Fig. 2From: Association of genetic polymorphism of NUDT15, TPMT and ITPA gene in the toxicity and efficacy of azathioprine-based regimen in Egyptian inflammatory bowel disease patientsMetabolism of AZA involves three pathways: the first is degradation to TUA which is then excreted, then through methylation by TPMT into MeMP, and breakdown of MP into TIMP catalyzed by HPRT. Then, TIMP is further metabolized via IMPDH into TGMP. Kinases convert this into the TGNs. Approximately 15–20% of patients with IBD demonstrate hypermethylation when treated with thiopurines. That means that during thiopurine metabolism, methylated thiopurine metabolites are preferentially produced instead of TGNs [16]Back to article page