PMID- 26095714
OWN - NLM
STAT- MEDLINE
DCOM- 20160318
LR  - 20161125
IS  - 1097-9883 (Electronic)
IS  - 0360-2532 (Linking)
VI  - 47
IP  - 2
DP  - 2015 May
TI  - Pharmacogenetics of isoniazid-induced hepatotoxicity.
PG  - 222-8
LID - 10.3109/03602532.2014.984070 [doi]
AB  - Tuberculosis is still a major problem in some developed and developing countries. 
      The poor compliance to the treatment of tuberculosis patients due to the adverse 
      events was supposed to be an important factor contributing to the high 
      prevalence. This review aims to clarify the role and the pharmacological 
      mechanism of the genes involved in the isoniazid-induced hepatotoxicity. We 
      selected English articles of studies in human from PubMed up to May 2014 with the 
      keywords pharmacogenetic, isoniazid and hepatotoxicity, N-acetyl transferase 2 
      (NAT2), CYP2E1 and glutathione S transferase (GST). Polymorphisms of NAT2, CYP2E1 
      and GST1 could increase patients' susceptibility to isoniazid-induced 
      hepatotoxicity. The rapid acetylators of NAT2 and rapid metabolizers of CYP2E1 
      showed increased concentrations of hepatotoxic metabolites. However, the rapid 
      metabolizers of GST1 could decrease the concentration of hepatotoxic metabolites. 
      Some studies of human leukocyte antigen (HLA), Uridine 5'-dipphospho (UDP) 
      glucuronosyltransferase (UGT), nitric oxide synthase (NOS), Broad complex, 
      Tramtrack, Bric-a-brac (BTB) and cap'n'collar type of basic region leucine zipper 
      factor family (CNC) homolog (BACH) and Maf basic leucine zipper protein (MAFK) 
      polymorphisms showed their roles in isoniazid-induced hepatotoxicity by modifying 
      the expression of antioxidant enzymes. A better insight into the role of 
      polymorphisms of HLA, UGT, NOS, BACH and MAFK in addition to NAT2, CYP2E1 and 
      GST1 in the hepatotoxicity of isoniazid may support physicians in monitoring 
      patients hepatotoxicity symptoms and laboratory data and optimizing 
      pharmacotherapy. Future studies about the role of such polymorphisms in different 
      ethnicities are suggested.
FAU - Perwitasari, Dyah Aryani
AU  - Perwitasari DA
AD  - Faculty of Pharmacy, University of Ahmad Dahlan , Yogyakarta , Indonesia .
FAU - Atthobari, Jarir
AU  - Atthobari J
FAU - Wilffert, Bob
AU  - Wilffert B
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20141119
PL  - England
TA  - Drug Metab Rev
JT  - Drug metabolism reviews
JID - 0322067
RN  - 0 (Antitubercular Agents)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 1.14.13.- (Cytochrome P-450 CYP2E1)
RN  - EC 2.3.1.5 (Arylamine N-Acetyltransferase)
RN  - EC 2.3.1.5 (NAT2 protein, human)
RN  - EC 2.5.1.- (glutathione S-transferase T1)
RN  - EC 2.5.1.18 (Glutathione Transferase)
RN  - EC 2.5.1.18 (glutathione S-transferase M1)
RN  - V83O1VOZ8L (Isoniazid)
SB  - IM
MH  - Antitubercular Agents/adverse effects/*pharmacokinetics
MH  - Arylamine N-Acetyltransferase/genetics/metabolism
MH  - Chemical and Drug Induced Liver Injury/enzymology/etiology/*genetics
MH  - Cytochrome P-450 CYP2E1/genetics/metabolism
MH  - *Genetic Variation
MH  - Glutathione Transferase/genetics/metabolism
MH  - Humans
MH  - Isoniazid/adverse effects/*pharmacokinetics
MH  - Pharmacogenetics
MH  - Reactive Oxygen Species/metabolism
OTO - NOTNLM
OT  - Genetic
OT  - hepatotoxicity
OT  - oral antituberculosis
OT  - polymorphism
OT  - tuberculosis
EDAT- 2015/06/23 06:00
MHDA- 2016/03/19 06:00
CRDT- 2015/06/23 06:00
PHST- 2015/06/23 06:00 [entrez]
PHST- 2015/06/23 06:00 [pubmed]
PHST- 2016/03/19 06:00 [medline]
AID - 10.3109/03602532.2014.984070 [doi]
PST - ppublish
SO  - Drug Metab Rev. 2015 May;47(2):222-8. doi: 10.3109/03602532.2014.984070. Epub 
      2014 Nov 19.