A recent update of pharmacogenomics in drug-induced severe skin reactions

Chun Yu Wei, Tai-Ming Ko, Chen Yang Shen*, Yuan Tsong Chen

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


Summary: In some adverse drug reactions (ADRs), genetic predisposition plays a significant role in pathogenesis, and the skin is the most frequently reported target. These severe cutaneous ADRs include bullous fixed drug eruptions (FDE), acute generalized exanthematous pustulosis (AGEP), drug-induced hypersensitivity syndrome (HSS), Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN). The putative contribution of individual effector cells in drug hypersensitivity is briefly mentioned. To trigger these drug hypersensitivities, certain class I HLA alleles (e.g., HLA-A and HLA-B alleles) and certain class II HLA alleles (e.g., HLA-DR alleles) have been recently found to be the genetic determinants. One of the best characterized examples mentioned in this article is HLA-B*1502 to determine the incidence of carbamazepine-induced SJS. How drugs are processed and presented by these HLA alleles to activate immune responses has been explained by several hypotheses. Further implication of pharmagenomic findings to prevent drug-induced severe skin reactions can be achieved by pre-screening putative risk HLA alleles before using drugs.

Original languageEnglish
Pages (from-to)132-141
Number of pages10
JournalDrug Metabolism and Pharmacokinetics
Issue number1
StatePublished - 1 Jan 2012


  • Adverse drug reactions
  • Drug allergic reaction
  • Genetic polymorphism
  • Immunotoxicology
  • Pharmacogenomics
  • Skin

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