Anaphylaxis occurs in an individual after reexposure to an antigen to which that person has produced a specific IgE antibody. The antigen to which one produces an IgE antibody response that leads to an allergic reaction is called an allergen. The IgE antibodies produced may recognize various epitopes of the allergen. These IgE antibodies then bind to the high-affinity IgE receptor (FcεRI) on the surface of mast cells and basophils. Upon reexposure to the sensitized allergen, the allergen may cross-link the mast cell or basophil surface-bound allergen-specific IgE resulting in cellular degranulation as well as de novo synthesis of mediators.[7] Histamine is thought to be the primary mediator of anaphylactic shock. Many of the signs and symptoms of anaphylaxis are attributable to binding of histamine to its receptors; binding to H1 receptors mediates pruritis, rhinorrhea, tachycardia, and bronchospasm. On the other hand, both H1 and H2 receptors participate in producing headache, flushing, and hypotension