SLC11A1 promoter gene polymorphisms and fibrosis progression in chronic hepatitis C

Romero‐Gómez, Manuel; Montes-Cano, Marco Antonio; Otero-Fernández, M A; Torres, Belén; Sánchez-Muñoz, Diego; Aguilar, Francisco; Barroso, Natalia; Gómez-Izquierdo, Lourdes; Castellano-Megias, Victor M.; Núñez‐Roldán, Antonio; Aguilar-Reina, José; González-Escribano, M F

doi:10.1136/gut.2003.028274

Cited by 30 publications

(23 citation statements)

References 29 publications

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“…b) Populations of Spanish healthy controls and HIV- or HCV- infected patients shows similar frequency of the genotypes tested [37], [44]. c) Data were similar when only those patients diagnosed of chronic hepatitis or cirrhosis by liver biopsy were considered .…”

Section: Discussionmentioning

confidence: 81%

Influence of Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Interleukin 10 Genes on the Risk of Liver Cirrhosis in HIV-HCV Coinfected Patients

Corchado

Márquez

et al. 2013

PLoS ONE

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ObjectiveAnalysis of the contribution of genetic (single nucleotide polymorphisms (SNP) at position -238 and -308 of the tumor necrosis factor alpha (TNF-α) and -592 of the interleukin-10 (IL-10) promotor genes) and of classical factors (age, alcohol, immunodepression, antirretroviral therapy) on the risk of liver cirrhosis in human immunodeficiency (HIV)-hepatitis C (HCV) virus coinfected patients.Patients and MethodsNinety one HIV-HCV coinfected patients (50 of them with chronic hepatitis and 41 with liver cirrhosis) and 55 healthy controls were studied. Demographic, risk factors for the HIV-HCV infection, HIV-related (CD4+ T cell count, antiretroviral therapy, HIV viral load) and HCV-related (serum ALT concentration, HCV viral load, HCV genotype) characteristics and polymorphisms at position -238 and -308 of the tumor necrosis factor alfa (TNF- α) and -592 of the interleukin-10 (IL-10) promotor genes were studied.ResultsEvolution time of the infection was 21 years in both patients’ groups (chronic hepatitis and liver cirrhosis). The group of patients with liver cirrhosis shows a lower CD4+ T cell count at the inclusion in the study (but not at diagnosis of HIV infection), a higher percentage of individuals with previous alcohol abuse, and a higher proportion of patients with the genotype GG at position -238 of the TNF-α promotor gene; polymorphism at -592 of the IL-10 promotor gene approaches to statistical significance. Serum concentrations of profibrogenic transforming growth factor beta1 were significantly higher in healthy controls with genotype GG at -238 TNF-α promotor gene. The linear regression analysis demonstrates that the genotype GG at -238 TNF-α promotor gene was the independent factor associated to liver cirrhosis.ConclusionIt is stressed the importance of immunogenetic factors (TNF-α polymorphism at -238 position), above other factors previously accepted (age, gender, alcohol, immunodepression), on the evolution to liver cirrhosis among HIV-infected patients with established chronic HCV infections.

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Section: Discussionmentioning

confidence: 81%

Influence of Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Interleukin 10 Genes on the Risk of Liver Cirrhosis in HIV-HCV Coinfected Patients

Corchado

Márquez

et al. 2013

PLoS ONE

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“…In considering the relationship between TNF -α -308 polymorphisms and the severity of disease, Barrett et al [35] and Hohler et al [45] reported an association between these factors in patients with chronic HCV infection; Romero-Gomez et al [47] found no association between TNF -α -308 polymorphisms and the severity of fibrosis in HCC. Hence, studies of TNF -α -308 polymorphisms and its effect on TNF-α production have been inconsistent but nevertheless indicate that this position likely influences the production of TNF-α, which may in turn affect the outcome of an HCV infection.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-alpha-308G/A polymorphism and risk of hepatocellular carcinoma in hepatitis C virus-infected patients

Talaat

Esmail²,

Elwakil³

et al. 2013

Chin J Cancer

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Tumor necrosis factor-alpha (TNF-α) is an important cytokine in generating an immune response against infection with hepatitis C virus (HCV). The functions of TNF-α may be altered by single-nucleotide polymorphisms (SNPs) in its gene structure. We hypothesized that SNPs in TNF-α may be important in determining the outcome of an HCV infection. To test this hypothesis, we investigated the role of the polymorphism -308G/A, which is located in the promoter region of the TNF-α gene, in the progression of HCV infection in Egyptian patients using a quantitative real-time polymerase chain reaction (qRT-PCR). The distribution of this polymorphism and its impact on the serum level of TNF-α was compared between 90 HCV-infected patients [45 with HCV-induced cirrhosis and 45 with HCV-related hepatocellular carcinoma (HCC)] and 45 healthy Egyptian volunteers without any history of liver disease. Our results showed that at the TNF-α -308 position, the G/G allele was most common (78.5%) in the study population, with the G/A and A/A alleles occurring less frequently (13.3% and 8.1%, respectively). Frequencies of G/G, G/A, and A/A genotypes were 87%, 7%, and 6% in patients with liver cirrhosis and were 94%, 4%, and 2% in patients with HCC, respectively. Serum levels of TNF-α were significantly higher in HCV-infected patients than in healthy controls, indicating that the TNF-α -308 polymorphism does not influence the production of TNF-α. The serum level of TNF-α was positively correlated with HCV infection. Taken together, these findings suggest that the TNF-α -308 polymorphism may not be a host genetic factor associated with the severity of HCV infection, but may be an independent risk factor for HCC.

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“…Several recent studies have identified possible polymorphisms in a number of candidate genes that influence the progression of liver fibrosis. Polymorphisms in genes encoding immunoregulatory proteins, proinflammatory cytokines, and fibrogenic factors may influence disease progression in patients with alcohol-induced liver disease, primary biliary cirrhosis, obesity, and particularly chronic hepatitis C [73][74][75][76][77][78][79]. However, some of the studies have yielded contradictory results, and large-scale, welldesigned studies are required to clarify the actual role of this factor and other genetic variants in liver fibrosis.…”

Section: Genetic Studiesmentioning

confidence: 99%

Fibrosis in chronic liver diseases: diagnosis and management

Pinzani

Rombouts

Colagrande

2005

Journal of Hepatology

242

179

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SLC11A1 promoter gene polymorphisms and fibrosis progression in chronic hepatitis C

Cited by 30 publications

References 29 publications

Influence of Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Interleukin 10 Genes on the Risk of Liver Cirrhosis in HIV-HCV Coinfected Patients

Influence of Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Interleukin 10 Genes on the Risk of Liver Cirrhosis in HIV-HCV Coinfected Patients

Tumor necrosis factor-alpha-308G/A polymorphism and risk of hepatocellular carcinoma in hepatitis C virus-infected patients

Fibrosis in chronic liver diseases: diagnosis and management

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