| Revista: | Annals of hepatology |
| Base de datos: | PERIÓDICA |
| Número de sistema: | 000412937 |
| ISSN: | 1665-2681 |
| Autores: | Ampuero, Javier1 Campo, José A. del1 Rojas, Lourdes1 García Lozano, José R2 Solá, Ricard3 Andrade, Raúl4 Pons, José A5 Navarro, José M6 Calleja, José L7 Buti, María8 González Escribano, María F2 Forns, Xavier9 Diago, Moisés10 García Samaniego, Javier11 Romero Gómez, Manuel1 |
| Instituciones: | 1Hospital Universitario Valme, Unit for Clinical Management of Digestive Diseases and Ciberehd, Sevilla. España 2Hospital Virgen del Rocío, Unidad de Inmunología, Sevilla. España 3Hospital del Mar, Barcelona. España 4Hospital Virgen de la Victoria, Unidad de Sistema Digestivo y ciberehd, Málaga. España 5Hospital Universitario Virgen de la Arrixaca, Murcia. España 6Hospital Costa del Sol, Málaga. España 7Hospital Puerta de Hierro, Madrid. España 8Hospital de la Vall d'Hebron, Unidad de Hepatología, Barcelona. España 9Institut d'Investigacions Biomediques August Pi i Sunyer, Unidad de Hígado y Ciberehd, Barcelona. España 10Hospital de Valencia, Departamento de Aparato Digestivo, Valencia. España 11Hospital Carlos III, Unidad de Aparato Digestivo y Ciberehd, Madrid. España |
| Año: | 2014 |
| Periodo: | Jul-Ago |
| Volumen: | 13 |
| Número: | 4 |
| Paginación: | 356-363 |
| País: | México |
| Idioma: | Inglés |
| Tipo de documento: | Artículo |
| Enfoque: | Aplicado, analítico |
| Resumen en inglés | Hepatitis C virus (HCV) is associated with a higher prevalence of steatosis compared to the general population. Aim. Our aim was to assess the impact of PNPLA3 rs738409 G-allele on steatosis in HCV patients. Material and methods. We included 474 HCV patients treated with peginterferon plus ribavirin. PNPLA3 rs738409 was genotyped and patients were classified according to alleles and genotypes. Steatosis was detected in 46.4% (220/474). Fibrosis was assessed by Scheuer score. Gene expression was analyzed in Huh7.5 and Huh7 cells using Real Time-PCR. Results. PNPLA3 allele-G was associated with steatosis [54.1% (126/233) vs. 39% (94/241)] (p = 0.0001). In HCV-1, allele-G was related to steatosis [50.6% (82/162) vs. 32.3% (53/164)] (p = 0.001), but did not in HCV-3 [61.9% (26/42) vs. 62% (31/50)] (p = 0.993). PNPLA3 allele-G was associated with steatosis in patients with IL28B-CT/TT [57.7% (82/142) vs. 37.1% (56/151)] (p = 0.0001), but did not in IL28B-CC [47.8% (43/90) vs. 42% (37/88)] (p = 0.442). Independent variables associated with steatosis were: PNPLA3 G-allele [O.R. 1.84 (CI95%: 1.06-3.21); p = 0.007], age [O.R. 1.04 (CI95%: 1.01-1.07); p = 0.017], HCV-genotype 3 [O.R. 2.46 (CI95%: 1.30-4.65); p = 0.006], HOMA > 4 [O.R. 2.72 (CI95%: 1.27-5.82); p = 0.010]. Since PNPLA3 RNA could not be detected on PBMC from HCV patients, an in vitro analysis was performed. Huh7.5 cells infected with JFH1 had a decreased PNPLA3 gene expression (fold inhibition = 3.2 ± 0.2), while Huh7 cells presented increased PNPLA3 gene expression (fold induction = 1.5 ± 0.2). Conclusion. PNPLA3 allele-G modulated the development of steatosis, particularly in patients with HCV-1 and IL28B-CT/TT genotype, but was not associated with SVR. Metabolic but not viral steatosis seems to be PNPLA3 regulated. Gene interaction may result in differential PNPLA3 gene expression levels in HCV infection |
| Disciplinas: | Medicina |
| Palabras clave: | Gastroenterología, Virus, Genética, Hepatitis C, VHC, Polimorfismo de nucleótido único, Replicación viral, Dislipidemia, Biopsia hepática |
| Keyword: | Medicine, Gastroenterology, Virus, Genetics, Hepatitis C, HCV, Single nucleotide polymorphism (SNPs), Viral replication, Liver biopsy, Dyslipidemia |
| Texto completo: | Texto completo (Ver PDF) |
