Atopic dermatitis is a chronic, relapsing, inflammatory skin manifestation. Its incidence is increasing in all industrialised nations. ^[1]

Two competing (and complementary) hypotheses ^[5][8]:

Four key factors for eczema (from Dermatology PBL) ^[6]:

1. Exaggerated cutaneous immune reaction to normally harmless antigens, with paradoxically weakened response to bacteria/viruses (explaining susceptibility to S. aureus, HSV)
2. Abnormal skin barrier function → dryness is a hallmark
3. Superantigen abnormality → infections and vaccinations can cause deterioration
4. Self-protein/keratin mimicry → skin self-proteins can mimic allergens → scratching worsens it (itch-scratch cycle)

Triggers include: irritants (soaps/detergents, disinfectants, tobacco smoke), xerosis (dry skin), microbial agents (S. aureus, viral infections, dermatophytes), heat/sweating, contactants including dust mites, psychological factors, foods (IgE-induced and those with vasodilatory properties), aeroallergens, and climate. ^[1]

60% of patients develop AD by 1 year of age. 85% develop AD by age 5. It is rare to see AD after age 50. 50–60% of AD patients develop respiratory allergies. ^[1]

• Majority clear of eczema by late childhood (50% by 12y, 75% by 16y) ^[5]
• Risk factors for persistence: onset 6–11 years, severe disease, prolonged disease, female sex ^[5]

Secondary infection: ^[1]

• a) Bacterial: Impetiginisation (S. aureus)
• b) Viral: Localised (verruca, molluscum, herpes) and Systemic (Kaposi's varicelliform eruption / eczema herpeticum)
• c) Mycotic: Dermatophyte, Candidal

Patients will suffer: disruption of family life, poor quality of life, lack of sleep, absence from school, failure to thrive. ^[1]

This is testable in SAQs asking about psychosocial impact — remember to mention all five domains.

1) Prevent and reduce flares of atopic dermatitis. 2) Improve overall long-term control of eczema. 3) Improve sleep and quality of life. ^[1]

AD Conventional therapy: ^[1]

1. Educate and develop correct conceptions
2. Avoid irritants and trigger factors
3. Emollients and bath oils
4. Sedating antihistamines
5. Oral or topical antibiotics
6. Topical steroids

Wrong use of steroid: ^[1]

• Stop using after once or twice
• Stop using after partial improvement
• Inadequate use
• Wrong use will result in deterioration!

Correct use of steroid: ^[1]

• Use as soon as AD develops
• Use different levels of concentration of steroid according to the seriousness of AD
• Stop using one to two days after the dermatitis improves
• Use according to doctors' prescription

Treatment strategy from Dermatology PBL ^[6]:

• Start with stronger steroid first to gain rapid control
• Then step down to maintenance with a lower-potency steroid to prevent flares
• Maintain as long as possible; if flare occurs, reset with higher potency
• Slowly wean off steroids over time
• Topical steroids >>> oral steroids in AD (flare-up following oral steroid withdrawal requires even more oral steroid next time — rebound phenomenon)

How wet wrap dressings work: ^[1]

• Rehydration and cooling of skin, reduce itchiness
• Prevent scratching when itchy
• Trap moisture and therefore reduce itchiness after wrapping
• Enhance absorption of topical steroid ointment and therefore reduce the total dose of topical steroid required

Technique: Apply emollient/diluted topical steroid → wrap with wet inner layer → dry outer layer → leave on for hours or overnight. The lecture shows dramatic improvement 3 days after wet wrap. ^[1]

Intermediate treatment with topical calcineurin inhibitors (TCI) for refractory AD ^[1]

• Examples: Tacrolimus (Protopic), Pimecrolimus (Elidel)
• Mechanism: Inhibit calcineurin → block T-cell activation and cytokine release (IL-2, IL-4, IL-5) → local immunosuppression without skin atrophy
• Advantage over steroids: No skin atrophy, safe for face/eyelids/intertriginous areas
• Disadvantage: Burning sensation on initial application; theoretical (unproven) concern about lymphoma risk (FDA black box warning)

Systemic therapy: ^[1]

• Oral steroids (short course)
• Azathioprine (often prolonged)
• Cyclosporin A
• Mycophenolate mofetil
• Methotrexate
• Phototherapy

Eczema can be managed! ^[1]

• Correct understanding of eczema
• Act according to prescriptions and instructions
• Ensure the moisture of the skin
• Correct use of steroid to control dermatitis
• No scratching
• Maintain a relaxed and happy mood; join more extra-curricular activities

Food allergy classification: ^[1] Adverse reaction → Toxic vs Non-toxic Non-toxic → Intolerance, Psychologic factors, Immunity (= food allergy)

Adverse Food Reaction
├── Toxic (affects anyone given sufficient dose, e.g. bacterial toxins)
└── Non-toxic
    ├── Food Intolerance (non-immune, e.g. lactose intolerance = enzyme deficiency)
    ├── Psychologic factors (aversion)
    └── Immune-mediated = TRUE Food Allergy
        ├── IgE-mediated (Type I hypersensitivity)
        ├── Cell-mediated (T-lymphocyte, delayed onset)
        ├── Mixed (e.g. atopic dermatitis itself)
        └── Other mechanisms

Why this classification matters for exams: Food intolerance (e.g. lactose intolerance) is NOT food allergy. Allergy requires an immune mechanism. Sensitisation (positive SPT/specific IgE) does NOT equal allergy unless clinical reaction occurs on exposure. ^[5][9]

Food allergy: ^[1]

1. IgE-mediated
2. Cell-mediated reactions: T lymphocytes – delayed onset
3. Mixed types (atopic dermatitis)
4. Other mechanisms

Prevalence: ^[1]

1. General population: 2%
2. Young children ( < 3 years): 8%
3. Hong Kong children: 5%

Specific groups: 4. Young children with severe eczema: 70–90% 5. Children with asthma: < 10%

Key link between AD severity and food allergy:

Children with moderate-severe AD: 33% have food allergy. Increasing severity of AD correlates with increasing risk of food allergy. Adults have low incidence ( < 2%). ^[1]

The 8 major food allergens: Hen's egg, Cow's milk, Peanut, Tree nuts, Wheat, Soya bean, Fish, Shellfish ^[1]

Mnemonic for outgrown: MEWS (Milk, Egg, Wheat, Soy) → these are the ones kids grow out of.

Manifestations: ^[1]

1. SKIN: urticaria – angioedema, eczema
2. RESPIRATORY: rhinitis – asthma
3. GI TRACT: diarrhoea – vomiting, eosinophilic gastroenteritis, enterocolitis
4. GENERAL: anaphylactic shock
5. OTHER: migraine, hyperactivity, sleep disturbances, failure to thrive

Common culprits – Hong Kong children: ^[1]

• Infants: cow's milk, hen's egg
• Older children: seafood (shellfish), herbs, eggs, peanuts, bird's nest

Triggers of anaphylaxis in HK children (2006–2008): ^[1]

1. Shellfish, fish & seafood
2. Cow's milk and dairy
3. Egg
4. Peanut & tree nut
5. Miscellaneous (bird's nest, fruits, legumes, mushroom, Chinese herbs)

Important: Food is the number one trigger of anaphylaxis in HK children. ^[1]

Every food has its own story… ^[1]

• Cow's milk allergy: peaks at 6 months, resolves by ~3 years
• Hen's egg allergy: peaks slightly later, resolves by ~5 years
• Peanuts, fish, seafood: persistent, may not resolve

Treatment: Epinephrine (adrenaline), Desensitisation, Anti-IgE therapy ^[1]

From supporting notes ^[5]:

Anaphylaxis is diagnosed when ≥1 of the following criteria is met:

1. Acute onset involving skin/mucosal tissue PLUS ≥1 of respiratory or cardiovascular compromise
2. ≥2 of the following after exposure to a likely allergen: (1) skin/mucosal involvement, (2) respiratory compromise, (3) cardiovascular compromise, (4) GI symptoms
3. Hypotension after exposure to a known allergen

Paediatric hypotension thresholds:

• 1 month–1 year: BP < 70 mmHg
• 1–10 years: BP < 70 + (2 × age) mmHg
• 11–18 years: BP < 90 mmHg

Signs of MILD TO MODERATE allergic reaction: ^[1]

• Swelling of lips, face, eyes
• Hives (urticaria)
• Abdominal pain, vomiting

Signs of ANAPHYLAXIS: ^[1]

• Difficulty/noisy breathing
• Swelling of tongue
• Swelling/tightness in throat
• Difficulty talking and/or hoarse voice
• Wheeze or persistent cough
• Loss of consciousness and/or collapse
• Pale and floppy (young children)

If in doubt, give EpiPen! ^[1]

IM adrenaline 1:1,000 (1 mg/mL) at 0.01 mL/kg/dose: ^[1]

• Children 10–20 kg: 150 µg (0.15 mg)
• Children > 20 kg and adults: 300 µg (0.3 mg)

Administration technique (from lecture action plan) ^[1]:

1. Form fist around EpiPen, pull off grey safety cap
2. Place black end against outer mid-thigh (anterolateral thigh)
3. Push down HARD until click is heard/felt → hold for 10 seconds
4. Remove EpiPen; massage injection site for 10 seconds
5. May repeat every 5–15 minutes if suboptimal response ^[5]

The atopic march connects this lecture to GC 040 (Cough and wheezing/asthma) and GC 141 (Chronic cough in children). In children with AD, always screen for:

• Nocturnal cough, exercise-induced wheeze → asthma
• Sneezing, nasal congestion, allergic salute → allergic rhinitis
• Dennie-Morgan folds → allergic conjunctivitis ^[9]

Food allergy can manifest as acute urticaria and progress to anaphylaxis. GC 093 covers the broader differential of urticaria (including chronic urticaria, which is rarely food-related). The key overlap: food allergy is the #1 trigger of paediatric anaphylaxis in HK. ^[1]

Some immunodeficiencies feature eczema-like rashes:

• Wiskott-Aldrich syndrome: eczema + thrombocytopenia + recurrent infections (X-linked)
• Hyper-IgE syndrome (Job syndrome): eczema + very high IgE + cold staphylococcal abscesses
• Ataxia telangiectasia: may feature eczema-like lesions + raised IgE ^[10]

When eczema is associated with severe/unusual infections, growth failure, or lymphopenia, think immunodeficiency rather than simple AD.

Children with multiple food allergies are at risk of nutritional deficiency and failure to thrive. Dietary counselling by a paediatric dietitian is essential. If cow's milk allergic, ensure appropriate formula substitution (extensively hydrolysed or amino acid-based formula). ^[1]

1. A 6-month-old with severe eczema is most likely allergic to which food? → Cow's milk or hen's egg (HK infant culprits)
2. Which food allergies tend to be outgrown? → Milk, egg, soy, wheat (not peanut, tree nuts, fish, shellfish)
3. First-line treatment for anaphylaxis? → IM adrenaline (NOT antihistamines, NOT steroids)
4. Anaphylaxis is mediated by which cells? → Mast cells (IgE cross-linking)
5. Gold standard for food allergy diagnosis? → Oral food challenge

1. Name 3 questions about worsening eczema (from 2019 minicase ^[15]): triggers (new soaps, heat, infection), compliance with emollients/steroids, signs of secondary infection (crusting, oozing, fever)
2. Two relevant personal/family history points: personal history of other atopic diseases (asthma, rhinitis); family history of atopy
3. Two management approaches: correct use of topical steroids + emollients; education about trigger avoidance and steroid compliance

1. Counsel a parent about correct topical steroid use
2. Demonstrate EpiPen administration technique
3. Take a history from a child with suspected food allergy (timeline, reproducibility, systems involved)