AI Article Synopsis
- The study examined how genetic variations impact the levels of certain metabolites in patients with inflammatory bowel disease taking azathioprine (AZA) or mercaptopurine (MP).
- Carriers of a specific GSTM1-null genotype showed significantly lower 6-methylmercaptopurine ribonucleotide (6-MMPR) levels while on AZA compared to those with normal GSTM1 genes.
- However, there were no significant differences in 6-MMPR levels among patients on MP or in the levels of another metabolite (6-thioguanine nucleotide) based on GSTM1, GSTA1, or GSTA2 genetic variations.
Article Abstract
The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2). We designed a case-control study with data from the TOPIC trial to explore the effects of genetic variation on steady state 6-methylmercaptopurine ribonucleotide (6-MMPR) and 6-thioguanine nucleotide (6-TGN) metabolite levels. We included 199 patients with inflammatory bowel disease (126 on AZA and 73 on MP). GSTM1-null genotype carriers on AZA had two-fold lower 6-MMPR levels than AZA users carrying one or two copies of GSTM1 (2239 (1006-4587) versus 4371 (1897-7369) pmol/8 × 10 RBCs; P<0.01). In patients on MP (control group) 6-MMPR levels were comparable (6195 (1551-10712) versus 6544 (1717-11600) pmol/8 × 10 RBCs; P=0.84). The 6-TGN levels were not affected by the GSTM1 genotype. The presence of genetic variants in GSTA1 and GSTA2 was not related to the 6-MMPR and 6-TGN levels.
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| http://dx.doi.org/10.1038/tpj.2016.87 | DOI Listing |
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