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Drug Allergy
2013[May]; ? (?): 37-90
PMIDC7120502
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Allergic reactions to drugs are not always the result of the drug?s
protein-binding capacity, biotransformation, or degradation. Mediator release may
occur via cross-linking of cell-bound IgE by di-(multi-) valent free drug.
Physiological and pharmacological effects of histamine are mediated through four
receptors, H(1), H(2), H(3), and H(4.) The H(3) receptor has a regulatory role in
the release of neurotransmitters such as serotonin and dopamine; the H(4)
receptor exerts a chemotactic effect on several cell types associated with
allergy and asthma. Cysteinyl leukotrienes and PAF are powerful mediators of
anaphylaxis, asthma, and shock. Sphingosine-1-phosphate, elevated in the lungs of
asthmatics, regulates pulmonary epithelium permeability and contributes to the
pathogenesis of anaphylaxis. Urticaria is a heterogeneous disease with many
subtypes. Both ACE inhibitors and angiotensin II receptor blockers may cause
angioedema. Abacavir changes the shape of the HLA antigen-binding cleft producing
an alteration in the repertoire of self-peptides that bind HLA-B*57:01 and a T
cell response to self-proteins. Drug-induced delayed-type cutaneous
hypersensitivity reactions are mediated by CD4+ and CD8+ CD3+ T cells in the
dermis and epidermis. Granulysin appears to be a key molecule for keratinocyte
killing in TEN/SJS. Drugs provide good examples of types II (immune hemolytic
anemia, drug-induced thrombocytopenia) and III (serum sickness-like)
hypersensitivities.
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