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Whose TPMT activity is it anyway?

Loretta Ford¹, Catherine Prout, Dairena Gaffney

¹Clinical Biochemistry Department, City Hospital, Birmingham B18 7QH, UK.

Annals of Clinical Biochemistry

|December 14, 2004

Summary

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Testing thiopurine S-methyltransferase (TPMT) activity before azathioprine is crucial. This case highlights how recent transfusions can affect TPMT results, emphasizing the need for careful interpretation and pre-treatment testing.

Area of Science:

Pharmacogenetics
Clinical Biochemistry
Drug Metabolism

Background:

Azathioprine therapy requires pre-treatment thiopurine S-methyltransferase (TPMT) activity assessment to mitigate risks of severe toxicity.
TPMT enzyme activity influences the metabolism of thiopurine drugs, with low or deficient activity correlating to increased adverse events.

Observation:

A patient developed pancytopenia during azathioprine treatment without prior TPMT status determination.
Initial TPMT activity measurement was low, consistent with heterozygosity, but a subsequent test revealed deficient activity, indicating homozygosity for mutant alleles.
The patient had received red blood cell and platelet transfusions shortly before the initial TPMT activity measurement.

Findings:

The case demonstrates that recent blood transfusions can confound TPMT activity measurements.

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Delayed TPMT testing revealed deficient activity, confirming a high risk for myelosuppression from thiopurine drugs.

The patient's clinical course underscores the critical need for pre-azathioprine TPMT genotyping or phenotyping.

Implications:

Accurate pre-treatment TPMT activity assessment is vital for safe azathioprine initiation.
Clinicians must consider recent transfusion history when interpreting TPMT activity results.
This case advocates for proactive TPMT testing over dose-titration strategies to prevent severe thiopurine-related toxicity.