Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2025
Changes in Hepatitis B Core Antigen and Hepatitis B Surface Antigen Expression Following Antiviral Therapy and Their Role in Outcome of Patients With Chronic Hepatitis B.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Shaik Mohammed Rifat, Apodaca Lauren, Auh Sungyoung, Kattapuram Meera, Cloherty Gavin A, Kleiner David E, Ghany Marc G
Аннотация
BACKGROUND & AIMS: Hepatitis B core antigen (HBcAg) and surface antigen (HBsAg) can be detected through immunostaining of liver tissue. This study examined the extent and patterns of HBcAg and HBsAg staining before and after long-term nucleos(t)ide analogue (NA) therapy.
METHODS: Liver biopsies performed before and after 4 years of NA treatment were analyzed from patients with HBeAg-positive and HBeAg-negative chronic hepatitis B participating in 3 treatment trials. Immunostaining for HBcAg and HBsAg was evaluated using semiquantitative scales for both extent and distribution. HBV DNA, HBV RNA, HBeAg status, and quantitative HBsAg (qHBsAg) were correlated with changes in immunostaining. Baseline HBcAg and HBsAg staining were correlated with clinical outcomes.
RESULTS: Ninety-one patients had a pretreatment biopsy, and 81 had paired pretreatment and year 4 biopsies. Pretreatment, three-quarters were positive for HBcAg, predominantly in a cytoplasmic staining pattern, and 86% had detectable HBsAg, with 79% exhibiting a scattered granular pattern. Following 4 years of NA treatment, the proportion of biopsies without HBcAg staining increased from 26% to 63% and HBsAg staining from 14% to 26% compared with baseline. Inhibition of replication was associated with a significant decline in HBcAg staining, and loss of HBcAg staining was related to the duration of replication inhibition. In contrast, long-term NA therapy had minimal effect on the extent of HBsAg staining. The absence of contiguous granular HBsAg pattern was associated with HBsAg loss.
CONCLUSIONS: NA-related inhibition of viral replication was associated with marked reduction in HBcAg expression in HBeAg-positive and HBeAg-negative patients but minimal changes in extent of HBsAg staining, likely reflecting HBsAg production from integrated HBV DNA.
METHODS: Liver biopsies performed before and after 4 years of NA treatment were analyzed from patients with HBeAg-positive and HBeAg-negative chronic hepatitis B participating in 3 treatment trials. Immunostaining for HBcAg and HBsAg was evaluated using semiquantitative scales for both extent and distribution. HBV DNA, HBV RNA, HBeAg status, and quantitative HBsAg (qHBsAg) were correlated with changes in immunostaining. Baseline HBcAg and HBsAg staining were correlated with clinical outcomes.
RESULTS: Ninety-one patients had a pretreatment biopsy, and 81 had paired pretreatment and year 4 biopsies. Pretreatment, three-quarters were positive for HBcAg, predominantly in a cytoplasmic staining pattern, and 86% had detectable HBsAg, with 79% exhibiting a scattered granular pattern. Following 4 years of NA treatment, the proportion of biopsies without HBcAg staining increased from 26% to 63% and HBsAg staining from 14% to 26% compared with baseline. Inhibition of replication was associated with a significant decline in HBcAg staining, and loss of HBcAg staining was related to the duration of replication inhibition. In contrast, long-term NA therapy had minimal effect on the extent of HBsAg staining. The absence of contiguous granular HBsAg pattern was associated with HBsAg loss.
CONCLUSIONS: NA-related inhibition of viral replication was associated with marked reduction in HBcAg expression in HBeAg-positive and HBeAg-negative patients but minimal changes in extent of HBsAg staining, likely reflecting HBsAg production from integrated HBV DNA.