Anaphylaxis can occur in response to any allergen. Common triggers include insect bites or stings, foods, medication and latex rubber.
Food
Many foods can trigger anaphylaxis. The most common are peanut, tree nuts, shellfish, fish, milk, and egg. Severe cases are usually the result of ingesting the allergen. This is usually due to a toxic reaction, rather than the immune system mechanism that occurs with "true" anaphylaxis.
The symptoms, risk for complications without treatment, and treatment are the same, however, for both types of reactions. Some vaccinations are also known to cause "anaphylactoid" reactions.
Venom
Venom from stinging or biting insects such as Hymenoptera or Hemiptera may induce anaphylaxis in susceptible people. These immune mediators cause many symptoms, including common symptoms of allergic reactions, such as itching, hives, and swelling.
Anaphylactic shock is an allergic reaction to an antigen that causes circulatory collapse and suffocation due to bronchial and tracheal swelling.
Different classes of antibodies are produced by B cells to bind and destroy substances that the immune system has identified as potentially dangerous pathogens. Each B cell produces thousands of identical antibodies that can attack a single, small part of a pathogen.
In susceptible individuals, antibodies may be produced against innocuous antigens or allergens, such as components of common foods or plants.
One class, the IgE antibodies, can trigger anaphylaxis.
Production of IgE antibodies may persist for months, even in the complete absence of the allergen. These IgE antibodies associate with a receptor on the surface of mast cells. If the antibody binds to its specific antigen, then the antibody triggers degranulation of the mast cell.
Mast cells become the major effector cells for immediate hypersensitivity and chronic allergic reactions.
Mast cells are large cells found in particularly high concentrations in vascularized connective tissues just beneath epithelial surfaces, including the submucosal tissues of the gastrointestinal and respiratory tracts, and the dermis that lies just below the surface of the skin. Once the FcεR1 are aggregated by the cross-linking process, the immunoreceptor tryrosine-based activation motifs (ITAMs) in both the β and γ chains are phosphorylated by LYN, a protein tryrosine kinase (PTK) belonging to the Src family.
The ITAM domain is simply conserved sequence motif generally composed of two YXXL/I sequences separated by about six to nine amino acids, where Y is tyrosine, L is leucine, I isoleucine and X any amino acid. These SH2 domains (Src homology 2 domian) are found in a numerous cell-signaling proteins and bind to phosphotyrosine through a very specific sequence.
The most notable of these LAT affected molecules is Phospholipase C (PLC). As in many cell signaling pathways PLC hydrolyzes the phosphodiester bond in phosphoatidylinositol-4,5-bisphosphate to yield diacylglycerol (DAG) and inositol-1,4,5-triphosphate (IP¬¬3)¬. A well-characterized second messenger, IP¬3¬, signals the release of calcium from the endoplasmic reticulum.
The influx of cytosolic Ca2+ and phosphoatidylserine further active Phosphokinase C (PKC) bound to DAG. Together, it is the cytosolic Ca2+ and PKC signal the degranulation of the mast cell.4
Although less well mapped, similarly prevailing cell signaling molecules, such as Ras, a monomeric G protein, SOS (son of sevenless homologue) and MAPK (mitogen-activated protein kinase) lead to the upregulation of cytokines and the previously mentioned eicosanoids, prostaglandin D2¬ and leukotriene C4. However, not all IgE are equally capable of inducing such as secretion.
Therefore, researchers have divided all invariant IgEs into two major categories: highly cytokinergic(HC), where the production and secretion of various cytokines and other activation events including degranulation is inducible, and poorly cytokinergic (PC) in which no autocrine signaling is observed.
The former, HC IgE, brings forward a reaction in which cytokines are exocytosed and act as autocrine and paracrine signaling molecules. As such, mast cells with bound HC IgE attract other mast cells even in the absence of antigen crosslinking.
- Symptom onset within minutes to several hours of allergen exposure with involvement of the skin or mucosal tissue and any of the following: hives, itchiness, or swelling of the airway; plus either respiratory difficulty or a low blood pressure.
- Any two or more of the following symptoms within minutes to several hours of allergen exposure: a. Involvement of the skin or mucosa b. Respiratory difficulties c. Low blood pressure d. Gastrointestinal symptoms
- Low blood pressure within minutes to several hours after exposure to known allergen
Apart from its clinical features, blood tests for tryptase (released from mast cells) might be useful in diagnosing anaphylaxis.
Allergy testing may help in determining what triggered the anaphylaxis. In this setting, skin allergy testing (with or without patch testing) or RAST blood tests can sometimes identify the cause.
Further Reading
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"Anaphylaxis"
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