Polymorphisms in the transforming growth factor‐β1 gene (TGF‐β1) and the risk of advanced alcoholic liver disease

Oliver, Javier; Agúndez, José A. G.; Morales, Sonia; Fernández‐Arquero, Miguel; Fernández‐Gutiérrez, Benjamín; Concha, Emilio G. de la; Dı́az-Rubio, Manuel; Martı́n, Javier; Ladero, José M.

doi:10.1111/j.1478-3231.2005.01150.x

Cited by 24 publications

(17 citation statements)

References 25 publications

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“…This implies that the genetic polymorphism at codon 10 does not exert great effects on the development of ALC as a host factor. In the study reported by Oliver et al9 and Bathgate et al29 the development of ALC was not associated with the genetic polymorphism at the codon 10, which is consistent with the results of this study.…”

Section: Discussionsupporting

confidence: 93%

“…Nevertheless, contradictory to this, it has been also reported that in the P/P genotype, the serum concentration of TGF-β1 is higher than other genotypes,23-26 and liver fibrosis progresses rapidly in the genotype containing proline 13,26. On the other hand, it has been also reported that the genotype at codon 10 is not associated with liver fibrosis 9,12,27,28. It is thought that the reason of such results contradictory to each other may be the effect of the sample size, races, and the difference of the cause of liver diseases such as HBV, hepatitis C virus (HCV), and alcohol.…”

Section: Discussionmentioning

confidence: 91%

“…As described above, TGF-β1 is involved in the mechanism of liver fibrosis induced by alcohol 8,9. The genetic polymorphism of TGF-β1 can effect on the level of its production 10.…”

Section: Introductionmentioning

confidence: 94%

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Genetic polymorphism at codon 10 of the transforming growth factor-β1 gene in patients with alcoholic liver cirrhosis

et al. 2011

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Background/AimsTransforming growth factor beta1 (TGF-β1) is a key cytokine in the production of extracellular matrix. A genetic polymorphism at codon 10 of the TGF-β1 gene is associated with liver fibrosis. We investigated the effect of genetic polymorphisms at codon 10 on the development of alcoholic liver cirrhosis (ALC).MethodsIn total, 119 controls and 182 patients with ALC, were enrolled in the study. Clinical and laboratory data including total lifetime alcohol intake were collected at enrollment. The genotype at codon 10 was determined for each patient by single-strand conformation polymorphism.ResultsThere were three types of genetic polymorphism at codon 10: homozygous proline (P/P), heterozygous proline/leucine (P/L), and homozygous leucine (L/L). Among the controls, the proportions of P/P, P/L, and L/L were 26.1%, 44.5%, and 29.4%, respectively in the ALC group, these proportions were 23.1%, 43.4%, and 33.5%, respectively. The genotype distribution did not differ between the controls and the ALC group. In the ALC group, age, total lifetime alcohol intake, and distribution of Child-Pugh class did not differ with the genotype. Of the male patients with ALC (n=164), the proportions of P/P, P/L, and L/L were 20.1%, 44.5%, and 35.4%, respectively the genotype distribution did not differ between the male controls and the male ALC patients.ConclusionsThe genotype at codon 10 in TGF-β1 does not appear to influence the development of ALC. Further study is needed to investigate other genetic factors that influence the development of ALC in patients with chronic alcohol intake.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 91%

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Genetic polymorphism at codon 10 of the transforming growth factor-β1 gene in patients with alcoholic liver cirrhosis

et al. 2011

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“…In contrast to hepatitis B infection, iron deposits are found in more than 50% of patients with HCV infection or chronic ethanol consumption [96,[106][107][108][109] . Even mild to moderate alcohol consumption has recently been shown to increase the prevalence of iron overload [110] .…”

Section: Ethanol and Hcv Lead To Hepatic Iron Accumulationmentioning

confidence: 99%

Evaluation of standard liver volume formulae for Chinese adults

Shi¹,

Yan²,

Li³

et al. 2009

WJG

105

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Alcoholic liver disease (ALD) and hepatitis C virus (HCV) infection represent, either alone or in combination, more than two thirds of all patients with liver disease in the Western world. This review discusses the epidemiology and combined impact of ALD and HCV on the progression of liver disease. ALD and HCV affect the progression of liver disease to liver cirrhosis and hepatocellular carcinoma (HCC) in a synergistic manner. Thus, the risk for HCC increases five times with a daily alcohol consumption of 80 g; in the presence of HCV it is increased 20-fold, and a combination of both risk factors leads to a more than 100-fold risk for HCC development. Alcohol consumption also decreases the response to interferon treatment which is probably due to a lack of compliance than a direct effect on HCV replication. Several molecular mechanisms are discussed that could explain the synergistic interaction of alcohol and HCV on disease progression. They include modulation of the immune response and apoptosis, increased oxidative stress via induction of CYP2E1 and the hepatic accumulation of iron. Thus, both HCV and alcohol independently cause hepatic iron accumulation in > 50% of patients probably due to suppression of the liver-secreted systemic iron hormone hepcidin. A better understanding of hepcidin regulation could help in developing novel therapeutic approaches to treat the chronic disease in the future. For now, it can be generally concluded that HCV-infected patients should abstain from alcohol and alcoholics should be encouraged to participate in detoxification programs.

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“…With regard to ALD, two studies have failed to find any association between ALD and the codon 25 Arg/Pro SNP in the TGF-b1 gene. 90,91 The only relevant study thus far in this regard in NAFLD reported that obese patients possessing both the high TGF-b1 and angiotensinogen-producing SNPs may be more susceptible to advanced fibrosis. 92 However interpretation of this study is limited by small numbers.…”

Section: Genes Influencing the Severity Of Fibrosismentioning

confidence: 97%

Genetics of Alcoholic Liver Disease and Nonalcoholic Fatty Liver Disease

2007

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Polymorphisms in the transforming growth factor‐β₁ gene (TGF‐β₁) and the risk of advanced alcoholic liver disease

Abstract: The polymorphisms at the TGF-beta(1) gene analysed in this study are probably not related to the risk of advanced ALD.

Cited by 24 publications

References 25 publications

Genetic polymorphism at codon 10 of the transforming growth factor-β1 gene in patients with alcoholic liver cirrhosis

Genetic polymorphism at codon 10 of the transforming growth factor-β1 gene in patients with alcoholic liver cirrhosis

Evaluation of standard liver volume formulae for Chinese adults

Genetics of Alcoholic Liver Disease and Nonalcoholic Fatty Liver Disease

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