A study of association between regulatory polymorphism in the IL-10 gene promoter region and acute viral hepatitis, and acute liver failure.

Abstract

The level of inflammatory cytokine Interleukin (IL)-10 is increased in patients infected with hepatitis-related acute liver failure (ALF), and this was thought to be because of the regulatory polymorphism in the IL-10 gene promoter region. The present study was designed to analyze the possible association between IL-10 gene promoter polymorphism and acute viral hepatitis (AVH), and ALF. An attempt was made to quantify IL-10 levels at admission, during the hospital stay, and at the final outcome to study its relationship with liver injury among patients with AVH, ALF, and controls. The study included 40 patients each with ALF and AVH. IL-10 gene promoter polymorphism was detected by the PCR-RFLP method. Quantification of IL-10 was done using commercially available ELISA kits. The individuals with -592 AC, -819 TC, -1082 AA genotypes were found to have a significantly higher risk of ALF whereas those with -592 AA and - 819 CC polymorphism were found to be less susceptible. Individuals with - 819 CC were found to be more susceptible to AVH while those with -592 AA and -819 TT were less susceptible as compared to controls. Mean serum IL-10 at admission was significantly elevated in patients with ALF (38.4±11.3 pg/mL) as compared to patients with AVH (16.7±5.4pg/mL) and control population (8.3±3.6 pg/mL, p < 0.05). Regulatory polymorphism in the IL-10 gene promoter has a possible and significant association with severity and outcome in patients with AVH and ALF. Raised levels of IL-10 could be predictive of prognosis in patients with ALF.