Paediatrics JC116: A Child With Atopic Eczema And Food Allergy Flashcards
Atopic march
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
- Atopic eczema (AD) (first manifestation)
- Food allergy (exacerbate eczema / anaphylaxis / IgE-mediated food reaction)
- Asthma (1-3 years later, severity peaks at ***4-9 yo then ↓ severity)
- Rhinoconjunctivitis (start to develop 2 years later, ***↑ severity throughout life)
Indication: Once develop AD / FA —> more likely to develop Asthma —> Rhinoconjunctivitis
Atopic dermatitis (AD)
**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)
Triggers of itchiness for AD
- Irritants
- soaps / detergents
- disinfectants
- tobacco smoke - Xerosis (Dry skin)
- Microbial agents
- S. aureus
- Viral infection
- Dermatophytes
—> toxins enter skin to trigger inflammatory + immune response - Heat / Sweating
- Contactants
- including dust mites (aeroallergens) —> trigger Th2 response - Psychological stress
- vicious cycle - Foods
- IgE-induced + those having vasodilatory properties
- cowmilk, egg, soy, wheat, nut, fish - Aeroallergens
- Climate
- hot, dry
Food allergy and Atopic dermatitis (+ SpC Paed E-learning: Common Problems In Allergy)
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)
Complications of AD
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
- Viral
- localised: **Verruca, Molluscum, **Herpes
- systemic: ***Kaposi’s herpetiform eruption (Eczema herpeticum) - Mycotic
- **Dermatophyte
- **Candidal
Natural history of AD
- 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
Treatment of Atopic dermatitis
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
- Adjunctive therapy
- Bleach baths, **Wet wrap
- UV phototherapy
- **Biologics
—> Dupilumab: Anti-IL4/IL13 Ab
- ***Immunosuppressants
—> Cyclosporin
—> Methotrexate
—> Azathioprine
Effect of Refractory AD
- Disruption of family life
- Poor QoL
- Lack of sleep
- Absence from school
- Failure to thrive (weight loss, not able to reach full potential)
Use of steroid
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
Wet wrap dressings
- Rehydration + Cooling of skin
- ***Prevent scratching when itchy
- ***Trap moisture —> ↓ itchiness after wrapping
- ***Enhance absorption of topical steroid ointment —> ↓ total dose of topical steroid required
Systemic therapy for AD
- Oral steroids (short course) (not used commonly —> can have rebound effect)
- need slow tapering to avoid rebound - ***Azathioprine (often prolonged)
- ***Cyclosporin A
- Mycophenolate mofetil
- ***Methotrexate
- Phototherapy
Eczema can be managed!
- Correct understanding of eczema
- Act according to prescriptions + instructions of ***immunologist / allergists + dermatologists
- ***Ensure moisture of skin (∵ dry skin is trigger)
- ***Correct use of steroid to control dermatitis
- ***No scratching
- Maintain a relaxed + happy mood, join more extra-curricular activities
Food allergy vs Adverse reaction to food
Adverse reaction to food
1. Toxic
- Food poisoning
- 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
Mechanism of IgE-mediated food allergy
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)
Prevalence of food allergy
- General population: 2%
- Young children (<3): 8%
- HK children: 5%
Specific groups:
4. Young children with severe ***eczema: 70-90%
5. Children with asthma: <10%
Manifestations of food allergy
- Skin
- **Urticaria
- **Angioedema
- ***Eczema (mixed type) - Respiratory
- Rhinitis
- ***Asthma exacerbation - GI tract
- **Diarrhoea, Vomiting
- Eosinophilic GE
- **Enterocolitis - General
- ***Anaphylactic shock - Others
- Migraine
- Hyperactivity
- Sleep disturbances
- Failure to thrive
Regional differences in food allergy
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
Trigger anaphylaxis in HK children
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
Diagnosis of food allergy
- History
- Physical test
- ***Skin test / Blood test (only for confirmation)
- can have false positive
- skin prick: safe, multiple allergens in a session -
**RAST-test (In-vitro test)
- Radioallergosorbent test
- quantification of level of **food specific IgE (IgG not useful!!!) - ***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)
Treatment for Food allergy
-
**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 - Desensitisation
- ***Anti-IgE therapy
Allergy + Immunotherapy clinic
- Deal with cases referred by family doctors / specialists
- Assess condition of food allergy in children
- Conduct community surveys to understand prevalence of food allergy + public awareness of disease
- 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
