Fig 1.
Metabolism and transportation of AZA/6MP and its metabolites.
XO, xanthine oxidase; TPMT, thiopurine S-methyltransferase; HGPRT, hypoxanthine–guanine phosphoribosyl transferase; ITPA, inosine triphosphate pyrophosphatase; IMPDH, inosine monophosphate dehydrogenase; GMPS, guanosine monophosphate synthetase; AZA, azathioprine; 6-MP, 6-mercaptopurine; 6-TUA, 6-thiouric acid; 6-MeMP, 6-methylmercaptopurine; 6-MeMPR, 6-methylmercaptopurine ribonucleotide; 6-TIMP, 6-thioinosine monophosphate; 6-TIDP, 6-thioinosine diphosphate; 6-TITP, 6-thioinosine triphosphate; 6-MeTIMP, 6-methylthioinosine monophosphate; 6-MeTITP, 6-methylthioinosine triphosphate; 6-TXMP, 6-thioxanthosine 5’-monophosphate; 6-TGN, 6-thioguanine nucleotide; 6-MeTGN, 6-methylthioguanine nucleotide.
Table 1.
Baseline Patient Characteristics.
Table 2.
Patients with Adverse Reactions during AZA therapy for IBD.
Table 3.
Characteristics of Adverse Reactions.
Table 4.
Characteristics of Leukopenia.
Table 5.
Characteristics of patients with 94C/A ITPA mutation.
Fig 2.
Changes in 6-TGN concentrations in RBCs (pmol/8×108 RBCs) over time for the various groups.
a The average concentration of 6-TGN in the group with 94C>A tended to be higher than that in the group without 94C>A. However, there was no statistically significant difference between the groups. b c d There were no statistically significant differences between the groups with and without adverse reactions (ARs) or the groups with and without leukopenia or between the males and females.
Fig 3.
Correlations between WBC and 6-TGN.
No negative correlations were observed (r = -0.112, P < 0.01, n = 636).
Fig 4.
Estimates cumulative incidence of Leukopenia.
Kaplan-Meier estimates show that the cumulative incidence of leukopenia was higher in the patients with 94C>A compared with those without 94C>A.