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Anaphylaxis
(redirected from homologous anaphylaxis)

   Also found in: Dictionary/thesaurus, Medical, Wikipedia, Hutchinson 0.03 sec.
anaphylaxis (ăn'əfəlăk`sĭs), hypersensitive state that may develop after introduction of a foreign protein or other antigen into the body tissues. When an anaphylactic state exists, a second dose of the same protein (commonly an antibiotic such as penicillin, or certain insect venoms) will cause a violent allergic reaction. Anaphylaxis results from the production of specific antibodies in the tissues in very high concentration; the violent reaction is produced by the neutralization of antigens by the antibodies. The histamines released during the reaction are thought to cause the most damage, i.e., severe vasodilation and loss of capillary fluid, resulting in circulatory collapse. Other symptoms include urticaria or edema, choking, coughing, shock, and loss of consciousness. Death may occur within 5 to 10 min if no medical help is available. Anaphylaxis differs from immunity immunity, ability of an organism to resist disease by identifying and destroying foreign substances or organisms. Although all animals have some immune capabilities, little is known about nonmammalian immunity.
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; in immunity, antibodies circulate in the blood and neutralize antigens without producing a violent reaction. See also allergy allergy, hypersensitive reaction of the body tissues of certain individuals to certain substances that, in similar amounts and circumstances, are innocuous to other persons. Allergens, or allergy-causing substances, can be airborne substances (e.g.
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; serum sickness serum sickness, hypersensitive response that occurs after injection of a large amount of foreign protein. The condition is named for the serum taken from horses or other animals immunized against a particular disease, e.g., tetanus or diphtheria.
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anaphylaxis

Severe, immediate, potentially fatal bodily reaction to contact with a substance (antigen) to which the individual has previously been exposed. Often triggered by antiserum, antibiotics, or insect stings, the reaction's symptoms include skin flushing, bronchial swelling (with difficulty breathing), and loss of consciousness. Shock may follow. Milder cases may involve hives and severe headache. Treatment, consisting of injection of epinephrine, followed by antihistamines, cortisone, or similar drugs, must begin within minutes. Anaphylaxis may be caused by extremely small amounts of antigen.


Anaphylaxis

A generalized or localized tissue reaction occurring within minutes of an antigen-antibody reaction. Similar reactions elicited by nonimmunologic mechanisms are termed anaphylactoid reactions. In humans, the clinical manifestations of anaphylaxis include reactions of the skin with itching, erythema, and urticaria; the upper respiratory tract with edema of the larynx; the lower respiratory tract with dyspnea, wheezing, and cough; the gastrointestinal tract with abdominal cramps, nausea, vomiting, and diarrhea; and the cardiovascular system with hypotension and shock. Individuals undergoing anaphylactic reactions may develop any one, a combination, or all of the signs and symptoms. Anaphylaxis may be fatal within minutes, or may occur days or weeks after the reaction, if the organs sustained considerable damage during the hypotensive phase.

Anaphylaxis in humans is most often the result of the interaction of specific IgE antibody fixed to mast cells and antigen. Two molecules of IgE are bridged by the antigen, which may be a complex protein or chemical (hapten) bound to protein. The antigen-antibody interaction leads to increased cell-membrane permeability, with influx of calcium and release of either preformed or newly formed pharmacologic mediators from the granules. Preformed mediators include histamine and eosinophilic or neutrophilic chemotactic factors. Newly formed molecules include leukotrienes or slow-reacting substance of anaphylaxis and prostaglandins. The mediator action induces bronchoconstriction, vasodilation, cellular infiltration, and increased mucus production.

Another mechanism for induction of anaphylaxis in humans occurs when antigen binds to preformed IgG antibody and complement components interact with the antigen-antibody complex. The early components of the complement system bind to the antibody molecule, leading to activation of other complement components. During the activation, components known as anaphylatoxins (C3a and C5a) are released which may directly cause bronchoconstriction with respiratory impairment, and vasodilation with hypotension or shock. See Complement, Eicosanoids

Anaphylaxis due to IgE mechanisms has been associated with foreign proteins such as horse antitoxins, insulin, adrenocorticotropic hormone (ACTH), protamine, and chymopapain injected into herniated discs; drugs such as penicillin and its derivatives; foods such as shellfish, nuts, and eggs; and venom of stinging insects. Anaphylaxis mediated by IgG is seen in blood-transfusion reactions and following the use of cryoprecipitate, plasma, or immunoglobulin therapy.

After the identification of the inciting agent for the anaphylactic reaction, prevention is the best mode of therapy. Immunotherapy with insect venom and desensitization with certain drugs are effective prophylactic measures. Individuals with recurrent episodes of anaphylaxis, when the etiological cause is unknown and preventive measures are impractical, should be provided with epinephrine in a form that can be self-administered whenever symptoms occur. See Epinephrine

The treatment of anaphylaxis is aimed at reducing the effect of the chemical mediators on the end organs and preventing further mediator release. The drug of choice for this is epinephrine given subcutaneously in repeated doses. Additionally, a clear airway and appropriate oxygenation must be maintained; hypotension should be treated, as should any cardiac arrhythmia. See Antigen-antibody reaction, Hypersensitivity


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