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Artigo Produção Nacional Revisado por pares
BIBTEX RIS

TNF‐α and IL‐10 polymorphisms increase the risk to hepatocellular carcinoma in HCV infected individuals

2016; Wiley; Volume: 88; Issue: 9 Linguagem: Inglês

10.1002/jmv.24501

ISSN

1096-9071

Autores

D.C.B.L. Aroucha, Rodrigo Feliciano do Carmo, Luydson Richardson Silva Vasconcelos, Raul Emídio de Lima, T.F. Mendonça, Lucia Elena Alvarado-Arnez, Maria do Socorro Mendonça Cavalcanti, Maria Tereza Cartaxo Muniz, Marcílio L Aroucha, Érika Rabelo Forte de Siqueira, Luciano Beltrão Pereira, Patrícia Moura, Leila Maria Moreira Beltrão Pereira, Maria Rosângela Cunha Duarte Coêlho,

Tópico(s)

Hepatitis B Virus Studies

Resumo

Hepatitis C virus (HCV) is the major cause of hepatocellular carcinoma (HCC). The risk to develop HCC increases with the severity of liver inflammation and hepatic fibrosis. It is believed that a balance between the releases of pro‐ and anti‐inflammatory cytokines will determine the clinical course of HCV and the risk to develop HCC. The inteleukin‐10 (IL‐10) and the tumor necrosis factor alpha (TNF‐α) play key roles in the Th1 and Th2 balance during the inflammatory response against HCV. The aim of the present study was to investigate the association between polymorphisms in TNF‐α ‐308 G>A (rs1800629), IL‐10 ‐1082 G>A (rs1800896) and ‐819/‐592 (rs1800871/rs1800872) with HCC risk in individuals with HCV. The present study evaluated 388 chronic HCV patients. Polymorphisms were determined by real‐time PCR. Diplotypes associated with low IL‐10 production and the TNF‐α GG genotype were significantly associated with HCC occurrence after multivariate logistic regression analysis ( P = 0.027 and P = 0.029, respectively). Additionally, the IL‐10 ‐819 (‐592) TT (AA) genotype was significantly associated with multiple nodules and HCC severity according to BCLC staging ( P = 0.044 and P = 0.025, respectively). Patients carrying low production haplotypes of IL‐10 and the TNF‐α GG genotype have higher risk to develop HCC. J. Med. Virol. 88:1587–1595, 2016 . © 2016 Wiley Periodicals, Inc.

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