alexa Thiopurine S-Methyltransferase Phenotype and Genotype i
ISSN: 2329-6887

Journal of Pharmacovigilance
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Review Article

Thiopurine S-Methyltransferase Phenotype and Genotype in Pediatric Patients with Inflammatory Bowel Disease; Implication for Azathioprine Treatment

Maciej Jankowski1,2*, Piotr Landowski3 , Robert Kowalski1 , Ewelina Kreft1 , Irena Audzeyenka2 , Małgorzata Kasztan1 , Barbara Kamińska3 , and Mirosława Szczepańska-Konkel1
1Department of Therapy Monitoring and Pharmacogenetics, Medical University of Gdańsk, Poland
2Laboratory of Cellular and Molecular Nephrology, Mossakowski Medical Research Centre PAS, Warsaw, Poland
3Department of Pediatric Gastroenterology, Hepatology and Nutrition, Medical University of Gdańsk, Poland
Corresponding Author : Maciej Jankowski
Department of Therapy Monitoring and Pharmacogenetics
Medical University of Gdansk, Poland
Tel: (+4858) 3492776
Fax: (+4858) 3492784
E-mail: [email protected]
Received June 1, 2013; Accepted August 17, 2013; Published August 30, 2013
Citation: Jankowski M,Landowski P,Kowalski R,Kreft E,Audzeyenka I, et al., (2013) Thiopurine S-Methyltransferase Phenotype and Genotype in Pediatric Patients with Inflammatory Bowel Disease; Implication for Azathioprine Treatment. J Pharmacovigilance 1:113. doi: 10.4172/2329-6887.1000113
Copyright: © 2013 Jankowski M, et al., This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Inflammatory Bowel Disease (IBD) is more prevalent in children than adults, and the incidence is increasing. IBD is treated with thiopurines, metabolized by thiopurine S-methyltransferase (TPMT) and inter-individual variability in activity of TPMT affecting therapy efficiency and drug toxicity arises from genetic polymorphisms, mainly TPMT*2, *3A, and *3C. The aim was to investigate the frequency distribution of TPMT activity, determine the penetration rate of TPMT*2, *3A, and *3C alleles in children, and compare TPMT activity in children and adults with IBD. The study included 85 children, 45% with Crohn’s disease (CD) and 55% with ulcerative colitis (UC), and 31 adults with IBD. TPMT activity was measured with radiochemistry. TPMT*2, *3A, and *3C alleles were investigated with PCR and restriction fragment length polymorphism analyses. Children showed median TPMT activities of 13.12 and 13.19 U/ml RBC in CD and UC, respectively, with 4.8-fold variability (range, 4.74 - 22.56 U/ml RBC). TPMT activity was similar in children and adults; ranges: 5.56-21.34 vs. 9.61-17.84 U/ml RBC, respectively, in CD; and 4.74-22.56 vs. 5.19-21.98 U/ml RBC, respectively, in UC. Patients with CD and UC treated with azathioprine displayed similar TPMT activities, similar adverse event frequencies, and similar numbers of non-responders. One out of 85 patients (1.18%) was heterozygous with TPMT*1/TPMT*2 (TPMT activity: 5.19 ± 0.05 U/ml RBC). Individuals with low-intermediate TPMT activity (<8 U/ ml RBC) did not carry mutant alleles *3A or *3C. TPMT phenotypes were similar in children and adults with inflammatory bowel disease.

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