Allergies and Children Allergies and Children Richard E. Freeman MD MPH

Korin Trumpie, PA-CLock Haven University

2013

Allergic DiseasesAllergic Diseases

Includes

◦Asthma◦Food allergies◦Atopic dermatitis (eczema)◦Allergic rhinitis◦Urticaria

AllergyAllergy

Allergies: (allos=other & ergon=reaction)

◦Used the term when referring to his patients who expressed an “altered state of reactivity” to common environmental antigens Clements von Pirquet- Austrian Pediatrician 1906

1960’s discovered that most patients with allergy problems produced IgE in response to antigens

ALLERGEN:a type of antigen that produces an

abnormally vigorous immune response in which the immune system fights off a perceived threat that would otherwise be harmless to most persons

by stimulating a type-I hypersensitivity reaction in atopic individuals through Immunoglobulin E (IgE) responses

ATOPY:/ˈætəpi/; Greek ἀτοπία - placelessness, out

of place, special, unusual, extraordinary)Hereditary (familial) predisposition in which

a individual responds to several or many common environmental allergens but only after sensitization.

BUT NOT ALL Allergic REACTIONS ARE ATOPIC

Not all allergic reactions are IgE mediated

Non IgE mediated◦More poorly understood◦T-cell mediated (Th1)◦Usually delayed in onset 4-28 hours after

exposure

Non-allergic rhinitis

THE ALLERGIC PATHWAYTHE ALLERGIC PATHWAY

Antigen Presenting Cells-Antigen Presenting Cells-Step1Step1

Antigen-presenting cells◦Dendritic cell, Landerhan cells, macrophages

◦Induce allergic inflammation by “presenting” allergens to T- cells Dendritic and Langerhan cells can “prime” naïve

T-cells◦Dendritic cells in skin, intestine and lung are

immature Actively phagocytize antigens Cells migrate to area lymph nodes Antigens are fully processed & converted

◦ Causing T-cells to proliferate and differentiate

T helper Cell Type 2 (TH2)T helper Cell Type 2 (TH2) Step 2 Step 2

T helper cells Type 2 (TH2)◦Atopic persons respond by activation of TH2

helper cells◦Secrete cytokines that favor IgE mediated

responses◦Also secrete interleukins which

Switch immunoglobulin isotypes to IgE Enhance IgE synthesis Differentiate and develop eosinophils (from stem cells) Contribute to mast cell development

◦Th2 thought to play big role in development of asthma and allergies

T helper cells Type 1 (TH1)

Non-atopic person: responds to exposure to potential allergens by making

TH1 cells

Secrete cytokines that stimulate IgG responses

IgE – it’s role: STEP 3IgE – it’s role: STEP 3

IgE◦Derived from Plasma cells (activated

Lymphocytes)◦memory

◦Acute allergic response is dependent on IgE and its ability to bind to allergen

◦Binding initiates intracellular cascade

EOSINOPHILS- Step 4EOSINOPHILS- Step 4

Eosinophils◦Help defend against parasites◦Found in peripheral blood and tissue◦Accumulate where allergic rxns take place◦Contain intracellular granules that are sources of inflammatory proteins These proteins

◦Damage epithelial cells◦Induce airway hyper-responsiveness◦Degranulate basophils and mast cells

EosinophilsEosinophils

MAST CELLS-MAST CELLS-

Mechanisms of Allergic InflammationMechanisms of Allergic Inflammation

Three patterns of inflammatory reactions◦EARLY PHASE RESPONSE◦LATE PHASE RESPONSE◦CHRONIC RESPONSE

Early Phase ResponseEarly Phase Response

◦IMMEDIATE (from mast cell degranulation)

◦Occurs within minutes of allergen exposure

◦Resolves within 1 to 3 hours◦Associated with increased local vascular permeability

Tissue swelling Sneezing Increased blood flow Wheezing Itching Abdominal

cramps

Late Phase ResponseLate Phase Response

◦Occur within hours of exposure◦Reach peak at 6 to 12 hours◦Resolve by 24 hours◦Associated with infiltration of neutrophils and eosinophils, then basophils, monocytes,macrophages and TH2 cells

Skin – redness, edema, induration Nose - sustained nasal blockage Lungs - wheezing

Chronic ResponseChronic Response

◦Persist for days to years◦Seen in patients with chronic allergic diseases

◦Contributing factorsRecurrent exposure to allergens and microbial agents

Tissue remodeling leading to irreversible changes in target organs

TH2 cytokines can maintain active inflammation

Genetic Basis for AtopyGenetic Basis for Atopy

Familial pre-disposition seenEnvironment plays a big role

◦ie. Hygiene hypothesisGenetic basis

◦Controversial◦Genetic coding controls

systemic expressions of atopy, increased IgE synthesis and eosinophilia

◦Control local inflammatory response, asthma and atopic dermatitis

HYGIENE HYPOTHESISHYGIENE HYPOTHESIS

THE CLEANER OR MORE STERILE THE ENVIRONMENT THE HIGHER THE RISK OF ALLERGIC DISORDERS.

MORE CHILDREN in house – LESS ALLERGIESPLAYING IN DIRT/OUTSIDE EARLIER- LESS

ALLERGIESFREQUENT BATHING/ANTIBACTERIAL SOAPS-

◦ MORE ALLERGIES

Diagnosis of Allergic DiseaseDiagnosis of Allergic Disease

HISTORY◦A careful History and P/E remain the most

effective diagnostic means of diagnosis.

◦Description of symptoms- severity◦Triggers- inhaled, food, pets, ◦Place-home, school, outside, bedroom,daycare◦Age at presentation

Infants and young children-- food, environment Older children-- seasonal

◦Timing-Seasonal vs Perennial, night-time, morning, activity

◦- How long do the symptoms last?

DESCRIPTION OF SYMPTOMS

◦HEENT: Congestion, rhinorrhea, type of nasal discharge,, sneezing or pruritus of nose or eyes

◦Lungs: Wheezing, Cough, Shortness of Breath

◦Skin: Rash, (eczema, contact dermatitis, uricaria)

◦GI tract: nausea, diarrhea, abdominal pain

◦Other complaints: headache, fatigue, lethargy, impaired concentration, and difficulty in learning.

◦?

ALLERGY HISTORY -contALLERGY HISTORY -cont

◦MEDICATIONS: Meds used and how he/she responds to them

◦PAST MEDICAL HISTORY atopic conditions,( i.e. eczema), drug allergy, food allergy,

recurrent infections such as sinusitis and otitis media

◦FAMILY HISTORY 50% risk with one positive parent 66% risk if both parents have positive history

HistoryHistory

Behaviors

◦Allergic salute – rubs nose upward with palm of hand

◦Allergic click – tongue against roof of mouth to scratch soft palate

◦Rubbing of eyes

PEPE

◦PE: TOROUGH◦ALLERGIC FACIES◦Allergic shiner – gray purple color to lower lids

Found in 60% allergic patients Found in 40% of non-allergic patients Dennie-Morgan lines- creases from inner canthus

parallel and underneath rim of lower lid◦Allergic transverse nasal crease◦Elongated facial structures-

mouth breathing

Allergic shiners &Allergic shiners &Dennie-Morgan linesDennie-Morgan lines

Denne-Morgan lines

Transverse Nasal crease- Transverse Nasal crease- Prolonged nasal saluteProlonged nasal salute

Nasal crease

Allergic FaciesAllergic Facies

PEPE

Physical Exam◦Allergic facies◦Skin – dry, urticaria, eczema◦Eyes - ropy discharge, cobblestoning of

conjunctivae◦Ears - check for serous fluid◦Nose – Turbinates- boggy, pale to purple

rather than beefy red◦Mouth-High arched palate from chronic

mouth breathing, and tongue thrusting Dental malocclusion

◦Lungs – wheezing

The Snotty NoseThe Snotty Nose

Diagnostic TestingDiagnostic Testing

Eosinophilia;◦ peripheral smear and mucous of nose (Hensel Stain)◦ Parasites/allergies

Total serum IgE:◦ Sometimes elevated (neither sensitive or specific)

RAST – Radioallergosorbent test,◦ documents allergen specific IgE (less sensitive than skin

tests)

ELISA

Skin Allergy Testing –◦ inject allergen subq. Some patients have late phase

response

Methacholine Challenge Test- bronchial provocation. Non-asthmatics do not

constrict. Requires 20% decrease in FEV-1

TreatmentTreatment

Environmental Control

◦Majority of our time spent indoors

◦Improved building causes increase humidity and concentration of indoor allergens

◦Dust mite In bedding, carpet, upholstered furniture Fecal pellets are source of allergen Do not survive in humidity <50% Emphasize control in bedroom

TreatmentTreatment

Environment

◦PETS Cats more sensitizing than dogs Hair, dander, saliva main sources of allergens Remove pet – still takes 6 months to clear

allergens Keep one room pet free

◦Insects and pests Mice, cockroaches Limit access to home and food

TreatmentTreatment

Environment

◦Irritants Tobacco smoke Wood burning stove Kerosene heaters

◦Fungi Aspergillis and Penicillium Keep humidity < 50% Wipe down walls and floors

TreatmentTreatment

PHARMACOLOGIC

◦Adrenergic agents- ◦ 2 adrenergic receptor sites

Alpha-adrenergics◦Constriction of small blood vessels in the bronchial mucosa◦Used for nasal congestion: pseudoephedrine (CAUTION)

Beta-adrenergics- short and long action ◦Used in treatment of asthma◦B-2 produces bronchodilation

Epinephrine has alpha and beta effectsDRUG OF CHOICE FOR ANAPHYLAXIS

TreatmentTreatment

Pharmacologic

◦ Anticholinergic agents Diphenhydramine (Benadryl)

◦ Use: Skin manifestations- urticaria, itching◦ Sedating, ◦ Avoid in asthma

Ipratroprium bromide (atrovent) – atropine-like◦Inhibits vagally mediated responses◦MDI or nebulized for asthma◦Nasal spray,◦ limited to severe cases,

does not alleviate sneezing, congestion or pruritis

TreatmentTreatment

Pharmacologic

◦Antihistamines Most frequently used H-1 receptor causes allergic inflammation, pain,

pruritis, vasodilation, increased mucous production

1st generation H-1 antihistamines cause somnolence and impaired cognition – benadryl, phenergan

2nd generation negligible side effects and once a day dosing- loratadine

TreatmentTreatment

Pharmacologic

◦Chromones (chromoglycates) Inhibit mast cell degranulation/ mediator release Safe Usually require multiple dosing (short half life) Better for prophylaxis

Cromolyn sodium Nedocromil sodium

TreatmentTreatment

Pharmacologic

◦Glucocorticoids- Widely used Block more mediators Topical

◦Ophthalmic drops◦Nasal sprays◦ Inhaled

Oral or IV

TreatmentTreatment

Pharmacologic

◦Leukotriene inhibitors Inhibit either production or receptor binding of

leukotrienes Mild anti-inflammatory and bronchodilator effect Mainly used in asthma Singulair

◦Asthma◦Allergic rhinitis◦Exercise induced asthma

◦IMMUNOTHERAPY◦ (ALLERGY SHOTS)

◦ Reserved for diseases that responds to this form of treatment

◦. ◦Insect anaphylaxis-highly recommend◦DRAW BACKS:

Expensive-usually under Allergist supervision (initiation phase)

◦ painful,◦ long-term treatment

Not for food or latex allergies◦Anaphylaxis risk◦ALWAYS-

ALLERGY SHOTSANAPHYLAXIS RISK

◦Initiation of new regimen◦Dosage/allergen change◦Local reaction at the last injection site (worse)◦Hx of anaphylaxis to allergen in shot

ALWAYS ALWAYS ALWAYS Check patients name, dose, last reaction in chart. Name on bottle matches

patient Have a second person check dosage Keep patient for designated time post-shot Have Anaphylaxis meds readily available Educate staff in all aspects ANY questions call Allergist

ALLERGIC RHINITIS

ALLERGIC RHINITISALLERGIC RHINITIS

Two factors needed for diagnosis◦Sensitivity to allergen◦Presence of allergen in environment

Itchy nose, mouth, eyes, throat, skin, or any area

Problems with smellRunny noseSneezingTearing eyes

◦SEASONAL ALLERGIC RHINITIS (SAR)

◦20% Itching of ears, nose, palate or throat is the prominent feature

Sneezing with tearing of eyes is common

Runny and/or stuffy nose with a non-productive cough 2o to post-nasal drainage

Sinus headache or earache with altered smell and taste

◦PERENNIAL ALLERGIC RHINITIS (PAR)

◦40%Persistent, chronic and generally less severe than SAR

Nasal congestion is the most common symptom

Patient complains of a “persistent cold” or “chronic sinusitis”

ATOPIC DERMATITIS (ECZEMA)

Atopic DermatitisAtopic Dermatitis

Pruritic skin disease◦“itch that rashes”

Occurs in 10% of population

80% with AD develop allergic rhinitis and/or asthma

Pathology◦T-cells in skin produce decrease in interferon◦Develops intercellular edema in acute lesions

◦Chronic lesions have hyperplastic epidermis, ◦hyperkeratosis and decreased intercellular edema

Genetics suggest strong maternal influence

Atopic DermatitisAtopic Dermatitis

Usually begins in infancy◦50% by 1 year◦Additional 30% between 1 and 5 years

Pruritis is worse at nightScratching leads to eczematous lesions

and secondary infections

Atopic DermatitisAtopic Dermatitis

Diagnosis◦Main featuresPruritisFacial or extensor eczema in infants and children

Flexural eczema in adolescents (elbows, knees, wrists)

Chronic or relapsing dermatitisPersonal or family history of atopic disease

Atopic DermatitisAtopic Dermatitis

Treatment

◦Identify and eliminate triggers

Irritants – soaps, chemical, smoke, abrasive clothing Foods – must take careful history, milk protein Aero-allergens – fungi, dander, grass, ragweed Infection – viral, bacterial or fungal

◦Systemic

Antihistamines Glucocorticoids Cyclosporine (psoriasis) Interferon

Atopic dermatitisAtopic dermatitis

Treatment◦Topical

Hydration of skin Glucocorticoids Immunomodulators – Elidel (primecrolimus) Tar preparations Phototherapy

Atopic DermatitisAtopic Dermatitis

Complications◦Repeated infections◦Chickenpox, herpes can spread over body◦Smallpox vaccination can be fatal

Prognosis◦Spontaneous remission after age 5 yrs in some◦Poor prognosis

Widespread AD in childhood Early onset of AD Allergic rhinitis or asthma Only child Family history Very high IgE

Other Allergic Disorders

Other Allergic DiseaseOther Allergic Disease

ANAPHYLAXIS◦Outside hospital

usually due to food- peanuts, seafood, insect stings Peanut Butter and schools

◦Inside hospital due to meds or latex

◦Clinical manifestations Usually very apparent Diffuse Edema – facial, oral, laryngeal Hypotension & Tachycardia SHOCK like state Sometimes nausea and abdominal cramps are presenting

symptoms

ANAPHYLAXIS:TREATMENT:Oxygen, Fluids, monitor

Epinephrine-SQBenadryl- IV IMCorticosteriods - IV

Other Allergic DiseaseOther Allergic Disease

URTICARIA AND ANGIOEDEMA◦IgE mediated reaction◦Usually self-limited◦Chronic if symptoms last > 6 weeks◦Treatment: Usually requires systemic meds◦Antihistamines◦steroids

Other Allergic DiseasesOther Allergic Diseases

DRUG REACTIONS◦True allergic response requires prior

sensitization◦Pseudo-allergic reactions – immune

mechanisms not involved◦Ampicillin/EB viral eruption- labeled as allergic

◦Treatment:◦ STOP offending MED◦ Systemic meds

Other Allergic DiseasesOther Allergic Diseases

SERUM SICKNESS◦Immune complex mediated vasculitis

◦Begins 7 to 21 days after injection of foreign protein

◦Original site may become red and swollen

◦Sx – fever, malaise, rash, may have joint pain

◦Rashes are morbilliform and urticarial

◦Treat with antihistamines and glucocorticoids

Foods that may cause a Foods that may cause a reactionreaction

Old way of thinking was that certain foods are more likely to cause a rxn in infants and should be avoided until after 12 months◦ Eggs, nuts, seeds, legumes, wheat, corn, citrus fruits and

juices, seafood-shellfish

However there is no evidence to support this theory, and it is now thought that WAITING to begin foods can INCREASE the likelihood of developing food allergies

Whole Cow’s milk can be started at 1 y/o

No honey (carries the risk of botulism)

~Questions?