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.
Bonkovsky, Herbert L., "YKL-40 Genetic Polymorphisms and the Risk of Liver Disease Progression in Patients with Advanced Fibrosis Due to Chronic Hepatitis C" (2012). Articles - Research. 160.