Abstract
Interleukin 6 (IL6) plays an essential role in the regulation of immune response to chronic disease. In this study, the three known single nucleotide polymorphisms (SNPs) in the IL6 promoter region were genotyped in a large chronic hepatitis B cohort to evaluate the effects of IL6 promoter variants. The single base extension method was used for this genotyping. Haplotypes were constructed by the three SNPs in IL6. Allele frequencies were compared for; i) patients with chronic hepatitis (CH) and chronic carriers vs. chronic hepatis patients with clinical evidence of liver cirrhosis (LC) (i.e., portal hypertension), ii) cirrhotic patients with hepatocellular carcinoma (HCC) vs. without HCC by logistic regression, and iii) with respect to the time intervals from the onset of infection to HCC. Results were analyzed by Cox relative hazard analysis on the assumption that all the patients were infected during early infancy. The frequencies of each SNP were 0.002 (IL6-597 G>A), 0.25 (IL6-572 C>G) and 0.002 (IL6-174 G>C), respectively, in the Korean population (n = 1,046). No significant associations were detected between IL6-572 C>G and chronic hepatitis B outcome in this study; i.e., LC occurrence on CH (OR = 0.16-1.27, P = 0.13- 0.71) and HCC occurrence on LC (OR = 1.04-1.23, P = 0.89-0.60) of heterozygotes and homozygotes for G allele in referent comparison to homozygotes for common allele (C/C genotype), and time interval to HCC (RH = 0.67-1.00; P = 0.14-0.99). In conclusion, there appeared to be no significant associations between IL6 promoter variants and disease outcome in chronic hepatitis B.
Highlights
Korea is an endemic area of chronic hepatitis B virus (HBV) infection
The different outcomes of HBV infection might be explained by virus-host interactions (Cruz et al, 1987)
Little is known about the host genetic factors that are involved in the progress of HBV infection
Summary
Korea is an endemic area of chronic hepatitis B virus (HBV) infection. The sequelae of chronic HBV infection vary from an inactive carrier state to the development of cirrhosis and hepatocellular carcinoma (HCC). Chronic carriers of HBV have a high risk of developing HCC compared with uninfected individuals (Blumberg, 1984; Huh et al, 1998; Merican et al, 2000). HCC is the most common primary liver cancer and is one of the ten most common carcinomas in the world. The incidence of HCC shows geographical variation and is most common in Asia and Africa, where HBV infection is highly endemic and where chronic infection is usually acquired in early infancy (Yu et al, 2000a). The development of HCC occurs 30-50 years after the onset of HBV infection; HCC is far more likely to be seen in individuals exposed to HBV perinatally rather than horizontally in adult life
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