Data from: Influence of hepatitis C virus and IL28B genotypes on liver stiffness

Objective: Liver fibrosis has been associated with hepatitis C virus (HCV)
genotype and genetic variation near the interleukin 28B (IL28B) gene, but
the relative contribution is unknown. We aimed to investigate the relation
between HCV genotypes, IL28B and development of liver stiffness. Patients
and Methods: This cross-sectional study consists of 369 patients with
chronic hepatitis C (CHC). Liver stiffness was evaluated using transient
elastograhy (TE). Factors associated with development of liver fibrosis
were identified by logistic regression analysis. Results: We identified
369 patients with CHC. 235 were male, 297 Caucasians, and 223 had been
exposed to HCV through intravenous drug use. The overall median TE value
was 7.4 kPa (interquartile range (IQR) 5.7–12.1). HCV replication was
enhanced in patients carrying the IL28B CC genotype compared to TT and TC
(5.8 vs. 5.4 log10 IU/mL, p = 0.03). Patients infected with HCV genotype 3
had significantly higher TE values (8.2 kPa; IQR, 5.9–14.5) compared to
genotype 1 (6.9 kPa; IQR, 5.4–10.9) and 2 (6.7 kPa; IQR, 4.9–8.8) (p =
0.02). Within patients with genotype 3, IL28B CC genotype had the highest
TE values (p = 0.04). However, in multivariate logistic regression, using
various cut-off values for fibrosis and cirrhosis, only increasing age
(odds ratio (OR) 1.09 (95% confidence interval (CI), 1.05–1.14 per year
increment)), ALT (OR 1.01 (95% CI, 1.002–1.011), per unit increment) and
HCV genotype 3 compared to genotype 1 (OR 2.40 (95% CI, 1.19–4.81), were
consistently associated with cirrhosis (TE>17.1 kPa). Conclusions:
Age, ALT and infection with HCV genotype 3 were associated with cirrhosis
assessed by TE. However, IL28B genotype was not an independent predictor
of fibrosis in our study.