Anaphylaxis: Prior sensitization has resulted in an immune response initially mediated by CD4 lymphocytes (of the Th2 variety) that promote mast cell proliferation and plasma cell production of IgE. The IgE becomes bound to mast cells in places such as respiratory tract mucosa. Encountering the allergen again leads to mast cell degranulation with release of primary mediators (such as histamine, serotonin) which cause vasodilation, bronchoconstriction, etc. and release of secondary mediators (such as leukotrienes, prostaglandin) which lead to inflammatory cell infiltrates. The process of mast cell degranulation is diagrammed below:
There are two forms of anaphylaxis:
Systemic anaphylaxis: In some individuals, a severe reaction occurs within minutes, leading to symptomatology such as acute asthma, laryngeal edema, diarrhea, urticaria, and shock. Classic examples are penicillin allergy and bee sting allergy.
Local anaphylaxis (atopy): About 10% of people have "atopy" and are easily sensitized to allergens that cause a localized reaction when inhaled or ingested. This can produce hay fever, hives, asthma, etc. Classic examples are food allergies and hay fever to ragweed pollen.
Laboratory Findings
Type 1 hypersensitivity reactions may be accompanied by an increase in eosinophils, as noted with differential count of peripheral white blood cells.
The serum tryptase may be increased in the hour following mast cell activation.
Measurement of serum total IgE and levels of specific IgE for certain antigens may be undertaken when allergy therapies are planned. Testing for total or specific IgE should be done only when the history is consistent with allergy and specific allergens are suspected as the cause.
Treatment: A standard adult dose of self-injecting epinephrine is 0.3 mg of 1:1000 epinephrine, which raises blood epinephrine from 0.035 ng/mL at rest to about 10 times that amount, the same as for vigorous exercise. In children, the dose is 0.01 mg per kilogram. Injection is subcutaneous or intramuscular. The injection can be repeated 3 times at 10 minute intervals if indicated. The epinephrine can be life-saving for the acute phase of type I hypersensitivity. Additional therapies including albuterol, antihistamines, and corticosteroids may be indicated for the late phase reaction.
Type I hypersensitivity (or immediate hypersensitivity), in the Gell and Coombs classification of allergic reactions, is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen.[1] Type I is distinct from type II, type III and type IV hypersensitivities. The relevance of the Gell and Coombs classification of allergic reactions has been questioned in the modern-day understanding of allergy, and it has limited utility in clinical practice.[2]
Exposure may be by ingestion, inhalation, injection, or direct contact.
Pathophysiology[edit]
Flowchart depicting the pathophysiology of Type I Hypersensitivity reactions [3]
In type I hypersensitivity, B cells are stimulated (by CD4+ Th2 cells) to produce IgE antibodies specific to an antigen. The difference between a normal infectious immune response and a type 1 hypersensitivity response is that in type 1 hypersensitivity, the antibody is IgE instead of IgA, IgG, or IgM. During sensitization, the IgE antibodies bind to FcεRI receptors on the surface of tissue mast cells and blood basophils.[4] Mast cells and basophils coated by IgE antibodies are "sensitized". Later exposure to the same allergen cross-links the bound IgE on sensitized cells, resulting in anaphylactic degranulation, which is the immediate and explosive release of pharmacologically active pre-formed mediators from storage granules and concurrent synthesis of inflammatory lipid mediators from arachidonic acid;[5] some of these mediators include histamine, leukotriene (LTC4 and LTD4 and LTB4), and prostaglandin, which act on proteins (e.g., G-protein coupled receptors) located on surrounding tissues.[5] The principal effects of these products are vasodilation and smooth-muscle contraction.
Type I hypersensitivity can be further classified into immediate and late-phase reactions. Within minutes of exposure to an antigen, the immediate hypersensitivity occurs, releasing histamines and lipid mediators which are responsible for the initial allergic reaction response. However, about 4-12 hours after antigen exposure, a cough and wheezing may persist in the patient, along with swelling and redness of the skin. This is known as the late-phase hypersensitivity reaction which can last from approximately 1-3 days and is caused by the release of additional mediators from the mast cells and basophils. [6]
The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock.
Treatment and prognosis[edit]
If multiple systems are involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.
Treatment usually involves adrenaline (epinephrine) because it counteracts anaphylaxis by increasing blood flow and relaxing bronchial muscles that block one’s airways.[8] Antihistamines and corticosteroids are also commonly used in less severe reactions.[9]