Allergic reactions, drugs immune mechanisms

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

In some drug reactions, several of these hypersensitivity responses may present simultaneously. Some adverse reactions to drugs may be mistakenly classified as allergic or immune when they are actually genetic deficiency states or are idiosyncratic and not mediated by immune mechanisms (eg, hemolysis due to primaquine in glucose-6-phosphate dehydrogenase deficiency, or aplastic anemia caused by chloramphenicol). 

Drug reactions mediated by immune responses can have several different mechanisms. Thus, any of the four major types of hypersensitivity discussed earlier in this chapter (page 967) can be associated with allergic drug reactions ... 

Several types of adverse drug reactions do not easily fit into Cell and Coomb s classification scheme. These include most cutaneous hypersensitivity reactions (such as toxic epidermal necrolysis), immune-allergic hepatitis and hypersensitivity pneumonitis. Another difficulty is that allergic drug reactions can occur via more than one mechanism picryl chloride in mice induces both type 1 and type IV responses. Although other classification schemes have been proposed. Cell and Coomb s system remains the most widely utilized scheme [4-7]. 

---