Age-specific prognosis following spontaneous hepatitis B e antigen seroconversion in chronic hepatitis B

Abstract

Hepatitis B e antigen (HBeAg) seroconversion in chronic hepatitis B virus infection confers a favorable prognosis, but untoward outcomes may develop in some patients. The impact of the age of HBeAg seroconversion on prognosis is not clearly known. HBeAg-positive patients with biopsy-proven chronic hepatitis B were followed up long-term.

Predictors of hepatitis B e antigen‐negative hepatitis in chronic hepatitis B virus‐infected patients from childhood to adulthood

“…[1][2][3] HBeAg seroconversion after 40 years of age has been reported to increase the risk of chronic liver insufficiency, liver cirrhosis, and even hepatocellular carcinoma. [4][5][6] Although HBeAg seroconversion is an important hallmark during chronic HBV infection, some patients still experience HBeAg-negative hepatitis after HBeAg seroconversion. The annual incidence of HBeAg-negative hepatitis was estimated to be 2%-4% in adult patients, 2,3,5,6 although this patient population may represent only the chronic HBV-infected subjects who experienced delayed HBeAg seroconversion in adulthood and the risk of HBeAg-negative hepatitis remains unclear in subjects who experience HBeAg seroconversion at a young age.…”

“…[4][5][6] Although HBeAg seroconversion is an important hallmark during chronic HBV infection, some patients still experience HBeAg-negative hepatitis after HBeAg seroconversion. The annual incidence of HBeAg-negative hepatitis was estimated to be 2%-4% in adult patients, 2,3,5,6 although this patient population may represent only the chronic HBV-infected subjects who experienced delayed HBeAg seroconversion in adulthood and the risk of HBeAg-negative hepatitis remains unclear in subjects who experience HBeAg seroconversion at a young age. 6,7 Previous studies have noted the presence of the HBV basal core promoter (BCP) and precore/core gene mutations during the immune-clearance phase before HBeAg seroconversion and hepatitis B core antigen cytoplasmic retention in hepatocytes of HBeAg-negative hepatitis patients.…”

“…The annual incidence of HBeAg-negative hepatitis was estimated to be 2%-4% in adult patients, 2,3,5,6 although this patient population may represent only the chronic HBV-infected subjects who experienced delayed HBeAg seroconversion in adulthood and the risk of HBeAg-negative hepatitis remains unclear in subjects who experience HBeAg seroconversion at a young age. 6,7 Previous studies have noted the presence of the HBV basal core promoter (BCP) and precore/core gene mutations during the immune-clearance phase before HBeAg seroconversion and hepatitis B core antigen cytoplasmic retention in hepatocytes of HBeAg-negative hepatitis patients. [8][9][10][11][12] Chronic HBV genotype B-infected subjects experience HBeAg seroconversion earlier than those with HBV genotype C infection.…”

“…[15][16][17][18] However, the relationship between HBV genotype, gender, and HBeAg-negative hepatitis remains controversial. 5,6,19 Prior nucleos(t)ide analogue treatment was also reported as a risk factor for hepatitis reactivation after HBeAg seroconversion, but the differences among various antiviral agents are unclear. 19 We conducted this study to investigate the impact of possible risk factors, including HBV genotype, gender, age at HBeAg seroconversion, antiviral treatment prior to HBeAg seroconversion, and relevant HBV BCP and precore/core gene mutations on incidence of HBeAgnegative hepatitis in a long-term and large-scale cohort study that followed patients from childhood to adulthood.…”

Management of Chronic Hepatitis B: An Overview of Practice Guidelines for Primary Care Providers

“…30 If HBeAg seroconversion occurs late in life (after the age of ϳ40 years), however, the prolonged immune response may still allow liver disease to progress. 31 Importantly, HBV reactivation may occur, either as a result of HBeAg seroreversion (ie, restored HBeAg positivity caused by reactivation of wildtype HBV), or, more frequently, as a result of the emergence of HBV mutants that no longer express HBeAg (ie, precore or basal core promoter [PC/BCP] mutants); the latter event, which results in HBeAg-negative CHB, is particularly common among patients from Asia or the Mediterranean, where the prevalence of PC/BCP mutants is high. 32 HBV reactivation can occur after years or decades of the inactive carrier state and represents, especially in the case of HBeAg-negative CHB, a late stage of the infection generally associated with advanced liver disease.…”