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Mechanisms of drug eruptions: Part I
Author(s) -
Breathnach SM
Publication year - 1995
Publication title -
australasian journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.67
H-Index - 53
eISSN - 1440-0960
pISSN - 0004-8380
DOI - 10.1111/j.1440-0960.1995.tb00953.x
Subject(s) - toxic epidermal necrolysis , medicine , drug eruption , erythema multiforme , drug , angioedema , immunology , serum sickness , acute generalized exanthematous pustulosis , dermatology , immune system , pemphigus , allergy , vasculitis , drug reaction , disease , antibody , pharmacology , pathology
SUMMARY The pathogenetic mechanisms underlying common, and less common but severe, adverse cutaneous drug reactions are reviewed. Pharmacogenetic variability may account for a susceptibility to serious drug reactions to sulphonamides and anticonvulsants, as well as to lupus erythematosus (LE)‐like syndrome. Exanthematous drug reactions may have an immunological basis. Cell mediated cutaneous drug reactions, including lichenoid reactions, LE‐like syndrome, fixed drug eruption, erythema multiforme, Stevens‐Johnson syndrome and toxic epidermal necrolysis, will inevitably involve elements of the skin immune system. Graft‐versus‐host disease provides a useful model for aspects of these drug‐induced disorders. Urticaria, angioedema, anaphlyaxis and anaphylactoid reactions may involve Type I immunoglobulin (Ig)‐mediated or Type III hypersensitivity, or may be caused by pharmacological, non‐allergic means. Drug‐induced vasculitis, serum sickness and the Arthus phenomenon are manifestations of the immune complex disease. Drug‐induced pemphigus may involve immune dysregulation, but several thiol‐containing drugs are able to cause antibody‐independent acantholysis directly.