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Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C

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Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C. / Stättermayer, Albert F; Rutter, Karoline; Beinhardt, Sandra; Wrba, Fritz; Scherzer, Thomas-Matthias; Strasser, Michael; Hofer, Harald; Steindl-Munda, Petra; Trauner, Michael; Ferenci, Peter.

in: LIVER INT, Jahrgang 34, Nr. 3, 01.03.2014, S. 388-95.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Stättermayer, AF, Rutter, K, Beinhardt, S, Wrba, F, Scherzer, T-M, Strasser, M, Hofer, H, Steindl-Munda, P, Trauner, M & Ferenci, P 2014, 'Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C', LIVER INT, Jg. 34, Nr. 3, S. 388-95. https://doi.org/10.1111/liv.12269

APA

Stättermayer, A. F., Rutter, K., Beinhardt, S., Wrba, F., Scherzer, T-M., Strasser, M., Hofer, H., Steindl-Munda, P., Trauner, M., & Ferenci, P. (2014). Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C. LIVER INT, 34(3), 388-95. https://doi.org/10.1111/liv.12269

Vancouver

Stättermayer AF, Rutter K, Beinhardt S, Wrba F, Scherzer T-M, Strasser M et al. Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C. LIVER INT. 2014 Mär 1;34(3):388-95. https://doi.org/10.1111/liv.12269

Bibtex

@article{48801bb1f01342c48e4e806cc0f62a29,
title = "Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C",
abstract = "BACKGROUND: In chronic hepatitis C (CHC), steatosis is associated with fibrosis and impaired response to antiviral therapy. Recently, a polymorphism of single nucleotide polymorphism SNP rs2645424 of farnesyl diphosphate farnesyl transferase 1 (FDFT1) was identified in NAFLD/NASH as a possible causal link to steatosis and fibrosis progression. SNP rs738409 in the adiponutrin gene (PNPLA3) is a well described factor for steatosis. This study evaluated the relation of these SNPs on steatosis, fibrosis and treatment response in CHC.METHODS: The SNPs rs738409478 and rs2645424 were determined by real-time PCR in 478 patients with CHC (m/f: 314/164; mean age: 44.9 ± 10.7; GT1: 387, GT4: 91) who completed treatment with peg-IFN-α-2a/ribavirin. All had a pretreatment liver biopsy. Steatosis and fibrosis were graded by board-certified pathologists according to Brunt and METAVIR respectively.RESULTS: The distribution of FDFT1 rs2645424 was GG: 186 (38.9%), AG: 222 (46.4%) and AA: 70 (14.6%) and of the rs738409 PNPLA3 allele: CC: 269 (56.3%), CG: 177 (37.0%) and GG: 32 (6.7%). Overall, FDTF1 polymorphism was not linked to the extent of steatosis or fibrosis. However, in patients without steatosis the AA genotype was associated with advanced fibrosis [AA: 8/20 (40.0%), AG: 6/70 (8.5%), GG: 9/57 (16.1%), P = 0.003]. In contrast, the minor PNPLA3 allele was associated with both steatosis and advanced fibrosis (P < 0.001). Both SNPs did not influence treatment response.CONCLUSION: The minor allele in FDFT1 was associated with advanced fibrosis in the non-steatotic but not in the steatotic subgroup. This may reflect different metabolic pathways in fibrosis progression for steatotic and non-steatotic patients with CHC.",
author = "St{\"a}ttermayer, {Albert F} and Karoline Rutter and Sandra Beinhardt and Fritz Wrba and Thomas-Matthias Scherzer and Michael Strasser and Harald Hofer and Petra Steindl-Munda and Michael Trauner and Peter Ferenci",
note = "{\textcopyright} 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.",
year = "2014",
month = mar,
day = "1",
doi = "10.1111/liv.12269",
language = "English",
volume = "34",
pages = "388--95",
journal = "LIVER INT",
issn = "1478-3223",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - Role of FDFT1 polymorphism for fibrosis progression in patients with chronic hepatitis C

AU - Stättermayer, Albert F

AU - Rutter, Karoline

AU - Beinhardt, Sandra

AU - Wrba, Fritz

AU - Scherzer, Thomas-Matthias

AU - Strasser, Michael

AU - Hofer, Harald

AU - Steindl-Munda, Petra

AU - Trauner, Michael

AU - Ferenci, Peter

N1 - © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

PY - 2014/3/1

Y1 - 2014/3/1

N2 - BACKGROUND: In chronic hepatitis C (CHC), steatosis is associated with fibrosis and impaired response to antiviral therapy. Recently, a polymorphism of single nucleotide polymorphism SNP rs2645424 of farnesyl diphosphate farnesyl transferase 1 (FDFT1) was identified in NAFLD/NASH as a possible causal link to steatosis and fibrosis progression. SNP rs738409 in the adiponutrin gene (PNPLA3) is a well described factor for steatosis. This study evaluated the relation of these SNPs on steatosis, fibrosis and treatment response in CHC.METHODS: The SNPs rs738409478 and rs2645424 were determined by real-time PCR in 478 patients with CHC (m/f: 314/164; mean age: 44.9 ± 10.7; GT1: 387, GT4: 91) who completed treatment with peg-IFN-α-2a/ribavirin. All had a pretreatment liver biopsy. Steatosis and fibrosis were graded by board-certified pathologists according to Brunt and METAVIR respectively.RESULTS: The distribution of FDFT1 rs2645424 was GG: 186 (38.9%), AG: 222 (46.4%) and AA: 70 (14.6%) and of the rs738409 PNPLA3 allele: CC: 269 (56.3%), CG: 177 (37.0%) and GG: 32 (6.7%). Overall, FDTF1 polymorphism was not linked to the extent of steatosis or fibrosis. However, in patients without steatosis the AA genotype was associated with advanced fibrosis [AA: 8/20 (40.0%), AG: 6/70 (8.5%), GG: 9/57 (16.1%), P = 0.003]. In contrast, the minor PNPLA3 allele was associated with both steatosis and advanced fibrosis (P < 0.001). Both SNPs did not influence treatment response.CONCLUSION: The minor allele in FDFT1 was associated with advanced fibrosis in the non-steatotic but not in the steatotic subgroup. This may reflect different metabolic pathways in fibrosis progression for steatotic and non-steatotic patients with CHC.

AB - BACKGROUND: In chronic hepatitis C (CHC), steatosis is associated with fibrosis and impaired response to antiviral therapy. Recently, a polymorphism of single nucleotide polymorphism SNP rs2645424 of farnesyl diphosphate farnesyl transferase 1 (FDFT1) was identified in NAFLD/NASH as a possible causal link to steatosis and fibrosis progression. SNP rs738409 in the adiponutrin gene (PNPLA3) is a well described factor for steatosis. This study evaluated the relation of these SNPs on steatosis, fibrosis and treatment response in CHC.METHODS: The SNPs rs738409478 and rs2645424 were determined by real-time PCR in 478 patients with CHC (m/f: 314/164; mean age: 44.9 ± 10.7; GT1: 387, GT4: 91) who completed treatment with peg-IFN-α-2a/ribavirin. All had a pretreatment liver biopsy. Steatosis and fibrosis were graded by board-certified pathologists according to Brunt and METAVIR respectively.RESULTS: The distribution of FDFT1 rs2645424 was GG: 186 (38.9%), AG: 222 (46.4%) and AA: 70 (14.6%) and of the rs738409 PNPLA3 allele: CC: 269 (56.3%), CG: 177 (37.0%) and GG: 32 (6.7%). Overall, FDTF1 polymorphism was not linked to the extent of steatosis or fibrosis. However, in patients without steatosis the AA genotype was associated with advanced fibrosis [AA: 8/20 (40.0%), AG: 6/70 (8.5%), GG: 9/57 (16.1%), P = 0.003]. In contrast, the minor PNPLA3 allele was associated with both steatosis and advanced fibrosis (P < 0.001). Both SNPs did not influence treatment response.CONCLUSION: The minor allele in FDFT1 was associated with advanced fibrosis in the non-steatotic but not in the steatotic subgroup. This may reflect different metabolic pathways in fibrosis progression for steatotic and non-steatotic patients with CHC.

U2 - 10.1111/liv.12269

DO - 10.1111/liv.12269

M3 - SCORING: Journal article

C2 - 23870067

VL - 34

SP - 388

EP - 395

JO - LIVER INT

JF - LIVER INT

SN - 1478-3223

IS - 3

ER -