乙型肝炎病毒携带者的肝脏病理学特点

Liver histopathological features of chronic HBV carriers and inactive HBsAg carriers

目的研究慢性HBV携带者和非活动性HBsAg携带者的肝脏组织病理改变。方法对219例HBsAg阳性且血清ALT持续正常6个月以上的HBV携带者进行了肝组织病理学和免疫组织化学检查,同时检测血清HBV DNA和HBV血清标记物,研究HBV携带者肝组织炎症和纤维化的发生率和程度,分析感染者组织学改变与血清病毒水平、HBeAg及年龄的关系。结果HBV携带者中95．0％（208／219）肝脏组织学有改变,其中轻度炎症和（或）纤维化（G0～1／S0～1）者占50．0％（104／208）,有8．7％（18／208）炎症活动度和（或）纤维化程度在3级（期）或以上。炎症活动度和纤维化程度的分布在慢性HBV携带者与非活动性HBsAg携带者两组间比较,差异无统计学意义;在慢性HBV携带组中,以HBeAg阳性和阴性分层分析,炎症活动度在两组间差异无统计学意义,但纤维化性程度在HBeAg阴性组严重于HBeAg阳性组（χ^2=9．551,P〈0．05）;不同年龄组炎症活动度和纤维化程度总体上差异无统计学意义,但40岁以上年龄组S3～4占21．1％,18岁以下年龄组S3～4仅占7．7％。免疫组织化学检查219例HBsAg全部阳性,HBcAg在慢性HBV携带者组均是阳性,在非活动性HBsAg携带者组中10例阳性（33．3％）。结论绝大部分HBV携带者存在不同程度肝脏炎症和纤维化,其中约50％为轻度改变,8．6%炎症和（或）纤维化程度在3级（期）或以上。炎症活动度和纤维化程度与血清病毒水平无显著相关。

Objective To study the liver histopathological features of chronic HBV carriers and inactive HBsAg carriers. Methods Liver biopsies were performed on 189 chronic HBV carriers and 30 inactive HBsAg carriers （219 cases in total）. All of them had a normal serum ALT value; they were then followed-up for more than 6 months. HBsAg and HBcAg were detected by immunohistochemistry. The circulating HBV DNA loads and serologic markers of HBV were examined at the same time. Grades of liver necrosis/inflammation and fibrosis were compared between the patients regarding their HBV DNA positivity or negativity. The relationships between the HBeAg positivity and degrees of liver histological changes were evaluated. The grades of liver necrosis/inflammation and fibrosis were compared between three age groups： younger than 18 years, 18-40, and older than 40 years. Results Two hundred eight carriers of the total 219 （95.0%） had histological liver changes. Fifty percent （104/208） of them had mild histological changes （GO-1/ SO-1）, while more severe changes （G3-4 and/or S3-4） were found in 18 out of the 208. There were no significant differences in the grades of liver necrosis/inflammation and fibrosis between the chronic HBV carriers and the inactive HBsAg carders. Among the serologic HBV DNA positive carriers, hepatic fibrosis was more severe in the HBeAg negative group than in the positive group （χ^2 = 9.551, P = 0.008）, but no differences of the necrosis/inflammation grades were seen between the two groups. The rate of severe fibrosis （S3-4） was 21.1% in those carriers older than 40 years but was 7.7% in patients younger than 18 years. However, no statistically significant differences in degrees of liver inflammation and fibrosis were found among the three age groups. HBcAg positive rate was 100% in the liver tissues of all the chronic HBV carriers, but only in 33.3% in the inactive HBsAg carders. Conclusions The majority of our HBV carriers have liver inflammation and fibrosis. More severe histological changes were found in 8.65% of them. Liver fibrosis existed in the carriers with negative HBeAg and in those older than 40 years. HBcAg was found in hepatic tissues while their serological HBV DNA was negative.