Document Type



Medicine and Health Sciences




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).


YKL-40 promoter polymorphisms were determined in 456 HALT-C Trial 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.


Mean patient age was 49.5 years, 70.4% were male, 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 to 48 weeks of peginterferon/ribavirin therapy. Serum YKL-40 levels remained significantly lower during follow-up in the randomized TT homozygotes compared to CT heterozygotes and CC homozygotes (p <0.001). Despite this association, YKL-40 genotype was not associated with the risk of clinical or histologic liver disease progression.


A reduced frequency of the protective YKL-40 promoter polymorphism was not observed in the HALT-C Trial 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.


Liver Int. Author manuscript; available in PMC 2013 April 1. Published in final edited form as: Liver Int. 2012 April; 32(4): 665–674. Published online 2011 November 22. doi: 10.1111/j.1478-3231.2011.02686.x PMCID: PMC3299849 NIHMSID: NIHMS334352