Acute Systemic Anaphylaxis

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Acute Systemic Anaphylaxis

Anaphylaxis is a systemic allergic reaction involving the respiratory and/or the cardiovascular system; it has a rapid onset with the possibility of causing death. However, less severe reaction may be also defined as “anaphylaxis” if there is a high index of suspicion for allergic reaction in the setting of previously diagnosed allergy (Sanchez et al. 1999; Simons et al. 2007; Tang and Liew, 2008). It was observed by Simons (2006) that anaphylaxis is a disease of modern times; sporadic cases report of anaphylaxis were only published in 17th, 18th and 19th centuries and within the past four decades, the rates of allergic diseases have been increasing dramatically. The most common identifiable triggers of anaphylaxis would be food, insect venom or medication while less commonly by allergen such as natural rubber latex or physical factor such as exercise (Simons, 2006). It is usually mediated by immunological mechanism which could result in the sudden systemic release of mast cells and basophils mediator. It will consist of some or all of the following signs and symptoms with the onset within 5 – 30 minutes; diffuse erythema, pruritus, urticaria and/or angioedema; brochospasm; laryngeal edema; hyperperistalsis; hypotension and/or cardiac arrhythmias. Other symptoms that might occur would be nausea, vomiting, lightheadedness, headache, feeling of impending doom and unconscious. However, it must be noted that reaction sometimes might not develop for several hours (Kemp and Lockey, 2002). In many individual, anaphylaxis is mediated by the expansion of T helper 2 cell (TH2-cell), a subset of T cells, together with isotype switching of B cells to generate IgE antibodies specific for common environment allergens (Holgate and Polosa, 2008). Thus, IgE is seen as having a crucial role in anaphylaxis where it would be synthesized in response to an allergen exposure and becoming fixed to FcεRI on the surface of mast cells and basophils. Then, during the re-exposure to the same allergen, it will result in cellular activation, mediator release and immediate hypersensitivity response (Gould and Sutton, 2008; Simons, 2008). Either than the IgE, there are also other potential immunological mechanisms in anaphylaxis which includes the involvement of immune aggregates, IgM, IgG, platelets and T cells; shift in eicosanoid metabolism toward leukotriene formation; and activation of the complement systems. There are also non-immunological factor which could activate mast cell by mechanism not fully understood yet; it includes exercise, cold air, radiation and many more. Regardless of which mechanism the anaphylaxis follows, mast cells and basophils are the one initiating and amplifying the acute allergic response (Simons, 2008).

Anaphylaxis is first initiated by the uptake of allergen by professional antigen presenting cells (APCs) which will present selected peptides on MHC class II molecule to naive T cells. This will then direct them in favour of a TH¬2- cell phenotype where the transcription factor GATA3 mediates cytokine secretion. This process is known as the “sensitization” stage where the dendritic cells play a crucial role as the professional APCs. Then in the presence of co-stimulation, T-cells coordinately upregulate expression of the genes encoded on human chromosome 5q31-33 where the cytokines will be synthesized. There are involved in the class-switching of B cells to IgE synthesis (Interleukin-3 [IL-3] and IL-4), maturation of eosinophils and basophils (IL-3 and IL-4) and the recruitment of mast cells (IL-4, IL-9 and IL13) which are the main mediator-secreting effector cells of the allergic response (Holgate and Polosa, 2008). Once an individual is sensitized to a particular allergen, subsequent encounter to the allergen will cause the crosslinking of IgE-FcεRI complex on the mast-cell surface. This will lead to the “early stage of the allergic reaction” involving the mast-cell degranulation and...
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