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?