PMID- 27154258
OWN - NLM
STAT- MEDLINE
DCOM- 20170627
LR  - 20220317
IS  - 1346-8138 (Electronic)
IS  - 0385-2407 (Linking)
VI  - 43
IP  - 7
DP  - 2016 Jul
TI  - Severe cutaneous adverse drug reactions.
PG  - 758-66
LID - 10.1111/1346-8138.13430 [doi]
AB  - The clinical manifestations of drug eruptions can range from mild maculopapular 
      exanthema to severe cutaneous adverse drug reactions (SCAR), including 
      drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and 
      systemic symptoms, Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis 
      (TEN) which are rare but occasionally fatal. Some pathogens may induce skin 
      reactions mimicking SCAR. There are several models to explain the interaction of 
      human leukocyte antigen (HLA), drug and T-cell receptor (TCR): (i) the 
      "hapten/prohapten" theory; (ii) the "p-i concept"; (iii) the "altered peptide 
      repertoire"; and (iv) the "altered TCR repertoire". The checkpoints of molecular 
      mechanisms of SCAR include specific drug antigens interacting with the specific 
      HLA loci (e.g. HLA-B*15:02 for carbamazepine-induced SJS/TEN and HLA-B*58:01 for 
      allopurinol-induced SCAR), involvement of specific TCR, induction of 
      T-cell-mediated responses (e.g. granulysin, Fas ligand, perforin/granzyme B and 
      T-helper 1/2-associated cytokines) and cell death mechanism (e.g. 
      miR-18a-5p-induced apoptosis; annexin A1 and formyl peptide receptor 1-induced 
      necroptosis in keratinocytes). In addition to immune mechanism, metabolism has 
      been found to play a role in the pathogenesis of SCAR, such as recent findings of 
      strong association of CYP2C9*3 with phenytoin-induced SCAR and impaired renal 
      function with allopurinol SCAR. With a better understanding of the mechanisms, 
      effective therapeutics and prevention for SCAR can be improved.
CI  - (c) 2016 Japanese Dermatological Association.
FAU - Chung, Wen-Hung
AU  - Chung WH
AD  - Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, 
      Chang Gung Memorial Hospitals, Tapei, Linko and Keelung, Taiwan.
AD  - College of Medicine, Chang Gung University, Taoyuan, Taiwan.
AD  - Chang Gung Immunology Consortium, Chang Gung Memorial Hospital and Chang Gung 
      University, Taoyuan, Taiwan.
AD  - Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial 
      Hospital, Keelung, Taiwan.
FAU - Wang, Chuang-Wei
AU  - Wang CW
AD  - Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, 
      Chang Gung Memorial Hospitals, Tapei, Linko and Keelung, Taiwan.
AD  - Chang Gung Immunology Consortium, Chang Gung Memorial Hospital and Chang Gung 
      University, Taoyuan, Taiwan.
FAU - Dao, Ro-Lan
AU  - Dao RL
AD  - Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, 
      Chang Gung Memorial Hospitals, Tapei, Linko and Keelung, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20160506
PL  - England
TA  - J Dermatol
JT  - The Journal of dermatology
JID - 7600545
SB  - IM
MH  - Drug Eruptions/classification/genetics/*immunology/therapy
MH  - Humans
OTO - NOTNLM
OT  - Stevens-Johnson syndrome
OT  - drug reaction with eosinophilia and systemic symptoms
OT  - drug-induced hypersensitivity syndrome
OT  - severe cutaneous adverse drug reactions
OT  - toxic epidermal necrolysis
EDAT- 2016/05/08 06:00
MHDA- 2017/06/28 06:00
CRDT- 2016/05/08 06:00
PHST- 2015/12/23 00:00 [received]
PHST- 2016/03/16 00:00 [accepted]
PHST- 2016/05/08 06:00 [entrez]
PHST- 2016/05/08 06:00 [pubmed]
PHST- 2017/06/28 06:00 [medline]
AID - 10.1111/1346-8138.13430 [doi]
PST - ppublish
SO  - J Dermatol. 2016 Jul;43(7):758-66. doi: 10.1111/1346-8138.13430. Epub 2016 May 6.