Dormeyer H H, Arnold W, Schönborn H, Braun B, Klinge O, Pfeifer U, Knolle J, Hess G, Kryger P, Nielsen J O, Meyer zum Büschenfelde K H
J Infect Dis. 1981 Jul;144(1):33-7. doi: 10.1093/infdis/144.1.33.
Eighty-eight asymptomatic carriers of hepatitis B surface antigen (HBsAg) were followed with biochemical, serologic, histologic, and immunohistologic studies over a period of four years. None of the 78 HBsAg carriers with normal or minimally changed liver tissue, antibody to hepatitis B e antigen (HBeAg) in serum, and no intranuclear hepatitis B core antigen (HBcAg) developed a chronic inflammatory liver disease. Four individuals lost circulatory HBsAg, and at least two individuals terminated their HBsAg carrier state. Seven asymptomatic HBsAg carriers with chronic hepatitis were characterized by HBeAg in serum and intranuclear HBcAg. However, three HBsAg carriers with chronic hepatitis and an absence of intrahepatocellular HBcAg were positive for antibody to HBeAg over the observation period. The mechanism that leads to chronic hepatitis in these patients remains to be determined.
对88名无症状乙肝表面抗原(HBsAg)携带者进行了为期四年的生化、血清学、组织学和免疫组织学研究。78名肝组织正常或仅有轻微改变、血清中存在乙肝e抗原(HBeAg)抗体且无核内乙肝核心抗原(HBcAg)的HBsAg携带者均未发展为慢性炎症性肝病。4人循环中的HBsAg消失,至少2人终止了HBsAg携带状态。7名无症状慢性乙型肝炎HBsAg携带者的特征为血清中有HBeAg和核内有HBcAg。然而,在观察期内,3名患有慢性肝炎且肝细胞内无HBcAg的HBsAg携带者HBeAg抗体呈阳性。导致这些患者发生慢性肝炎的机制仍有待确定。