Abstract
It is well appreciated that ethnicity influences the natural history and immune responses during a chronic hepatitis B infection. In this study, we explore the effect of ethnicity and treatment cessation on Hepatitis B surface Antigen (HBsAg) seroclearance in patients with Nucleos(t)ide Analogue (NA)-induced Hepatitis B e Antigen (HBeAg) seroconversion. We performed a multi-ethnic, multicentric observational cohort study. The analyzed cohort consisted of 178 mono-infected, predominantly male (75.3%) chronic hepatitis B patients of mixed ethnicity (44.4% Asians, 48.9% Caucasians) with nucleos(t)ide analogue-induced HBeAg seroconversion. Treatment was withdrawn in 105 patients and continued in 73, leading to HBsAg loss in 14 patients off- and 16 patients on-treatment, respectively. Overall, HBsAg loss rates were not affected by treatment cessation (hazard ratio 1.45, p = 0.372), regardless of consolidation treatment duration. Caucasian ethnicity was associated with an increased chance of HBsAg loss (hazard ratio 6.70, p = 0.001), but hepatitis B virus genotype was not (p = 0.812). In conclusion, ethnicity is the most important determinant for HBsAg loss after NA-induced HBeAg seroconversion, with up to six-fold higher HBsAg loss rates in Caucasians compared to Asians, irrespective of treatment cessation and consolidation treatment duration.
Highlights
With approximately 3% of the worldwide population infected, chronic hepatitis B (CHB) represents a serious global health problem
After expansion of the Nucleos(t)ide Analogue (NA) stop cohort with patients who continued treatment, the final cohort consisted of 178 predominantly male (75.3%) patients of well-balanced, mixed ethnicity (44.4% Asians, 48.9% Caucasians) with NA-induced Hepatitis B e Antigen (HBeAg) seroconversion after a median treatment duration of
We investigated hepatitis B surface antigen (HBsAg) loss following NA-induced HBeAg seroconversion in a multicentric, international CHB cohort that was well-balanced for ethnicity
Summary
With approximately 3% of the worldwide population infected, chronic hepatitis B (CHB) represents a serious global health problem. Chronic infections are associated with an up to 100-fold increased risk for liver-related complications, including cirrhosis, decompensation, and hepatocellular carcinoma. The hepatitis B virus (HBV) continues to kill over 700,000 people annually [2]. HBV integrates into the host genome and forms covalently closed circular DNA (cccDNA), a minichromosome in the nucleus of infected hepatocytes, which cannot be eradicated with the current therapeutic armamentarium [3]. Seroclearance of the virus from blood, marked by hepatitis B surface antigen (HBsAg) loss, confers excellent clinical outcomes and is regarded as the optimal endpoint in CHB treatment [4,5,6,7]
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