Azathioprine (AZA) and its metabolite, mercaptopurine (6-MP), are widely used immunosuppressant drugs
Xanthine oxidase/dehydrogenase (XDH) and aldehyde oxidase (AO) compete with
Purpose
Mutations in thiopurine methyltransferase ( TPMT) and inosine triphosphate pyrophosphohydrolase ( ITPA) genes account for the major genetic polymorphism
The
Azathioprine (AZA) is increasingly being prescribed to rheumatoid arthritis (RA) patients
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SNPs genotype TPMT (rs1800460) and ITPA gene (rs1127354) were significantly related to adverse effects among IBD patients receiving Azathioprine treatment
This gene encodes the enzyme that metabolizes thiopurine drugs via S-adenosyl-L-methionine as the S-methyl donor and S-adenosyl-L-homocysteine as a byproduct
The mechanism of
Gene pools upregulated by azathioprine in 559T and 592T and downregulated in 559T and 592T versus NHA were not significantly enriched in
May reduce anticoagulant effect of warfarin
Gene pools upregulated by azathioprine in 559T and 592T and downregulated in 559T and 592T versus NHA were not significantly enriched in
Polymorphisms thiopurine-S-methyltransferase (TPMT) and nudix hydrolase 15 (NUDT15) can increase the risk of azathioprine myelotoxicity, but little is known about other genetic factors that increase risk for azathioprine-associated side effects
6-MP or the prodrug AZA are purine analogues that stop the synthesis of adenine and guanine
Inter-individual variability to AZA effect and outcomes is related to its genetic polymorphism
An organism’s DNA affects how it looks, how it behaves, its physiology — all aspects of its life
A human example is cystic fibrosis
Xanthinuria Type I is caused by mutations in the xanthine dehydrogenase gene (XDH)
The patient had a heterozygous mutation of the thiopurine S-methyltransferase gene (TPMT*3A)