Type I Reaction
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Caused by the formation of drug/antigen-specific IgE that cross-links with
receptors on mast cells and basophils.
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This leads to immediate release of chemical mediators, including histamine and
leukotrienes.
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Clinical features: pruritus, urticaria, angio-oedema and, less commonly,
bronchoconstriction and anaphylaxis.
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Common drugs: aspirin, opioids, penicillins and some vaccines.
Type II Reaction
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Cytotoxic reactions based on IgG or IgM-mediated mechanisms.
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These involve binding of antibody to cells with subsequent binding of
complement and cell rupture.
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Mechanism accounts for blood cell dyscrasias such as haemolytic anaemia and
thrombocytopenia.
Type III Reaction
·
Mediated by intravascular immune complexes & arise when drug antigen and
antibodies, usually of IgG or IgM class, are both present in the circulation,
with the antigen present in excess. Slow removal of immune complexes by
phagocytes leads to their deposition in the skin and the microcirculation of
the kidneys, joints and gastrointestinal system.
·
Examples: serum sickness & vasculitis
Type IV Reaction
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Mediated by T cells causing ‘delayed’ hypersensitivity reactions.
·
Examples: contact dermatitis or delayed skin tests to tuberculin, drug-related
delayed-type hypersensitivity reactions include Stevens–Johnson syndrome and
toxic epidermal necrolysis (TEN).
·
Can be divided into four subtypes based on the T-lymphocyte subset and cytokine
expression profile involved.
References:
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