Pathophysiology, diagnosis and treatment of anaphylactic and anaphylactoidreactions.

Anaphylaxis is the product of IgE-dependent activation of mast cells and ba sophils, and results in the production of large amounts of mast cell- and b asophil-derived mediators, such as histamine. Anaphylactoid reactions are s imilar to anaphylactic reactions, but are the result of a non-IgE-dependent activation of mast cells and basophils. The pathophysiological role of his tamine in anaphylaxis and anaphylactoid reactions has been assessed in a la rge number of studies showing that plasma histamine levels and urinary conc entrations of methylhistamine increase during anaphylactic and anaphylactoi d reactions, and are significantly correlated with the severity of the reac tion. Moreover, histamine injections in experimental animals and healthy vo lunteers have been found to induce the same clinical symptoms and biologica l alterations as those associated with anaphylaxis. Some clinical manifesta tions of anaphylaxis such as bronchospasm are due to the direct action of h istamine on the cells and tissues, but others, e.g., cardiovascular alterat ions, are mediated by nitrogen oxide released by cells activated by histami ne. Finally, other mast cell- and basophil-derived mediators, such as plate let-activating factor and leukotrienes, may also play a pathophysiological role in anaphylaxis and anaphylactoid reactions. Interactions between the n euroendocrine and immune systems are also involved in anaphylaxis. It has b een shown that physiologic and pathologic alterations in the neuroendocrine system favor the onset of anaphylactic reactions, and that the mediators a nd cytokines involved in anaphylaxis induce alterations in the production o f neurohormones. A large number of substances can induce anaphylaxis, inclu ding food, drugs and hymenoptera venom. Emergency treatment for severe anap hylactic and anaphylactoid reactions is based on epinephrine injections. Th e prognosis for these reactions is poor when epinephrine injection is delay ed. The frequency of relapse is significantly reduced in patients in whom t he substances to which they are allergic or intolerant are known. Thus, all ergy tests should be performed in patients with anaphylaxis, to determine t he allergens responsible for anaphylactic reactions. Finally, the preventio n of relapse is based on allergen eradication (certain foods and drugs), an d on hyposensitization (hymenoptera venom). (C) 2000 Editions scientifiques et medicales Elsevier SAS.