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Allergies and Children Richard E. Freeman MD MPH Korin Trumpie, PA-C Lock Haven University 2013 Includes ◦Asthma ◦Food allergies ◦Atopic dermatitis (eczema) ◦Allergic rhinitis ◦Urticaria Allergic Diseases 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 Allergy 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 PATHWAY 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 Antigen Presenting Cells-Step1 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 T 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 helper Cell Type 2 (TH2) Step 2 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 ◦ 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 IgE – it’s role: STEP 3 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 EOSINOPHILS- Step 4 Eosinophils Mast cells ◦ Derived from cells in bone marrow ◦ Enter circulation and travel to peripheral tissues where they undergo tissue specific maturation ◦ Mature mast cells do not circulate ◦ Located throughout connective tissue and lie next to vessels ◦ Mast cell and basophil degranulate ◦ Releasing mediators of allergenic inflammation: histamine,serine proteases and proteolytics, lipids, cytokines, and chemokines = Allergic Response MAST CELLS- Three patterns of inflammatory reactions ◦ EARLY PHASE RESPONSE ◦ LATE PHASE RESPONSE ◦ CHRONIC RESPONSE Mechanisms of Allergic Inflammation ◦ 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 Increased blood flow Itching Sneezing Wheezing Abdominal cramps Early 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 Late Phase Response ◦ Persist for days to years ◦ Seen in patients with chronic allergic diseases ◦ Contributing factors Recurrent exposure to allergens and microbial agents Tissue remodeling leading to irreversible changes in target organs TH2 cytokines can maintain active inflammation Chronic Response Familial pre-disposition seen Environment plays a big role ◦ ie. Hygiene hypothesis Genetic basis ◦ Controversial ◦ Genetic coding controls systemic expressions of atopy, increased IgE synthesis and eosinophilia ◦ Control local inflammatory response, asthma and atopic dermatitis Genetic Basis for Atopy THE CLEANER OR MORE STERILE THE ENVIRONMENT THE HIGHER THE RISK OF ALLERGIC DISORDERS. MORE CHILDREN in house – LESS ALLERGIES PLAYING IN DIRT/OUTSIDE EARLIERLESS ALLERGIES FREQUENT BATHING/ANTIBACTERIAL SOAPS ◦ MORE ALLERGIES HYGIENE HYPOTHESIS 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? Diagnosis of Allergic Disease 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. ◦? ◦ 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 ALLERGY HISTORY -cont Behaviors ◦ Allergic salute – rubs nose upward with palm of hand ◦ Allergic click – tongue against roof of mouth to scratch soft palate ◦ Rubbing of eyes History ◦ 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 PE Denne-Morgan lines Allergic shiners & Dennie-Morgan lines Nasal crease Transverse Nasal creaseProlonged nasal salute Allergic Facies 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 PE The Snotty Nose Eosinophilia; Total serum IgE: RAST – Radioallergosorbent test, ELISA Skin Allergy Testing – Methacholine Challenge Testbronchial provocation. Non-asthmatics do not constrict. Requires 20% decrease in FEV-1 ◦ peripheral smear and mucous of nose (Hensel Stain) ◦ Parasites/allergies ◦ Sometimes elevated (neither sensitive or specific) ◦ documents allergen specific IgE (less sensitive than skin tests) ◦ inject allergen subq. Some patients have late phase response Diagnostic Testing 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 Treatment 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 Treatment Environment ◦ Irritants Tobacco smoke Wood burning stove Kerosene heaters ◦ Fungi Aspergillis and Penicillium Keep humidity < 50% Wipe down walls and floors Treatment 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 effects DRUG OF CHOICE FOR ANAPHYLAXIS Treatment 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 Treatment 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 Treatment Pharmacologic ◦ Chromones (chromoglycates) Inhibit mast cell degranulation/ mediator release Safe Usually require multiple dosing (short half life) Better for prophylaxis Cromolyn sodium Nedocromil sodium Treatment Pharmacologic ◦ Glucocorticoids Widely used Block more mediators Topical ◦ Ophthalmic drops ◦ Nasal sprays ◦ Inhaled Oral or IV Treatment 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 Treatment ◦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 SHOTS ANAPHYLAXIS 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 Two factors needed for diagnosis ◦ Sensitivity to allergen ◦ Presence of allergen in environment Itchy nose, mouth, eyes, throat, skin, or any area Problems with smell Runny nose Sneezing Tearing eyes ALLERGIC RHINITIS ◦ 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 nonproductive 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) Pruritic skin disease Occurs in 10% of population 80% with AD develop allergic rhinitis and/or asthma Pathology ◦ “itch that rashes” ◦ 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 Dermatitis Atopic Dermatitis Usually begins in infancy ◦ 50% by 1 year ◦ Additional 30% between 1 and 5 years Pruritis is worse at night Scratching leads to eczematous lesions and secondary infections Diagnosis ◦ Main features Pruritis Facial or extensor eczema in infants and children Flexural eczema in adolescents (elbows, knees, wrists) Chronic or relapsing dermatitis Personal or family history of atopic disease Atopic 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 Dermatitis Treatment ◦ Topical Hydration of skin Glucocorticoids Immunomodulators – Elidel (primecrolimus) Tar preparations Phototherapy Atopic 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 Atopic Dermatitis Other Allergic Disorders 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 Other Allergic Disease ANAPHYLAXIS: TREATMENT: Oxygen, Fluids, monitor Epinephrine-SQ Benadryl- IV IM Corticosteriods - IV URTICARIA AND ANGIOEDEMA ◦ ◦ ◦ ◦ ◦ ◦ IgE mediated reaction Usually self-limited Chronic if symptoms last > 6 weeks Treatment: Usually requires systemic meds Antihistamines steroids Other Allergic Disease 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 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 Other Allergic Diseases 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) Foods that may cause a reaction ~ Questions?