BACKGROUND: Hepatitis B virus (HBV) genotypes influence disease progression and treatment outcome. OBJECTIVES: To determine natural history and treatment outcome in patient chronically infected with HBV. STUDY DESIGN: A cohort study included 162 treatment naive patients with chronic HBV infection in order to analyze factors influencing natural history of infection and survival. RESULTS: Genotype A was far less prevalent, detected in 14.2%. The prevalence of HbeAg+ serology of 60.8% among patients infected with genotype A was significantly higher then 30.9% recorded among those with genotype D (P=0.02). Even though patients from two genotypes subgroups had significantly different prevalence of HBeAg serology, their viral loads were similar at the time of diagnosis (2.90 log10 and 3.31 log10 HBV DNK IU/μl plasma, for genotypes A and D, respectively). The analyses of viral loads across three serologic patterns of chronic HBV infection were: for HBeAg+/HBeAb-, HbeAg-/HBAb+, and both "e" antigen and antibodies negative: 4.24, 2.67 and 2.69 log10 IU/ml of HBV DNA IU/μl, respectively (P=0.01). Mean time to liver cirrhosis was 23.2±3.4 years and 15.1±8.4 years, for genotypes A and D, respectively (P=0.02). The overall estimated mean survival of patients with chronic HBV infection was 28.4 years, and was influenced by the stage of liver disease, but not by gender, age above 40, viral genotype and lamivudine therapy. CONCLUSIONS: Patients infected with genotype D had more rapid progression to ESLD regardless of levels of viral replication. All clinical and laboratory differences between genotypes did not affect survival of patients with chronic hepatitis B, regardless of lamivudine therapy.
BACKGROUND:Hepatitis B virus (HBV) genotypes influence disease progression and treatment outcome. OBJECTIVES: To determine natural history and treatment outcome in patient chronically infected with HBV. STUDY DESIGN: A cohort study included 162 treatment naive patients with chronic HBV infection in order to analyze factors influencing natural history of infection and survival. RESULTS: Genotype A was far less prevalent, detected in 14.2%. The prevalence of HbeAg+ serology of 60.8% among patients infected with genotype A was significantly higher then 30.9% recorded among those with genotype D (P=0.02). Even though patients from two genotypes subgroups had significantly different prevalence of HBeAg serology, their viral loads were similar at the time of diagnosis (2.90 log10 and 3.31 log10 HBV DNK IU/μl plasma, for genotypes A and D, respectively). The analyses of viral loads across three serologic patterns of chronic HBV infection were: for HBeAg+/HBeAb-, HbeAg-/HBAb+, and both "e" antigen and antibodies negative: 4.24, 2.67 and 2.69 log10 IU/ml of HBV DNA IU/μl, respectively (P=0.01). Mean time to liver cirrhosis was 23.2±3.4 years and 15.1±8.4 years, for genotypes A and D, respectively (P=0.02). The overall estimated mean survival of patients with chronic HBV infection was 28.4 years, and was influenced by the stage of liver disease, but not by gender, age above 40, viral genotype and lamivudine therapy. CONCLUSIONS:Patients infected with genotype D had more rapid progression to ESLD regardless of levels of viral replication. All clinical and laboratory differences between genotypes did not affect survival of patients with chronic hepatitis B, regardless of lamivudine therapy.