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Reducing risk in thiopurine therapy.

Anthony M Marinaki1, Monica Arenas-Hernandez1

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Xenobiotica; the Fate of Foreign Compounds in Biological Systems
|November 5, 2019
PubMed
Summary
This summary is machine-generated.

Genetic testing for thiopurine methyltransferase (TPMT) and NUDT15 variants is crucial for safe thiopurine drug therapy. Personalized dosing based on these genetic profiles minimizes severe toxicity and optimizes treatment response in immune disorders and leukemia.

Keywords:
NUDT15TPMTThiopurineazathioprinemercaptopurinethioguanine nucleotidethiopurine methyltransferase

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Area of Science:

  • Pharmacogenomics
  • Immunology
  • Oncology

Background:

  • Thiopurine drugs (azathioprine, mercaptopurine) are vital for immune regulation disorders and acute lymphoblastic leukemia.
  • Despite their age, thiopurines remain essential, often used with anti-TNF biologics as co-immunomodulators.
  • Significant advancements in patient management have reduced severe thiopurine toxicity.

Purpose of the Study:

  • To highlight the clinical utility of thiopurine methyltransferase (TPMT) and NUDT15 genetic testing.
  • To emphasize the importance of personalized thiopurine therapy based on pharmacogenetic profiles.
  • To discuss strategies for managing thiopurine toxicity and optimizing treatment response.

Main Methods:

  • Review of clinical management strategies for thiopurine therapy.
  • Analysis of thiopurine methyltransferase (TPMT) deficiency testing for dose adjustment.
  • Monitoring of red cell thioguanine nucleotide (TGN) and methylmercaptopurine (MMP) levels.
  • Evaluation of NUDT15 variants' role in myelotoxicity, particularly in Asian populations.
  • Assessment of combination therapy with low-dose thiopurines and allopurinol.

Main Results:

  • TPMT deficiency testing guides safe initial thiopurine dosing.
  • Red cell TGN monitoring aids dose adjustment and identifies non-responders or those at risk.
  • High MMP:TGN ratios indicate risk for hepatotoxicity and non-response.
  • Combination therapy with low-dose thiopurine and allopurinol resolves hepatotoxicity and improves response.
  • NUDT15 variants are a major cause of myelotoxicity in populations with low TPMT deficiency.

Conclusions:

  • Pre-treatment genetic testing for TPMT and NUDT15 deficiencies is clinically valuable for all populations.
  • Personalized thiopurine therapy, guided by pharmacogenetics, is essential for patient safety and efficacy.
  • These genetic screenings represent a critical first step in optimizing thiopurine treatment regimens.