Villa E, Theodossi A, Portmann B, Eddleston A L, Williams R
Gastroenterology. 1981 May;80(5 pt 1):1048-53.
Two patients, 1 with chronic active hepatitis, the other with Goodpasture's syndrome, became HBsAg-positive after the start of immunosuppressive drug therapy. At the same time of presentation, sera contained anti-HBc antibodies of IgM and IgG class in the absence of HBsAg or anti-HBs and immunofluorescent studies of liver biopsy specimens showed core antigen in the nuclei of liver cells. It is suggested that these findings reflected an unusual pattern of hepatitis B virus infection with a very low level of viral replication and that the appearance of HBsAg in both serum and liver cells after immunosuppressive drug therapy was due to reactivation of this infection, possibly as a result of changes in levels of antibodies which suppress viral replication. In 1 patients, the change in viral replication was associated with continuing liver cell necrosis and progressive deterioration in liver function.
两名患者,一名患有慢性活动性肝炎,另一名患有古德帕斯丘综合征,在开始免疫抑制药物治疗后出现HBsAg阳性。在出现症状的同时,血清中含有IgM和IgG类抗-HBc抗体,而无HBsAg或抗-HBs,肝活检标本的免疫荧光研究显示肝细胞细胞核中有核心抗原。提示这些发现反映了一种不寻常的乙肝病毒感染模式,病毒复制水平极低,免疫抑制药物治疗后血清和肝细胞中出现HBsAg是由于这种感染的重新激活,可能是由于抑制病毒复制的抗体水平发生变化所致。在1例患者中,病毒复制的变化与持续的肝细胞坏死和肝功能进行性恶化有关。