Paediatrics JC116: A Child With Atopic Eczema And Food Allergy

Question 1

Atopic march

Answer 1

Natural history or typical progression of allergic diseases that often begin early in life
0-3 years (peaks at ***0-3 yo then ↓ severity, may even resolve)

***記: AFAR

1. Atopic eczema (AD) (first manifestation)
2. Food allergy (exacerbate eczema / anaphylaxis / IgE-mediated food reaction)
3. Asthma (1-3 years later, severity peaks at ***4-9 yo then ↓ severity)
4. Rhinoconjunctivitis (start to develop 2 years later, ***↑ severity throughout life)

Indication: Once develop AD / FA —> more likely to develop Asthma —> Rhinoconjunctivitis

Question 2

Atopic dermatitis (AD)

Answer 2

**Chronic, **Relapsing, **Inflammatory skin manifestation
- usually get better when get older
- skin: normal areas + eczema areas
- cheeks, limbs
- infants: **extensor surface —> older: ***flexor surface

Epidemiology:
- Incidence of AD ↑ in all industrialised nations (unknown reason: processed food, pollution, climate change)

Mechanism (**Itch-rash cycle):
Acute stage:
Itchy —> Scratching —> Skin barrier defect —> Skin inflammation —> Allergens enter epidermis + dermis —> **Langerhans cells (APC) —> Detect + Processing Ag (i.e. allergens) to **Th2 —> **IL4 —> activate naive Th to become Th2 —> **Th2 skewing —> IL4, IL5, IL13 —> activate Eosinophil + **B cells —> produce ***IgE to bind to allergens, Mast cells, Eosinophils —> Degranulation

Chronic stage:
Scratching / Microbial toxins —> Cytokines + Chemokines —> naive T cells —> IL12 —> **Th1 —> IFNγ —> Eosinophils, **Macrophages —> Chronic inflammation —> chronic changes in 1-2 days (e.g. ***lichenification, bacterial infection (e.g. Staph aureus))

Aim: prevent chronic phase (uncomfortable)

Question 3

Triggers of itchiness for AD

Answer 3

1. Irritants
   - soaps / detergents
   - disinfectants
   - tobacco smoke
2. Xerosis (Dry skin)
3. Microbial agents
   - S. aureus
   - Viral infection
   - Dermatophytes
   —> toxins enter skin to trigger inflammatory + immune response
4. Heat / Sweating
5. Contactants
   - including dust mites (aeroallergens) —> trigger Th2 response
6. Psychological stress
   - vicious cycle
7. Foods
   - IgE-induced + those having vasodilatory properties
   - cowmilk, egg, soy, wheat, nut, fish
8. Aeroallergens
9. Climate
   - hot, dry

Question 4

Food allergy and Atopic dermatitis (+ SpC Paed E-learning: Common Problems In Allergy)

Answer 4

Epidemiology of Food allergy in children:
- Food allergy from birth to 14 yo: 4.8%
- 2-4 times more likely to have asthma, rhinoconjunctivitis, eczema
- 15.6% of food allergy are at risk of anaphylaxis
- All-cause fatal anaphylaxis increased by 6.2% per year
- Fatal food anaphylaxis increased by 9.7% per year

Children:
- moderate to severe AD (33%) have food allergy (anaphylactic type / IgE mediated food allergy)
- ↑ severity of AD —> ↑ risk of food allergy

Adults:
- Low incidence (<2%)
- ∵ Atopic March —> AD / food allergy improves over time

Food responsible (~85% of cases)
- Outgrown, occur earlier in life: cowmilk, egg, soy, wheat
- Persistent, occur later in life: **nuts (peanut, nuts), **seafood (fish, shellfish) (記: 花生+海產)

Question 5

Complications of AD

Answer 5

Skin barrier defect + Defect in molecules defending the skin (e.g. Defensin) —> at risk of infection

Secondary infection
1. Bacterial
- **Impetiginisation (Secondary infection of a lesion that is initially not infected)
—> Staph. aureus, Streptococcus
—> **Impetigo, ***Cellulitis

2. Viral
   - localised: **Verruca, Molluscum, **Herpes
   - systemic: ***Kaposi’s herpetiform eruption (Eczema herpeticum)
3. Mycotic
   - **Dermatophyte
   - **Candidal

Question 6

Natural history of AD

Answer 6

• 60% of patients develop AD by 1 yo
• 85% of patients develop AD by 5 yo
• Rare to see AD after 50 yo
• 50-60% AD patients develop respiratory “allergies” (Atopic March) —> Asthma —> Rhinoconjunctivitis

Question 7

Treatment of Atopic dermatitis

Answer 7

Aims:
1. Prevent + Reduce ***flares of AD
2. Improve overall long-term control of eczema
3. Improve sleep + QoL

Conventional therapy:
1. Educate + develop correct conceptions
2. **Avoid irritants + trigger factors (psychological support: acceptance, encouragement)
3. **Moisturiser, Emollient, Bathoils (1st line: keep skin from being dry)
4. **Topical Corticosteroids (for skin inflammation)
5. **Oral / Topical Antibiotics (for infection)
6. ***Sedating Antihistamines (for better sleep)

Refractory AD:
7. Intermediate treatment with ***Topical calcineurin inhibitors (TCI)
- not as effective as above
- use as adjunct

8. Adjunctive therapy
   - Bleach baths, **Wet wrap
   - UV phototherapy
   - **Biologics
   —> Dupilumab: Anti-IL4/IL13 Ab
   - ***Immunosuppressants
   —> Cyclosporin
   —> Methotrexate
   —> Azathioprine

Question 8

Effect of Refractory AD

Answer 8

1. Disruption of family life
2. Poor QoL
3. Lack of sleep
4. Absence from school
5. Failure to thrive (weight loss, not able to reach full potential)

Question 9

Use of steroid

Answer 9

Wrong use:
1. Stop using after once / twice
2. Stop using after partial improvement
3. Inadequate use
—> Wrong use will result in deterioration!

Correct use:
1. **Use as soon as AD develops (damp down inflammation —> stop vicious cycle of deterioration)
2. **Use different levels of concentration of steroid according to seriousness of AD in different parts of body
- avoid adrenal insufficiency from steroid overuse
3. ***Stop using 1-2 days after dermatitis resolves —> back to Emollient
4. Use according to doctors’ prescription

Question 10

Wet wrap dressings

Answer 10

1. Rehydration + Cooling of skin
2. ***Prevent scratching when itchy
3. ***Trap moisture —> ↓ itchiness after wrapping
4. ***Enhance absorption of topical steroid ointment —> ↓ total dose of topical steroid required

Question 11

Systemic therapy for AD

Answer 11

1. Oral steroids (short course) (not used commonly —> can have rebound effect)
   - need slow tapering to avoid rebound
2. ***Azathioprine (often prolonged)
3. ***Cyclosporin A
4. Mycophenolate mofetil
5. ***Methotrexate
6. Phototherapy

Question 12

Eczema can be managed!

Answer 12

1. Correct understanding of eczema
2. Act according to prescriptions + instructions of ***immunologist / allergists + dermatologists
3. ***Ensure moisture of skin (∵ dry skin is trigger)
4. ***Correct use of steroid to control dermatitis
5. ***No scratching
6. Maintain a relaxed + happy mood, join more extra-curricular activities

Question 13

Food allergy vs Adverse reaction to food

Answer 13

Adverse reaction to food
1. Toxic
- Food poisoning

2. Non-toxic
   - Intolerance
   - Psychologic factors
   - Immunity

Food allergy
Types:
1. **IgE-mediated (Anaphylaxis)
2. **Cell-mediated reactions (T lymphocytes: delayed onset —> AD deterioration)
3. Mixed types (Anaphylaxis + Atopic dermatitis deterioration)
4. Other mechanisms
- **Celiac disease
- **Food protein-induced allergic proctocolitis

Question 14

Mechanism of IgE-mediated food allergy

Answer 14

APC
—> Th2
—> IL
—> B cell —> Plasma cells
—> IgE against peanuts
—> IgE bind to Mast cells (become sensitised) / Basophils
—> Subsequent exposure to peanut
—> Degranulation
—> Systemic reactions (anaphylaxis)

Treatment:
- Anti-IgE (still not present)

Question 15

Prevalence of food allergy

Answer 15

1. General population: 2%
2. Young children (<3): 8%
3. HK children: 5%

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

Question 16

Manifestations of food allergy

Answer 16

1. Skin
   - **Urticaria
   - **Angioedema
   - ***Eczema (mixed type)
2. Respiratory
   - Rhinitis
   - ***Asthma exacerbation
3. GI tract
   - **Diarrhoea, Vomiting
   - Eosinophilic GE
   - **Enterocolitis
4. General
   - ***Anaphylactic shock
5. Others
   - Migraine
   - Hyperactivity
   - Sleep disturbances
   - Failure to thrive

Question 17

Regional differences in food allergy

Answer 17

Unknown reason
- Some studies suggest introduce the particular food earlier can prevent food allergies

Common culprits in HK children:
Infants
1. Hen’s egg
2. Cow’s milk

Older children
1. Seafood (shellfish)
2. Herbs
3. Eggs
4. Peanuts
5. Bird’s nest

***Cow’s milk / Hens egg: Can usually outgrown

Question 18

Trigger anaphylaxis in HK children

Answer 18

Children with acute anaphylaxis

***Food: number 1 trigger
1. Shellfish, fish, seafood
2. Cow milk, dairy
3. Egg
4. Peanut, tree nut
5. Miscellaneous (bird nest, fruits, legume, mushroom, chinese herbs)

• Outgrown, occur earlier in life: cowmilk, egg, soy, wheat
• Persistent, occur later in life: nuts (peanut, nuts), seafood (fish, shellfish)

Cross-reactive of food:
- Peanut allergy: allergic to peas, beans, lentils as well
- Tree nut: brazil, cashew, hazelnut
- Salmon: swordfish, sole
- Shrimp: crab, lobster
- Wheat: barley, rye
- Cow’s milk: hamburger

Question 19

Diagnosis of food allergy

Answer 19

1. History
2. Physical test
3. ***Skin test / Blood test (only for confirmation)
   - can have false positive
   - skin prick: safe, multiple allergens in a session
4. **RAST-test (In-vitro test)
   - Radioallergosorbent test
   - quantification of level of **food specific IgE (IgG not useful!!!)
5. ***Food challenge
   - gold standard
   - under medical supervision
   - potentially dangerous test —> might develop allergic reaction
   - pinch nose so subject cannot smell the food
   - safeguards: individual protocol, appropriate setting (i.e. hospital)

Question 20

Treatment for Food allergy

Answer 20

1. **Adrenaline
   - IM
   - **1:1000 (1 mg/ml)
   - ***0.01 ml/kg/dose
   - children (10-20kg): 150ug (0.15mg)
   - children >20kg / adults: 300ug (0.3mg)
   - use when difficulty breathing / low BP
   - schools, relatives, domestic helpers, food labels, restaurants should help protect the children
   - parents should remind children to be vigilant when dine out, should be taught to choose food correctly to protect themselves
2. Desensitisation
3. ***Anti-IgE therapy

Question 21

Allergy + Immunotherapy clinic

Answer 21

1. Deal with cases referred by family doctors / specialists
2. Assess condition of food allergy in children
3. Conduct community surveys to understand prevalence of food allergy + public awareness of disease
4. Long-term follow up to understand development of the condition

Research data:
1. Develop guidelines for schools
2. First 15-30 mins treatment on the spot most critical
3. Food labelling should be developed