Drug Hypersensi̇ti̇vity
Özet
Drug hypersensitivity reactions (DHRs) represent complex adverse drug reactions mediated by immunological or inflammatory pathways, contrasting with type A reactions that stem from predictable pharmacological properties. DHRs, or type B reactions, are categorized based on symptom onset, mechanisms of action, and immunologic types under the Gell and Coombs system. Immediate reactions, occurring within an hour, are typically IgE-mediated type I responses that pose anaphylaxis risks, commonly triggered by beta-lactam antibiotics. Delayed reactions manifest after six hours to several weeks and involve types II, III, and IV mechanisms. Type II reactions entail antibody-dependent cytotoxicity leading to conditions like hemolytic anemia, while type III reactions involve immune complex deposition as seen in serum sickness. Type IV reactions are T-cell mediated, driving severe cutaneous conditions like Stevens-Johnson syndrome, toxic epidermal necrolysis, and DRESS syndrome, which often present strong human leukocyte antigen (HLA) genetic associations. Additionally, pseudoallergic reactions mimic true allergies through direct, non-immunological mast cell stimulation via receptors like MRGPRX2, yet differ in diagnosis and prevention. Factors such as viral infections, dosage, and duration further influence these unpredictable hypersensitivity events, necessitating careful clinical evaluation.
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