Published online Apr 7, 2014. doi: 10.3748/wjg.v20.i13.3534
Revised: December 30, 2013
Accepted: January 19, 2014
Published online: April 7, 2014
Processing time: 156 Days and 13.2 Hours
Azathioprine is a purine antimetabolite drug commonly used to treat inflammatory bowel disease (IBD). In vivo it is active after reaction with reduced glutathione (GSH) and conversion to mercaptopurine. Although this reaction may occur spontaneously, the presence of isoforms M and A of the enzyme glutathione-S-transferase (GST) may increase its speed. Indeed, in pediatric patients with IBD, deletion of GST-M1, which determines reduced enzymatic activity, was recently associated with reduced sensitivity to azathioprine and reduced production of azathioprine active metabolites. In addition to increase the activation of azathioprine to mercaptopurine, GSTs may contribute to azathioprine effects even by modulating GSH consumption, oxidative stress and apoptosis. Therefore, genetic polymorphisms in genes for GSTs may be useful to predict response to azathioprine even if more in vitro and clinical validation studies are needed.
Core tip: Polymorphisms of glutathione-S-transferase-M1 may influence azathioprine effects in young patients with inflammatory bowel disease by increasing the drug activation and by modulating oxidative stress and apoptosis.