Allergies in Children

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ALLERGIES IN CHILDREN Present 3-15%, 3 million active cases 2025 expected 50% next pandemic after metabolic x, diabetes, obesity:

ALLERGIES IN CHILDREN Present 3-15%, 3 million active cases 2025 expected 50% next pandemic after metabolic x, diabetes, obesity DR UDAY PATHAK

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Poornamadah poornamidam purnat poornamaduchyate, Poornasya poornamadaya, Poornameva Vashishyate

Immunological fashions in Medicine:

Immunological fashions in Medicine 1960’s & 1970’s Immunoglobulin E 1970’s & 1980’s Mast cells & Eosinophils 1980’s & 1990’s Environment – ante-natal & adult, allergens, Th2 cells 1990’s & 2000’s Microbial experience, Epithelium, Tregs Although undoubtedly a useful model, the textbook ‘skew to Th2’ model is too simplistic to explain allergy Allergy is a disease of impaired immune regulation Where is the regulatory lesion?

Newer Concepts or Confusion:

Newer Concepts or Confusion Cough Variant Exercise Induced Infant , Childhood , and Adult Asthma and allergies Occupational 4 Step Diagnosis and treatment Mild Intermittent Mild persistent Moderate Persistent Severe persistent Upgraded treatment 3months last usually till 6 yrs Newer treatments -RAST, Prick, Asthma Action plan Hypoallergenic bedsheets and pillow covers Hepa Filters Indoor and Outdoor Intrinsic and Extrinsic New Drug responsive


P REVALENCE Every third person in this room suffers from some kind of allergy (66%) One Third have multiple forms. Ingestants, Contactents, Inhalents, Haptens, Injectants etc Only 30% GP, treat as per any protocol.

Factors predisposing to asthma::

Factors predisposing to asthma: 1. Genetic predisposition/family history 2. Atopy/high lgE/atopic dermatitis 3. Viral respiratory illness in early childhood (RSV) Respiratory Syncetial virus etc 4. Environmental exposures (aeroallergens, pollution, Tobacco smoke, Chulha, Dung smoke 5. Living in an urban area 6. Exposure to secondary smoking in childhood 7. Low birth weight 8. Duration of breast feeding 9. Antibiotic use in childhood eg Neomycin, Ampicillin, Sulphas etc 10. Western lifestyle 11. Obesity 12. Diet 13. Vitamin D deficiency

Features 1:

Features 1 Def: An altered state of reactivity to Environmental antigen. Most allergy have target organs that are open directly to the environment Gastrointestinal Respiratory ( Including Eye, Nose, Sinuses ) Skin


Features-2 A family disposition in >50% showing Dendritic cell surface marker D2. These act via Th2 cells of Mast cell, eosinophil and Basophilic origin leading to a production of IgE antibodies. A proliferation of new antigens, coupled with global warming, Lifestyle changes , pollution etc has shown a dramatic increase in allergies. Tracheal Dendritic Cells

Key Elements (6) :

Key Elements (6) 1. Allergens 2. T Cells 3.Antigen Presenting Cells (APC) 4. IgE and its receptors 5. Eosinophil 6. Mast Cells


1. ALLERGENS An allergen is something that triggers an IgE response in genetically predisposed individuals. Molecular weight 10-70 Kilodaltons (kDa). Whereas allergens < 10 kDa does not bridge the Fc region of the IgE antibody molecule, allergens > 70 kDa do not pass the mucus membrane barrier.

2 .T Cells:

2 .T Cells Babies are usually sterile at birth after which they are exposed to allergens and Infections. A Th-1 response produces cytokines that promote phagocytosis Th-2 cells are induced in genetically susceptible atopic individuals that secrete cytokines favoring IgE synthesis. These cytokines IL4 and IL13 act on Eosinophils, Mast cells and Basophils that leads to an outpouring of Histamine 1,2, and 3.

3.Antigen Presenting Cells (APCs):

In-vitro differentiated monocyte-derived Dendritic Cell 3.Antigen Presenting Cells (APCs) The following cells are APCs Dendritic Cells Langerhan Cells Monocytes Macrophages These carry either a DC 1, which promotes Th-1 and no allergy. In atopic individuals they carry DC 2 surface protein that causes Th-2 production and the allergy cascade.

4-IgE and its receptors :

4-IgE and its receptors Fc epsilon R1 and Fc epsilon R2 (CD23) bind to the Alpha chain of the IgE molecule. These are present on all APC cells. Cross linking of receptor bound IgE molecule initiates a complex intracellular leading to a release of various mediators of Inflammation


5.Eosinophils The degranulation of Eosinophils releases 1. Major Basic Protein 2. Eosinophil derived neurotoxin 3. Peroxidase 4. Cationic proteins These cause damage to epithelial cells Induce airway hyper responsiveness Cause degranulation of mast cells and Basophils The Major basic protein blocks muscarinic receptor 2 leading to increase Acetylcholine thereby increasing airway hyperresponse.

6. Mast Cell:

6. Mast Cell Derived from CD 34 progenitor cells in the marrow. Upon entering the circulation they migrate to the peripheral tissues where they mature and STAY. Unlike mature Eosinophils and Basophils, mature mast cells do not circulate in Blood. These lie amongst Epithelial cells of Organs exposed to the environment Preformed mediators e.g.: Histamine, Serine proteases, and proteoglycans are released on degranulation The most important mast cell derived lipid mediators act on the Arachidonic acid pathway ( Cyclooxygenase and Lipooxygenase causing inflammation.


MECHANISMS OF ALLERGY- Th2 Antihistamines work well in Allergic Rhinitis yet they are relatively contraindicated in Asthma where they do not seem to work ? Ipratropium is indicated in Asthma but not in Eczema or Allergic Rhinitis ? 3 Phases Early Phase Response Late Phase response Chronic allergy disease

EARLY PHASE RESPONSE (starts 0-10 minutes and subsides in 1-3 hours):

EARLY PHASE RESPONSE (starts 0-10 minutes and subsides in 1-3 hours) Immediate response caused by Mast cell degranulation which produces Itching, sneezing, wheezing, abdominal cramps etc depending on target organ. Increased vascular permeability..tissue swelling and shock.

LATE PHASE RESPONSE (Starts within hours and lasts 24 hrs:

LATE PHASE RESPONSE (Starts within hours and lasts 24 hrs Maximises around 6 hours producing SKIN- oedema, redness, swelling, itching NOSE- Blockage LUNG- Wheeze An infiltrate of Th-2 cells causing release of TNF and Adhesion molecule causing apoptosis and increased infiltration on Eosinophils


CHRONIC ALLERGIC DISEASE Tissue inflammation lasting days to years. IL3 and IL5 causing delayed apoptosis of cells and self generation of Eosinophil. Tissue remodeling leads to irreversible changes in target organs. Asthma: Thickening of airway wall, Increased submucosal tissue, and smooth muscle hypertrophy and hyperplasia causing a permanent impairment in Lung Function Test. Skin: Lichenification Nose : Initial hypertrophy and polyps, later atrophy

PowerPoint Presentation:

The hygiene hypothesis (Strachan, 1989) Based upon the epidemiology of hay fever “Declining family size, improved household amenities, and higher standards of personal cleanliness have reduced the opportunities for cross-infection in young families. This may have resulted in more widespread clinical expression of atopic disease" ..can be interpreted in terms of a failure to microbially modulate default Th2 responses in childhood Explains how Th2 arise, but… …does not explains why some individuals are allergic and others are not and why the incidence of allergy is increasing. Reduced numbers of IL-12 producing cells? Reduced ability to produce or respond to IL-12? Reduced stimulation of IL-12 by microbial substances?


GENETICS 1 Could be argued that the development of Th2 cells is the default pathway IN allergic individuals. …does not explain why some individuals are allergic and others are not and why the incidence of allergy is increasing. Reduced numbers of IL-12 producing cells? Reduced ability to produce or respond to IL-12? Reduced stimulation of IL-12 by microbial substances?

Genetics:2 :

Genetics:2 Strong Familial disposition 50% if one parent affected 66% if both parents affected 60% heritability in twin studies 5q 23-35 code for IL3,4,5,9,13 and GM-CSF resulting from a Cytosine to Thymidine change at position 589 of the IL4 promotor region. 11q13 codes for the IgE receptor Fc epsilon R1 Beta SPINK-5 gene coding for serine protease mutation causes Nethertons disease –Severe Eczema, asthma and eosinophilia

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Th2 Th1 Th2 Balanced Th1/Th2 at ~2yr Neonatal & infant immune systems The intrauterine environment is powerfully Th2 – this imprints Th2 dominance upon the neonate Serial infections Age Immune response

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Th1 Th2 Unbalanced Th1/Th2 Th2 dominance at ~2yr Delayed maturation of Th1 capacity Few serial infections – hygiene, small family size etc Age Immune response Longer period of time in which to make and establish Th2 responses to environmental antigens (i.e. allergens)

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Y Y Y T cell help to B cells B Antigen Th Th IL-4 and IL-13 CD40 Ligand CD40

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Allergen causes: Predisposition: Dust mite Genetics/family Hx Dog Atopic tendency/High lgE Cat Environmental Other furry pets Exposures -Aeroallergens, pollution, tobacco smoke Cockroaches Living in Western society Mold spores Tobacco exposure in early childhood Tree pollen Duration of breast feeding Grass pollen Antibiotic use in childhood Weed pollen Diet Viruses, Filaria, Bacteria RSV, Flagellates, Worms during Infancy Cow, Soy Milk Infancy, Childhood Food Additives New Chemical Challenge Metals Hapten

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It has been estimated that as many as 2,000 new compounds are introduced annually. chemical incitants, such as formaldehyde, 6 phenol, 7 chlorine, and petroleum alcohol. 8 Commonly encountered chemicals such as glycine, 9 chlorphenothane, toluene and turpentine, air pollutants such as suspended particulates, formaldehyde, and ozone

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L. destructor G. domesticus D. pteronyssinus D. pteronyssinus A. siro T. putrescentiae

Contact Dermatitis, Parthenium:

Contact Dermatitis, Parthenium


metals have been incriminated, among them nickel, cobalt, chromium, 14 , aluminum, 15 mercury, 16 and platinum. 17 Other common environmental chemical incitants include xylene, 18 various acylates, 19 and acrylated prepolymers, 20 benzoyl peroxide, carbon tetrachloride, 21 sulfates, 22 dithiocarbamates, 23 and isocyanates. 24 Metals


urticarial reactions with several additives, such as p-hydroxybenzoic acid methylester, p-hydroxybenzoic acid propylester, benzoic acid, sodium benzoate, ponceau rouge, and indigo carmine. Monroe=s 34 data indicate a causal role played by tartrazine azo dyes and salicylates in the provocation of vascular alterations. Other additives, including sodium nitrite and sodium glutamate, have been found to trigger migraine phenomena in susceptible patients. 35 Additives


Time and space limitations allow only a cursory review of the numerous hygienic products which have been revealed as noxious for the chemically susceptible individual. Among these are a wide variety of cosmetics, 40,41 particularly those containing glycerin, propylene, glycol, or butylene glycol, 42 perfumes, 43,44 and hair products such as dyes, 45,46 creams, 47 sprays, 48 and shampoos. 49 Moreover, sensitivities have been demonstrated to occur in association with lip salve, 50 fingernail preparations, 51 soaps, 52 sanitary napkins, 53 mouthwash, 54 antiperspirants, 55 contact lenses, 56 contact lens solutions, 57 and suntan lotions. 58 Cosmetics


Reports of sensitivities to textiles and to those chemicals used in the processing of clothing continue to apear. ElSaad 59 reports sensitivities to synthetic acrylic fibers, and Burrows= data indicate the existence of contact dermatitis secondary to polyester spin finishes. 60 Recently, the epoxy resins used in manufacturing many trousers have been isolated as triggering agents, and reports on synthetic clothing as environmental antigens are widespread. 61 Products such as spray starch used in the maintenance of fabrics may also be considered toxic for the chemically sensitive individual, 62 for whom, as Larsen=s interesting study suggests, even the metallic buttons on blue jeans may trigger reactions to nickel. 63 Textiles


HISTORY TAKING .1 All symptoms with time line and progression Recurrent and reversible Exposure to common allergens eg .Carpets,moulds, curtains, pollen and nuts etc. Response to previous therapy More than one organ system involved in 80%


HISTORY- 2 Certain charectoristic behaviours associated Allergic Salute (Nasal crease) Repeated sneezing Rubbing of eyes Rapid blinking of eyelids Allergic Cluck (Palatal itch) ADHD and irritability Glue ears ( Inattention)


HISTORY..3 During acute episodes look for aggravation factors. Viral infection Pets and animal contact Smoke exposure, high humidity Mites, Moulds, cockroachs Nuts, cheese, banana, eggs, chinese, foods etc


SEASONAL AEROALLERGENS Certain aeroallergens change with seasons temperature, and Geographic locations. Cold dry air can sometimes incite allergy. Hot humid air incide dust mite allergy Wild plants in India esp Parthenium, Wild grass, Devils tree, Litchi and Mango pollen Trees pollinate – March to July Grasses pollinate – July to October Weeds pollinate – October- March


PERRENIAL (YEAR –ROUND) Once sensitive also to seasonal baseline and worsening in March - April and Sept -Oct Dust mites Animal Dander Cockroach- Inner city Fungi Aspergillus, Pennicilinum,-- Indoor Alternaria– both Indoor and Indoor


History-4 Age is important in both causation and presentation. Infants and young children are first sensitized to Perennial allergens e.g. dust mite, animal dander and fungi. Children getting worm infestations early are protected Th-1 Relevant sensitization to seasonal aerogens takes several years. Food Allergies- more common in infants and young children– GI and skin. If lungs think super infection with RSV, CMV, Herpes, Cytoplasma etc, attaches to the basilar layer of epithelium and triggers Th2 response. Infants seborrhoeic dermatitis, converts to flexural eczema ( Darriers disease), in toddlers and converts to Extensor ecze ma later !


PHYSICAL EXAM- 1 PEFR or Spirometry should be performed to confirm diagnosis of Asthma and to follow up useful in age 5 and above. (reversibility demonstrated) If respiratory distress –Pulse Oximetry. All. Rhinoconjunctivitis observe for mouth breathing, cheilitis, sneezing, sniffing, runny nose and eyes Higher incidence of atopy with cradle cap Age 4 and above, counting upto 20 in a single breath gives a gross value of lung function In Infants and toddlers flexural and facial eczema later converts to extensor eczema of knees and elbows

Physical Exam 2::

Physical Exam 2: Allergies present a dynamic spectrum of Asthma , Eczema and hay fever witch appears to wax and wane. Allergy to something as common as cow milk can mimic Coeliac disease, GERD, Severe Iron deficiency, and chronic diarrhoea. 30% of Cow milk allergies are also allergic to soy protein History of recurrent pneumonia suggests Asthma Pulsus Paradoxus Glue ear, Polyps nasal, Pale boggy mucosa with stringy discharge Skin Xerosis

Physical Exam: 3:

Physical Exam: 3 Lower eyelid puffiness and blueness (Allergic shiners) Dennie Morgan folds. Subconjunctival hgg suggests bronchiolitis or pertussis Improvement with bronchodilators suggests Asthma Fever and purulent discharge not a feature Improvement with position suggests GERD

Physical Exam :4:

Physical Exam :4 Adenoidal hypertrophy, Tonsillar Hypertrophy Post nasal drip Snoring OSAS Pharyngeal submucus lymphoid hypertrophy cobblestoning


DIAGNOSTIC TESTING (vitro) Blood, Nasal secretion, Bronchial eosinophilia RAST 1. Spirometry 2. Allergy Test 3. Histamine Challenge Test 4. Bronchoscopy 5. Fe No Test 6. Hypoxia Challenge Test 7. Sleep Lab 8. Sniff Test 9. .. Environment Pollen Counter End Tidal CO Test Biopsy 10. Exercise Induced bronchoconstriction FEV1 < 12%

Asthma Medications:1:

Asthma Medications:1 Anti-inflammatory medications are most commonly needed. 1. Inhaled corticosteroids (ICS) Asmanex Advair Symbicort Flovent Azmacort Pulmicort Budecort Fluticasone 2. Leukotriene receptor antagonists Montelukast (Singulair) Zatirlukast (Accolate) 3. Leukotriene synthetase inhibitors Zileutin (Zyflo) 4. Short acting B-agonists (SABA) Albuterol HFA Levabuterol Pirbuterol (Maxair) etc 5. Long acting B-agonists (LABA) Salmeterol (Serevent) Fomoterol (Foradil) 6. Combination ICS/LABA


Medicines:2 6. Combination ICS/LABA 7. Theophylline 8. Oral corticosteroids 9. Anti-lgE antibody Omalizumab (Xolair) Plavizumab 10. Occasionally other immune inhibitors Methotrexate Cyclosporin 11. Intravenous , sublingual or subcutaneous immunotherapy

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