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Lupus, Vol. 17, No. 2, 132-134 (2008)
DOI: 10.1177/0961203307085255

Azathioprine-induced fatal myelosuppression in systemic lupus erythematosus patient carrying TPMT*3C polymorphism

U. Boonsrirat

Lupus Research Unit, Department of Medicine

S. Angsuthum

Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand

S. Vannaprasaht

Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand

J. Kongpunvijit

Lupus Research Unit, Department of Medicine

N. Hirankarn

Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

W. Tassaneeyakul

Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand

Y. Avihingsanon

Lupus Research Unit, Department of Medicine, yingyos{at}hotmail.com, yingyos.a{at}gmail.com

Azathioprine (AZA) is a commonly used immunosuppressant for systemic lupus erythematosus (SLE). Myelosuppression is a serious adverse reaction due to AZA and its metabolites. Thiopurine S-methyltransferase (TPMT) is the rate-limiting enzyme. Variations of TPMT enzyme activity may be responsible for myelosuppression. However, a correlation between certain mutant alleles of low TPMT enzyme activity and myelotoxicity has also been suggested as a factor. We describe herein a case of AZA-induced severe myelosuppression associated with TPMT*3C heterozygous mutant allele in a SLE patient. The patient presented with pancytopenia, sepsis, typhlitis and disseminated intravascular coagulopathy after a short period of AZA therapy. The patient had low TPMT activity and TPMT*3C genotype. Measurement of TPMT activity and determination of TPMT variant allele may identify patients at risk for AZA-induced myelosuppression. Lupus (2008) 17, 132—134.

Key Words: genetic polymorphism • myelosuppression • 6-mercaptopurine • pharmacogenetics • systemic lupus erythematosus • thiopurine S-methyltransferase


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