Evaluation of complement factor 5 variants as genetic risk factors for the development of advanced fibrosis in chronic hepatitis C infection.

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Evaluation of complement factor 5 variants as genetic risk factors for the development of advanced fibrosis in chronic hepatitis C infection. / Halangk, Juliane; Sarrazin, Christoph; Neumann, Konrad; Puhl, Gero; Mueller, Tobias; Teuber, Gerlinde; Klinker, Hartwig; Hinrichsen, Holger; Buggisch, Peter; Landt, Olfert; Weich, Viola; Bergk, Alexandra; Wiedenmann, Bertram; Neuhaus, Peter; Berg, Thomas; Witt, Heiko.

in: J HEPATOL, Jahrgang 49, Nr. 3, 3, 2008, S. 339-345.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Halangk, J, Sarrazin, C, Neumann, K, Puhl, G, Mueller, T, Teuber, G, Klinker, H, Hinrichsen, H, Buggisch, P, Landt, O, Weich, V, Bergk, A, Wiedenmann, B, Neuhaus, P, Berg, T & Witt, H 2008, 'Evaluation of complement factor 5 variants as genetic risk factors for the development of advanced fibrosis in chronic hepatitis C infection.', J HEPATOL, Jg. 49, Nr. 3, 3, S. 339-345. <http://www.ncbi.nlm.nih.gov/pubmed/18644651?dopt=Citation>

APA

Halangk, J., Sarrazin, C., Neumann, K., Puhl, G., Mueller, T., Teuber, G., Klinker, H., Hinrichsen, H., Buggisch, P., Landt, O., Weich, V., Bergk, A., Wiedenmann, B., Neuhaus, P., Berg, T., & Witt, H. (2008). Evaluation of complement factor 5 variants as genetic risk factors for the development of advanced fibrosis in chronic hepatitis C infection. J HEPATOL, 49(3), 339-345. [3]. http://www.ncbi.nlm.nih.gov/pubmed/18644651?dopt=Citation

Vancouver

Bibtex

@article{d25da13c5fb1476a8c15b6b3914350a8,
title = "Evaluation of complement factor 5 variants as genetic risk factors for the development of advanced fibrosis in chronic hepatitis C infection.",
abstract = "BACKGROUND/AIMS: Intercross studies in inbred mice susceptible or resistant to liver fibrosis revealed complement factor 5 as a quantitative trait gene associated with the development of fibrosis. In 277 patients with hepatitis C, two C5 SNPs, rs17611 and rs2300929, have been associated with advanced fibrosis. METHODS: We investigated the association of these C5 SNPs with advanced fibrosis in 1435 HCV infected patients and in 1003 patients with other liver diseases. We performed genotyping with melting curve analysis using fluorescence resonance energy transfer probes in the LightCycler. RESULTS: The defined high-risk genotypes (AA and TT) and alleles (A and T) were not associated with advanced fibrosis in HCV patients when Chi square testing and logistic regression analysis were applied (rs17611A 0.45 in F0-1 vs. 0.43 in F2-4, P=0.31; rs2300929T 0.91 F0-1 and 0.91 in F2-4, P=0.82). In the group of patients with liver diseases other than HCV we neither found an association of the C5 SNPs with advanced fibrosis nor an overrepresentation of the SNPs in patients with cirrhosis. CONCLUSIONS: We found no evidence that these C5 SNPs are genetic risk factors for the development of advanced fibrosis in chronic HCV infection or other chronic liver diseases.",
author = "Juliane Halangk and Christoph Sarrazin and Konrad Neumann and Gero Puhl and Tobias Mueller and Gerlinde Teuber and Hartwig Klinker and Holger Hinrichsen and Peter Buggisch and Olfert Landt and Viola Weich and Alexandra Bergk and Bertram Wiedenmann and Peter Neuhaus and Thomas Berg and Heiko Witt",
year = "2008",
language = "Deutsch",
volume = "49",
pages = "339--345",
journal = "J HEPATOL",
issn = "0168-8278",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Evaluation of complement factor 5 variants as genetic risk factors for the development of advanced fibrosis in chronic hepatitis C infection.

AU - Halangk, Juliane

AU - Sarrazin, Christoph

AU - Neumann, Konrad

AU - Puhl, Gero

AU - Mueller, Tobias

AU - Teuber, Gerlinde

AU - Klinker, Hartwig

AU - Hinrichsen, Holger

AU - Buggisch, Peter

AU - Landt, Olfert

AU - Weich, Viola

AU - Bergk, Alexandra

AU - Wiedenmann, Bertram

AU - Neuhaus, Peter

AU - Berg, Thomas

AU - Witt, Heiko

PY - 2008

Y1 - 2008

N2 - BACKGROUND/AIMS: Intercross studies in inbred mice susceptible or resistant to liver fibrosis revealed complement factor 5 as a quantitative trait gene associated with the development of fibrosis. In 277 patients with hepatitis C, two C5 SNPs, rs17611 and rs2300929, have been associated with advanced fibrosis. METHODS: We investigated the association of these C5 SNPs with advanced fibrosis in 1435 HCV infected patients and in 1003 patients with other liver diseases. We performed genotyping with melting curve analysis using fluorescence resonance energy transfer probes in the LightCycler. RESULTS: The defined high-risk genotypes (AA and TT) and alleles (A and T) were not associated with advanced fibrosis in HCV patients when Chi square testing and logistic regression analysis were applied (rs17611A 0.45 in F0-1 vs. 0.43 in F2-4, P=0.31; rs2300929T 0.91 F0-1 and 0.91 in F2-4, P=0.82). In the group of patients with liver diseases other than HCV we neither found an association of the C5 SNPs with advanced fibrosis nor an overrepresentation of the SNPs in patients with cirrhosis. CONCLUSIONS: We found no evidence that these C5 SNPs are genetic risk factors for the development of advanced fibrosis in chronic HCV infection or other chronic liver diseases.

AB - BACKGROUND/AIMS: Intercross studies in inbred mice susceptible or resistant to liver fibrosis revealed complement factor 5 as a quantitative trait gene associated with the development of fibrosis. In 277 patients with hepatitis C, two C5 SNPs, rs17611 and rs2300929, have been associated with advanced fibrosis. METHODS: We investigated the association of these C5 SNPs with advanced fibrosis in 1435 HCV infected patients and in 1003 patients with other liver diseases. We performed genotyping with melting curve analysis using fluorescence resonance energy transfer probes in the LightCycler. RESULTS: The defined high-risk genotypes (AA and TT) and alleles (A and T) were not associated with advanced fibrosis in HCV patients when Chi square testing and logistic regression analysis were applied (rs17611A 0.45 in F0-1 vs. 0.43 in F2-4, P=0.31; rs2300929T 0.91 F0-1 and 0.91 in F2-4, P=0.82). In the group of patients with liver diseases other than HCV we neither found an association of the C5 SNPs with advanced fibrosis nor an overrepresentation of the SNPs in patients with cirrhosis. CONCLUSIONS: We found no evidence that these C5 SNPs are genetic risk factors for the development of advanced fibrosis in chronic HCV infection or other chronic liver diseases.

M3 - SCORING: Zeitschriftenaufsatz

VL - 49

SP - 339

EP - 345

JO - J HEPATOL

JF - J HEPATOL

SN - 0168-8278

IS - 3

M1 - 3

ER -