severity and persistence probably relate to dose effect, i.e: the larger the no. of genes involved, the greater the effect
Genes inv. skin barrier function, over production of inflammatory cytokines, increased IgE production
Explain impaired barrier function in relation to eczema
Cornified cell envelope (CCE) is the main outer cutaneous layer that prevents water loss and prevent entry of infectious agents, irritants and allergens
Impaired barrier function is the MAJOR CAUSE of atopic eczema
What is fillagrin?
Protein present in keratohyalin granules in the granular layer of the epidermis
They help in the terminal differentiation of cells
Effects of fillagrin mutations?
Prevalent mutations cause ichthyosis vulgaris and predispose to atopy
NOTE - ichythyosis is a family of genetic skin conditions characterised by skin, thickened, scaly skin; vulgaris is the most common type
Phenotype of severe ichthyosis vulgaris?
Dry skin
Hyperlinear palms
NOTE - this is caused by fillagrin deficiency and has a strong assoc. with eczema
How common are fillagrin mutations?
1/10 people of European origin carry 1 filaggrin null mutation and have only 50% of the normal amount of fillagrin protein in their skin; these people have dry skin and/or mild ichthyosis vulgaris, with a high risk of atopic eczema
1/90 people carry 2 filaggrin null mutations and have no filaggrin protein in their skin; they have severe ichthyosis vulgaris and a very high risk of atopic eczema
Exacerbating factors of atopic eczema?
Irritants, xerosis (dryness), heat, scratching, infection, inhalent allergens, diet (infants), stress
Epidemiological factors affecting atopic eczema?
Higher in industrialised areas
Other related factors: • Increased washing • Central heating • Dietary factors • Hygiene hypothesis
PC of food allergy and eczema?
Usually infants who present with worsening or eczema +/- type 1 reactions and/or GI effects
Specific IgE levels/prick testing (egg and milks commonest)
NOTE - the majority are not due to food allergy
Prognosis of food allergies in infancy?
Milk allergy resolves by 2-3 years
Egg allergy resolves by 3-5 years
Uses of prick testing?
Tests for immediate type 1 hypersensitivity, e.g: food and latex allergy, although false positives are common
What hypersensitivity reaction is eczema classed as?
Delayed type IV +/- type I reactions