YKL ‐40 genetic polymorphisms and the risk of liver disease progression in patients with advanced fibrosis due to chronic hepatitis C
dc.contributor.author | Fontana, Robert John | en_US |
dc.contributor.author | Litman, Heather J. | en_US |
dc.contributor.author | Dienstag, Jules L. | en_US |
dc.contributor.author | Bonkovsky, Herbert L. | en_US |
dc.contributor.author | Su, Grace L. | en_US |
dc.contributor.author | Sterling, Richard K. | en_US |
dc.contributor.author | Lok, Anna Suk-Fong | en_US |
dc.date.accessioned | 2012-04-04T18:43:31Z | |
dc.date.available | 2013-06-11T19:15:43Z | en_US |
dc.date.issued | 2012-04 | en_US |
dc.identifier.citation | Fontana, Robert J.; Litman, Heather J.; Dienstag, Jules L.; Bonkovsky, Herbert L.; Su, Grace; Sterling, Richard K.; Lok, Anna S. (2012). " YKL ‐40 genetic polymorphisms and the risk of liver disease progression in patients with advanced fibrosis due to chronic hepatitis C ." Liver International 32(4): 665-674. <http://hdl.handle.net/2027.42/90574> | en_US |
dc.identifier.issn | 1478-3223 | en_US |
dc.identifier.issn | 1478-3231 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/90574 | |
dc.description.abstract | Background/Aims The aim of this study was to explore the association of a functional YKL ‐40 promoter polymorphism (rs4950928) with baseline disease stage, response to antiviral therapy and risk of liver disease progression in a group of patients with chronic hepatitis C ( CHC ). Methods YKL ‐40 promoter polymorphisms were determined in 456 H epatitis C A ntiviral L ong‐term T reatment against C irrhosis ( HALT ‐C) T rial patients with bridging fibrosis or cirrhosis entering a prerandomization lead‐in peginterferon/ribavirin 24‐week treatment phase and in 462 patients followed for a mean of 3.8 years after randomization to maintenance peginterferon or observation. Results Mean patient age was 49.5 years, 70.4% were men and 71.2% were Caucasian. The 17% frequency of the YKL ‐40 minor allele (T) was similar to that reported in the general population. YKL ‐40 genotype was associated significantly with baseline serum YKL ‐40 levels but was not associated with the likelihood of a virological response following 24–48 weeks of peginterferon/ribavirin therapy. Serum YKL ‐40 levels remained significantly lower during follow‐up in the randomized TT homozygotes compared with CT heterozygotes and CC homozygotes ( P < 0.001). Despite this association, YKL ‐40 genotype was not associated with the risk of clinical or histological liver disease progression. Conclusions A reduced frequency of the protective YKL ‐40 promoter polymorphism was not observed in the HALT ‐C T rial patient population. The absence of an association between YKL ‐40 promoter polymorphisms and baseline liver disease severity as well as with the risk of liver disease progression over time suggests that this polymorphism is not associated with disease progression in CHC patients with established fibrosis. | en_US |
dc.publisher | Wiley Periodicals, Inc. | en_US |
dc.subject.other | Virological Response | en_US |
dc.subject.other | Decompensation | en_US |
dc.subject.other | Cirrhosis | en_US |
dc.subject.other | Genetic Polymorphisms | en_US |
dc.subject.other | Hepatitis C | en_US |
dc.subject.other | Interferon | en_US |
dc.title | YKL ‐40 genetic polymorphisms and the risk of liver disease progression in patients with advanced fibrosis due to chronic hepatitis C | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.identifier.pmid | 22103814 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/90574/1/liv2686.pdf | |
dc.identifier.doi | 10.1111/j.1478-3231.2011.02686.x | en_US |
dc.identifier.source | Liver International | en_US |
dc.identifier.citedreference | Huang H, Shiffman ML, Friedman S, et al. A 7 gene signature identifies the risk of developing cirrhosis in patients with chronic hepatitis C. Hepatology 2007; 46: 297 – 306. | en_US |
dc.identifier.citedreference | Sztrolovics R, Recklies AD, Roughley PJ, Mort JS. Hyaluronate degradation as an alternative mechanism for proteoglycan release from cartilage during interleukin‐1beta stimulated catabolism. Biochm J 2002; 362: 473 – 9. | en_US |
dc.identifier.citedreference | Malinda KM, Ponce L, Kleinman HK, Shackleton LM, Millis AJ. Gp38k, a protein synthesized by vascular smooth muscle cells, stimulates directional migration of human umbilical vein endothelial cells. Exp Cell Res 1999; 250: 168 – 73. | en_US |
dc.identifier.citedreference | Nojgaard C, Johansen JS, Christensen E, et al. Serum levels of YKL‐40 and PIIINP as prognostic markers in patients with alcoholic liver disease. J Hepatol 2003; 39: 179 – 86. | en_US |
dc.identifier.citedreference | Mehta P, Ploutz‐Snyder R, Nandi J, et al. Diagnostic accuracy of serum hyaluronic acid, FIBROSpect II, and YKL‐40 for discriminating fibrosis stages in chronic hepatitis C. Am J Gastroenterol 2008; 103: 928 – 36. | en_US |
dc.identifier.citedreference | Rehli M, Krause SW, Andreesen R. Molecular characterization of the gene for human cartilage gp_39 (CHI3L1), a member of the chitinase protein family and marker for late stages of macrophage differentiation. Genomics 1997; 43: 221 – 5. | en_US |
dc.identifier.citedreference | Ober C, Tan Z, Sun Y, et al. Effect of variation in CHI3L1 on serum YKL‐40 level, risk of asthma, and lung function. N Engl J Med 2008; 358: 1682 – 91. | en_US |
dc.identifier.citedreference | Berres ML, Papen S, Pauels K, et al. A functional variation in CHI3L1 is associated with severity of liver fibrosis and YKL‐40 serum levels in chronic hepatitis C infection. J Hepatology 2009; 50: 370 – 6. | en_US |
dc.identifier.citedreference | Di Bisceglie AM, Shiffman ML, Everson GT, et al. Prolonged therapy of advanced chronic hepatitis C with low‐dose peginterferon. N Engl J Med 2008; 359: 2429 – 41. | en_US |
dc.identifier.citedreference | Shiffman ML, DiBisceglie AM, Lindsay KL, et al. Peginterferon alfa‐2a and ribavirin in patients with chronic hepatitis C who failed prior treatment. Gastroenterology 2004; 126: 1015 – 23. | en_US |
dc.identifier.citedreference | Fontana RJ, Goodman ZD, Dienstag JL, et al. Relationship of serum fibrosis markers with liver fibrosis stage and collagen content in patients with advanced chronic hepatitis C. Hepatology 2008; 47: 789 – 98. | en_US |
dc.identifier.citedreference | Fontana RJ, Bonkovsky HL, Naishadham D, et al. Serum fibrosis marker levels decrease after successful antiviral treatment in chronic hepatitis C patients with advanced fibrosis. Clin Gastroenterol Hepatol 2009; 7: 219 – 26. | en_US |
dc.identifier.citedreference | Fontana RJ, Dienstag JL, Bonkovsky HL, et al., the HALT‐C Trial Group. Serum fibrosis markers are associated with liver disease progression in non‐responder patients with chronic hepatitis C. Gut 2010; 59: 1401 – 9. | en_US |
dc.identifier.citedreference | Ishak KG. Chronic hepatitis: morphology and nomenclature. Mod Pathol 1994; 7: 690 – 713. | en_US |
dc.identifier.citedreference | Lok ASF, Everhart JE, Chung RT, et al. Hepatic steatosis in hepatitis C: comparison of diabetic and non‐diabetic patients in the Hepatitis C Antiviral Long‐term Treatment against Cirrhosis Trial. Clin Gastroenterol Hepatol 2007; 5: 245 – 54. | en_US |
dc.identifier.citedreference | Huang H, Shiffman ML, Cheung RC, et al. Identification of two gene variants associated with risk of advanced fibrosis in patients with chronic hepatitis C. Gastroenterology 2006; 130: 1679 – 87. | en_US |
dc.identifier.citedreference | Asselah T, Bieche I, Paradis V, et al. Genetics, genomics, and proteomics: implications for the diagnosis and the treatment of chronic hepatitis C. Sem Liv Dis 2007; 27: 13 – 27. | en_US |
dc.identifier.citedreference | Bataller R, North KE, Brenner DA. Genetic polymorphisms and the progression of liver fibrosis: a critical appraisal. Hepatology 2003; 37: 493 – 503. | en_US |
dc.identifier.citedreference | Zhao X, Tang R, Gaso B, et al. Functional variants in the promoter region of chitinase 3‐like 1 (CHI3L1) and susceptibility to schizophrenia. Am J Hum Genet 2007; 80: 12 – 8. | en_US |
dc.identifier.citedreference | Suppiah V, Moldovan M, Ahlenstiel G, et al. IL28B is associated with response to chronic hepatitis C interferon‐α and ribavirin therapy. Nat Genet 2009; 41: 1100 – 4. | en_US |
dc.identifier.citedreference | Thompson AJ, Muir AJ, Sulkowski MS, et al. Interleukin‐28B polymorphism improves viral kinetics and is the strongest pretreatment predictor of sustained virological response in genotype 1 hepatitis C virus. Gastroenterology 2010; 139: 120 – 9. | en_US |
dc.identifier.citedreference | O'Brien TR, Everhart JE, Chung RT, et al. An IL28B genotype‐based model for personalized prediction of response to pegylated‐Interferon alfa and ribavirin in the treatment of chronic hepatitis C (Abstract). Hepatology 2010; 62 ( Suppl. 1 ): A127. | en_US |
dc.identifier.citedreference | Curto TM, Lagier RJ, Lok AS, et al., and the HALT‐C Trial Group. Predicting Cirrhosis and clinical outcomes in patients with advanced chronic hepatitis C with a panel of genetic markers (CRS7). Pharmacogenet Genomics 2011; 21: 851 – 60. | en_US |
dc.identifier.citedreference | O'Brien TR, Everhart JE, Morgan TR, et al., and the HALT‐C Trial Group. An IL28‐B genotype‐based clinical prediction model for treatment of chronic hepatitis C. PLos One 2011; 6: e20904. | en_US |
dc.identifier.citedreference | Trepo E, Potthoff A, Pradat P, et al. Role of cirrhosis risk score for the early prediction of fibrosis progression in hepatitis C patients with minimal liver disease. J Hepatology 2011; 55: 38 – 44. | en_US |
dc.identifier.citedreference | Marcolongo M, Young B, Dal PF, et al. A seven‐gene signature (cirrhosis risk score) predicts liver fibrosis progression in patients with initially mild chronic hepatitis C. Hepatology 2009; 50: 1028 – 44. | en_US |
dc.identifier.citedreference | Kamal SM, Turner B, He Q, et al. Progression of fibrosis in hepatitis C with and without schistosomiasis correlation with serum markers of fibrosis. Hepatology 2006; 43: 771 – 9. | en_US |
dc.identifier.citedreference | Hu B, Trinh K, Figueira WF, Price PA. Isolation and sequence of novel human chondrocyte protein related to mammalian members of the chitinase protein family. J Biol Chem 1996; 271: 19415 – 20. | en_US |
dc.identifier.citedreference | Rehli M, Niller HH, Ammon C, et al. Transcriptional regulation of CHI3LI, a marker gene for late stages of macrophage differentiation. J Biol Chem 2003; 278: 44058 – 67. | en_US |
dc.identifier.citedreference | Baeten D, Boots AM, Steenbakkers PG, et al. Human cartilage gp‐39 + , CD16 + monocytes in peripheral blood and synovium: correlation with joint destruction in rheumatoid arthritis. Arthritis Rheum 2000; 43: 1233 – 43. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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