PMID- 21913872
OWN - NLM
STAT- MEDLINE
DCOM- 20120501
LR  - 20161125
IS  - 1097-9883 (Electronic)
IS  - 0360-2532 (Linking)
VI  - 44
IP  - 1
DP  - 2012 Feb
TI  - Genetic association studies in drug-induced liver injury.
PG  - 116-26
LID - 10.3109/03602532.2011.605790 [doi]
AB  - A large number of case-control association studies on genetic susceptibility to 
      drug-induced liver injury, involving both candidate gene and genome-wide 
      association approaches, have now been reported. The strongest associations have 
      been observed for human leukocyte antigen (HLA) class I and II genes and 
      N-acetyltransferase 2 (NAT2). The associations with HLA class I and II genes are 
      drug specific, though some apparently unrelated compounds show genetic 
      associations with the same alleles. The underlying mechanism for the HLA 
      association is likely to involve T-cell responses to either drug-protein adducts 
      or to drug alone, but needs further investigation. The NAT2 association relates 
      to liver injury induced by isoniazid, with most published studies finding an 
      increased risk of injury in slow acetylators lacking NAT2 enzyme activity, 
      presumably because of the accumulation of toxic metabolites. Other associations 
      with genes relevant to drug disposition, innate immunity, oxidative stress, and 
      mitochondrial function have also been reported, though these still need to be 
      confirmed by replication in independent cohorts.
FAU - Daly, Ann K
AU  - Daly AK
AD  - Institute of Cellular Medicine, Newcastle University Medical School, Newcastle 
      upon Tyne, United Kingdom. a.k.daly@ncl.ac.uk
FAU - Day, Christopher P
AU  - Day CP
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20110914
PL  - England
TA  - Drug Metab Rev
JT  - Drug metabolism reviews
JID - 0322067
RN  - 0 (Antitubercular Agents)
RN  - 0 (HLA Antigens)
RN  - 0 (Pharmaceutical Preparations)
RN  - V83O1VOZ8L (Isoniazid)
SB  - IM
MH  - Antitubercular Agents/adverse effects
MH  - Case-Control Studies
MH  - Chemical and Drug Induced Liver Injury/*genetics
MH  - Drug-Related Side Effects and Adverse Reactions
MH  - Genes, MHC Class I
MH  - *Genetic Predisposition to Disease
MH  - *Genome-Wide Association Study
MH  - Genotype
MH  - HLA Antigens/genetics
MH  - Humans
MH  - Immunity, Innate/genetics
MH  - Isoniazid/adverse effects
MH  - Oxidative Stress/genetics
MH  - Pharmaceutical Preparations/metabolism
MH  - Polymorphism, Genetic
EDAT- 2011/09/15 06:00
MHDA- 2012/05/02 06:00
CRDT- 2011/09/15 06:00
PHST- 2011/09/15 06:00 [entrez]
PHST- 2011/09/15 06:00 [pubmed]
PHST- 2012/05/02 06:00 [medline]
AID - 10.3109/03602532.2011.605790 [doi]
PST - ppublish
SO  - Drug Metab Rev. 2012 Feb;44(1):116-26. doi: 10.3109/03602532.2011.605790. Epub 
      2011 Sep 14.