Sánchez-Tapias J M, Vilar J H, Costa J, Bruguera M, Ballesta A M, Rodés J
J Hepatol. 1985;1(1):15-27. doi: 10.1016/s0168-8278(85)80064-7.
The status of viral replication at diagnosis and its relationship to the changes occurring during the natural history of the disease have been investigated in 26 patients with chronic persistent hepatitis (CPH) type B. Liver HBcAg and serum HBeAg were found in 73% of patients. During follow-up, serum transaminases normalized in 13/17 HBeAg-positive patients 1-6 years after diagnosis and 11 of them developed anti-HBe. HBe seroconversion was closely preceded by a transient elevation of transaminases in 5 patients in whom a repeated liver biopsy showed prominent lobular hepatitis and marked reduction of liver HBcAg. Such changes resulted in long-lasting biochemical normalization but only 1 patient became HBsAg-negative. These observations indicate that prolonged viral replication occurs in type B CPH. Termination of replication frequently implies a transient worsening caused by lysis of HBcAg-containing hepatocytes which leads to inactivation of the disease and to development of a healthy HBsAg carrier state.
对26例B型慢性持续性肝炎（CPH）患者诊断时的病毒复制状态及其与疾病自然史中发生变化的关系进行了研究。73%的患者肝脏中发现乙肝核心抗原（HBcAg）和血清中发现e抗原（HBeAg）。随访期间，17例HBeAg阳性患者中有13例在诊断后1至6年血清转氨酶恢复正常，其中11例产生了抗-HBe。5例患者在HBe血清转换之前转氨酶短暂升高，对这5例患者进行重复肝活检显示小叶性肝炎明显且肝脏HBcAg显著减少。这些变化导致生化指标长期正常，但只有1例患者乙肝表面抗原（HBsAg）转阴。这些观察结果表明，B型CPH中存在病毒的持续复制。复制的终止通常意味着由含HBcAg的肝细胞溶解引起的短暂恶化，这会导致疾病失活并发展为健康的HBsAg携带者状态。
