Data/hora: 05/06/2024 18:25:55

Provedor de dados: 	42	
País: 	Brazil	
Título: 	Polymorphisms in CYP2E1, GSTM1 and GSTT1 and anti-tuberculosis drug-induced hepatotoxicity	
Autores: 	BRITO,TAIS C.; POSSUELO,LIA G.; VALIM,ANDREIA R.M.; TODENDI,PÂMELA F.; RIBEIRO,ANDREZZA W.; GREGIANINI,TATIANA S.; JARCZEWSKI,CARLA A.; HUTZ,MARA H.; ROSSETTI,MARIA LUCIA R.; ZAHA,ARNALDO.	
Data: 	2014-06-01	
Ano: 	2014	
Palavras-chave: 	Hepatotoxicity; Isoniazid; Polymorphisms; Tuberculosis.	
Resumo: 	Anti-tuberculosis drug-induced hepatitis (ATD- induced hepatitis) has been linked to polymorphisms in genes encoding drug metabolizing enzymes. N-acetyltransferase 2 (NAT2), cytochrome P450 2E1 (CYP2E1) and glutathione S-transferase (loci GSTM1 and GSTT1) are involved in the metabolism of isoniazid, the most toxic drug for the treatment of tuberculosis (TB). This study was designed to determine the frequency and to evaluate whether polymorphisms at CYP2E1, GSTM1 and GSTT1 genes are associated with drug response, as well as to identify clinical risk factors for ATD-induced hepatitis. A total of 245 Brazilian patients undergoing treatment for TB were genotyped using polymerase chain reaction and restriction fragment length polymorphism and sequencing methods. The frequencies of the CYP2E1 polymorphic alleles RsaI, PstI and DraI are 8%, 8.5% and 12%, respectively. GSTM1 and GSTT1 genes are deleted in 42.9% and 12.4% of the population, respectively. Fifteen patients (6.1%) developed hepatotoxicity. Clinical (HIV, female sex and extrapulmonary TB) and genetic characteristics (CYP2E1 without any mutations, having NAT2 slow acetylator profile) are at higher risk of developing ATD-induced hepatitis in this population. Genotyping for GSTM1 and GSTT1 showed no influence on drug response.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652014000200855	
Editor: 	Academia Brasileira de Ciências	
Relação: 	10.1590/0001-3765201420130350	
Formato: 	text/html	
Fonte: 	Anais da Academia Brasileira de Ciências  v.86 n.2 2014	
Fonte: 	info:eu-repo/semantics/openAccess