Allergic Disease Dr Garry M. Walsh,
School of Medicine, University of Aberdeen
Allergic Disease Dr Garry M. Walsh,
School of Medicine, University of Aberdeen
Atopy
The predisposition to produce high quantities of Immunoglobulin (Ig)-E
Immediate (Type I hypersensitivity)
Mast cells, basophils, eosinophils, Th2 cells
Allergy
Allergic Disease is mediated by IgE
First described by Prausnitz & Kustner in 1921
Proposed the existence of “atopic reagin” in serum of allergic subjects
45 years later Ishizaka described a new class of immunoglobulin - IgE
Allergic Disease
Seen in 30-35% of the population
Perennial & seasonal allergic rhinitis
Allergic (extrinsic asthma)
Atopic and contact dermatitis
Urticaria
Food intolerance
Allergy
Elevated IgE levels seen in allergy and parasitic infection
Binds to mast cells and basophils
Often specific for harmless environmental factors - allergens
Seasonal (pollen, spores) or perennial (house dust mite)
Mucus production (Runny nose, nasal stuffiness
Itching & sneezing
Treat with antihistamines or nasal steroids
Urticaria
Wheal and flare
Itching
Allergen-induced
Idiopathic – pressure, cold etc.
Food – shellfish, strawberries, peanuts
Treat with antihistamines
Atopic dermatitis
Allergen –induced particularly milk protein from the gut enters blood stream –deposited in skin – mast cell degranulation
Exfoliating eczema and itching
Treat with antihistamines
May progress to asthma
Anaphylaxis
Very acute and severe reaction to allergen
Peanuts, shellfish, penicillin, insect stings
Allergen moves from gut to blood stream
Massive histamine release from mast cells and basophils
Vasodilatation leads to dramatic drop in blood pressure
Often fatal if not treated with adrenaline
Allergens
Environmental substances
Usually benign
Sub-group of individuals exhibit a hypersensitivity reaction (type 1)
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