BACKGROUND: Infection due to hepatitis B virus (HBV) could be due to wild or mutant (precore or surface) viruses. The prevalence and clinical profile of different viral forms in patients with chronic liver disease has not been established. METHODS: One hundred and twenty patients with histologically proven HBV-related chronic liver disease were studied. Patients with dual infection with HCV/HDV/HIV, past history of interferon therapy, or autoimmune hepatitis were excluded. Eighteen (15.5%) patients had the precore mutation (HBsAg +ve, HBeAg -ve/anti-HBe +ve, HBV DNA +ve), and 13 (10.8%) had the surface gene mutations (HBsAg -ve, HBeAg -ve, IgG anti-HBc, and HBV DNA +ve). The remaining 89 (74.2%) patients were infected with wild type HBV. The course of all patients with mutant forms and 41 of those with the wild type form was followed for a mean (+/- SD) of 4.4 +/- 2.4 yr. RESULTS: Compared with wild-type-infected patients, those with surface mutation were younger (39.9 +/- 14 vs. 30.1 +/- 12.4 yr, p < 0.05). Patients with precore mutations had a shorter illness than those with surface mutant (p < 0.01) and wild forms (p < 0.05). Histologically, patients with precore type had more active liver disease than wild type (39% vs. 15%, p < 0.05). Patients with precore mutations were always symptomatic, often presenting with ascites (67%) and jaundice (55%). Patients with surface mutant forms often presented with quiescent cirrhosis (77%) or cirrhosis with hepatoma (15%). CONCLUSIONS: One-fourth of HBV-related chronic liver disease in Asian Indians is attributable to mutant HBV forms. The presence of variant viruses alters the natural history of the disease, with the precore variance having a more aggressive course and the surface mutant, a more quiescent but unfavorable course, compared with the wild type.
BACKGROUND: Infection due to hepatitis B virus (HBV) could be due to wild or mutant (precore or surface) viruses. The prevalence and clinical profile of different viral forms in patients with chronic liver disease has not been established. METHODS: One hundred and twenty patients with histologically proven HBV-related chronic liver disease were studied. Patients with dual infection with HCV/HDV/HIV, past history of interferon therapy, or autoimmune hepatitis were excluded. Eighteen (15.5%) patients had the precore mutation (HBsAg +ve, HBeAg -ve/anti-HBe +ve, HBV DNA +ve), and 13 (10.8%) had the surface gene mutations (HBsAg -ve, HBeAg -ve, IgG anti-HBc, and HBV DNA +ve). The remaining 89 (74.2%) patients were infected with wild type HBV. The course of all patients with mutant forms and 41 of those with the wild type form was followed for a mean (+/- SD) of 4.4 +/- 2.4 yr. RESULTS: Compared with wild-type-infected patients, those with surface mutation were younger (39.9 +/- 14 vs. 30.1 +/- 12.4 yr, p < 0.05). Patients with precore mutations had a shorter illness than those with surface mutant (p < 0.01) and wild forms (p < 0.05). Histologically, patients with precore type had more active liver disease than wild type (39% vs. 15%, p < 0.05). Patients with precore mutations were always symptomatic, often presenting with ascites (67%) and jaundice (55%). Patients with surface mutant forms often presented with quiescent cirrhosis (77%) or cirrhosis with hepatoma (15%). CONCLUSIONS: One-fourth of HBV-related chronic liver disease in Asian Indians is attributable to mutant HBV forms. The presence of variant viruses alters the natural history of the disease, with the precore variance having a more aggressive course and the surface mutant, a more quiescent but unfavorable course, compared with the wild type.
Authors: Maja Thiele; Lise Lotte Gluud; Annette Dam Fialla; Emilie Kirstine Dahl; Aleksander Krag Journal: PLoS One Date: 2014-09-16 Impact factor: 3.240