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

The lecture includes a detailed immunopathogenesis diagram (Slide 5) showing the progression from uninvolved skin → acute phase → chronic phase ^[1]:

• Uninvolved skin: Th₂ cells and mast cells (MC) are present; skin barrier is intact
• Acute phase: Allergens penetrate the skin → taken up by Langerhans cells (LC) → presented to Th₂ cells → IL-4 drives TH0 → Th₂ differentiation → CLA⁺ Th₂ cells and IgE enter the circulation → mast cell activation
• Chronic phase: Scratching and microbial toxins damage the barrier further → release of cytokines and chemokines → Th₂ cytokines (IL-4, IL-5, IL-13) persist; additionally IL-12 drives TH0 → Th₁ → IFN-γ production → recruitment of eosinophils and macrophages into the tissue

This explains why chronic AD has a mixed Th₂/Th₁ cytokine profile, unlike the purely Th₂-driven acute phase.

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. Microbial superantigen effects → infection can amplify inflammation; routine vaccination should not be withheld merely because a child has AD
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]

The image-heavy slides add morphology that is easy to miss in text:

• Acute infantile AD: ill-defined erythematous papules and plaques on the cheeks and trunk, sometimes weeping or crusted.
• Chronic AD: dry, thickened, lichenified plaques with accentuated skin markings and excoriations - the visual footprint of the itch-scratch cycle.
• Impetiginised AD: rapidly wetter eczema with pustules, oozing or golden-yellow crust; distinguish this from simple dry scale.
• Eczema herpeticum: clusters of similar-looking vesicles or monomorphic punched-out erosions, often painful and associated with rapid deterioration. Uniform lesions are a key visual clue, whereas bacterial crusting is usually more irregular.
• After control: erythema, exudation and thickness settle first; residual lighter or darker pigmentation may remain and does not by itself mean persistent inflammation, treatment failure or a steroid burn. ^[1][16]

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]

Lecture-era AD conventional therapy list: ^[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]

What the before/after image demonstrates: the intense erythema and excoriation settle rapidly, while sharply visible brown patches remain. These are post-inflammatory pigmentary change rather than active eczema. Whole-body wet wraps, especially when combined with topical corticosteroids, should be initiated by a trained clinician because occlusion increases steroid absorption; do not occlude infected eczema. ^[16]

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)

Lecture-era systemic therapy list: ^[1]

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

The refractory-disease photographs show diffuse erythema, xerosis, papulation and thick excoriated plaques before systemic treatment, followed by near-clear skin with residual pigment. Judge treatment response by reduced inflammation, itch and thickening - not by immediate disappearance of pigment. ^[1]

Eczema can be managed! ^[1]

• Correct understanding of eczema
• Act according to prescriptions and instructions of immunologists / allergists and dermatologists
• 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

The lecture diagram (Slide 31) illustrates the full pathway from allergen exposure to anaphylaxis, and how anti-IgE therapy intervenes ^[1]:

The following figures are reproduced as lecture-era estimates and should not be treated as current universal prevalence values:

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 important clinical point is the direction of association - food allergy is more common with earlier and more severe eczema - not the exact 70-90% figure, which reflects selected older cohorts and conflicts with the broader 33% estimate elsewhere in the deck. Do not diagnose food allergy from eczema severity alone or start an elimination diet without an allergy-focused history and appropriate testing.

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

This is the lecture's classic "Big 8" teaching list, not a universal legal list. In Hong Kong, current prepackaged-food labelling rules specify eight substance groups: cereals containing gluten; crustacea; eggs; fish; peanuts/soybeans and their products; milk (including lactose); tree nuts; and sulphites at 10 ppm or more. The legal category is crustacea, not every molluscan shellfish. ^[22]

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

The lecture provides historical cross-reactivity estimates ^[1]:

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

Urticaria, angioedema, respiratory compromise, reproducible gastrointestinal symptoms and anaphylaxis fit established allergic phenotypes. Migraine, hyperactivity and isolated sleep disturbance are non-specific and should not be used to diagnose food allergy. Failure to thrive warrants evaluation for chronic gastrointestinal disease, nutritional restriction and other causes as well as possible non-IgE food allergy.

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 (historical 2006–2008 hospital cohort): ^[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)

Historical context: food was the leading trigger in that 2006-2008 Hospital Authority cohort. The ranking is useful local context but is not a current population surveillance estimate. ^[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

Treat these curves as schematic natural-history trends, not deadlines. Resolution varies with phenotype and the individual child, and suspected tolerance should be reassessed clinically - often with a supervised challenge - rather than by unplanned home re-exposure.

The lecture uses an older 1999 chart to show that dominant food allergens vary by country ^[1]:

The graph has no numeric y-axis and should be read qualitatively, not as current prevalence. It underscores why Hong Kong data cannot simply be extrapolated from Western allergen profiles, but modern local surveillance should be used for present-day counselling.

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

Using the current WAO criteria ^[18]:

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

1. Acute illness with skin/mucosal involvement plus respiratory compromise, reduced blood pressure/end-organ symptoms, or severe gastrointestinal symptoms.
2. Acute hypotension, bronchospasm or laryngeal involvement after a known or highly probable allergen, even without skin findings.

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

Severe crampy abdominal pain or repetitive vomiting, especially with another organ system involved, may meet anaphylaxis criteria; do not automatically classify all gastrointestinal symptoms as mild. ^[18]

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]

The slide's wording about waiting for difficulty breathing or low blood pressure is unsafe if read literally. Give IM adrenaline as soon as anaphylaxis is recognised or strongly suspected; do not wait for shock, and remember that skin findings may be absent. Call emergency services and position the child safely while treatment proceeds. ^[18][19]

For a healthcare professional using an ampoule, give 1 mg/mL adrenaline at 0.01 mg/kg (0.01 mL/kg) IM into the mid-anterolateral thigh, maximum 0.5 mg. If airway, breathing or circulation problems persist, repeat after 5 minutes and escalate emergency care. ^[18][19]

The lecture slide's 0.15 mg at 10-20 kg and 0.3 mg above 20 kg are historical device cut-offs. Auto-injectors deliver fixed doses, and available strengths, weight bands and instructions vary by brand and jurisdiction. Follow the child's current prescribed device and written action plan.

Auto-injector technique: train with the exact prescribed brand. Safety-cap colour, needle end, activation method and hold time are device-specific; the old grey-cap/black-end/10-second photograph in the lecture must not be generalised to every current device. Inject through clothing if necessary into the outer mid-thigh, call emergency services, and give a second prescribed device after 5 minutes if anaphylaxis persists. ^[19]

Never delay adrenaline to give an antihistamine, steroid or inhaler.

The HKU Department of Paediatrics and Adolescent Medicine set up the Allergy and Immunotherapy Clinic in 2003 to assess food allergy in children referred by family doctors and specialists. Key data points ^[1]:

• Approximately 1500 food challenge episodes since 2003
• The slide reports 1 in 10 as a severe reaction. This is historical clinic activity, not a general per-challenge risk estimate; it reinforces the need for a risk-appropriate medically supervised setting with anaphylaxis capability. ^[20]
• Community surveys have been conducted to understand prevalence and public awareness

Atopic dermatitis and food allergy have a profound impact on the social, personal, emotional and financial perspectives of afflicted families. Acceptance. Encouragement. ^[1]

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]