@article {3516,
	title = {Pharmacogenetics of azathioprine in inflammatory bowel disease: a role for glutathione-S-transferase?},
	journal = {World J Gastroenterol},
	volume = {20},
	year = {2014},
	month = {2014 Apr 7},
	pages = {3534-41},
	abstract = {<p>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.</p>},
	keywords = {6-Mercaptopurine, Animals, Apoptosis, Azathioprine, Glutathione, Glutathione Transferase, Humans, Immunosuppressive Agents, Inflammatory Bowel Diseases, Oxidative Stress, Pharmacogenetics, Polymorphism, Genetic},
	issn = {2219-2840},
	doi = {10.3748/wjg.v20.i13.3534},
	author = {Stocco, Gabriele and Pelin, Marco and Franca, Raffaella and De Iudicibus, Sara and Cuzzoni, Eva and Favretto, Diego and Martelossi, Stefano and Ventura, Alessandro and Decorti, Giuliana}
}
