Guptan R C, Thakur V, Sarin S K, Banerjee K, Khandekar P
Department of Gastroenterology, GB Pant Hospital, New Delhi, India.
Am J Gastroenterol. 1996 Jul;91(7):1312-7.
Infection due to hepatitis B virus (HBV) could be due to wild or mutant (precore or surface) viruses. The prevalence and clinical profile of different viral forms in patients with chronic liver disease has not been established.
One hundred and twenty patients with histologically proven HBV-related chronic liver disease were studied. Patients with dual infection with HCV/HDV/HIV, past history of interferon therapy, or autoimmune hepatitis were excluded. Eighteen (15.5%) patients had the precore mutation (HBsAg +ve, HBeAg -ve/anti-HBe +ve, HBV DNA +ve), and 13 (10.8%) had the surface gene mutations (HBsAg -ve, HBeAg -ve, IgG anti-HBc, and HBV DNA +ve). The remaining 89 (74.2%) patients were infected with wild type HBV. The course of all patients with mutant forms and 41 of those with the wild type form was followed for a mean (+/- SD) of 4.4 +/- 2.4 yr.
Compared with wild-type-infected patients, those with surface mutation were younger (39.9 +/- 14 vs. 30.1 +/- 12.4 yr, p < 0.05). Patients with precore mutations had a shorter illness than those with surface mutant (p < 0.01) and wild forms (p < 0.05). Histologically, patients with precore type had more active liver disease than wild type (39% vs. 15%, p < 0.05). Patients with precore mutations were always symptomatic, often presenting with ascites (67%) and jaundice (55%). Patients with surface mutant forms often presented with quiescent cirrhosis (77%) or cirrhosis with hepatoma (15%).
One-fourth of HBV-related chronic liver disease in Asian Indians is attributable to mutant HBV forms. The presence of variant viruses alters the natural history of the disease, with the precore variance having a more aggressive course and the surface mutant, a more quiescent but unfavorable course, compared with the wild type.
乙型肝炎病毒（HBV）感染可能由野生型或突变型（前核心区或表面区）病毒引起。慢性肝病患者中不同病毒形式的患病率和临床特征尚未明确。
对120例经组织学证实为HBV相关慢性肝病的患者进行研究。排除丙型肝炎病毒/丁型肝炎病毒/人类免疫缺陷病毒双重感染患者、既往有干扰素治疗史的患者或自身免疫性肝炎患者。18例（15.5%）患者存在前核心区突变（HBsAg阳性，HBeAg阴性/抗-HBe阳性，HBV DNA阳性），13例（10.8%）患者存在表面基因突变（HBsAg阴性，HBeAg阴性，IgG抗-HBc阳性，HBV DNA阳性）。其余89例（74.2%）患者感染野生型HBV。对所有突变型患者和41例野生型患者进行了平均（±标准差）4.4±2.4年的随访。
与野生型感染患者相比，表面基因突变患者更年轻（39.9±14岁对30.1±12.4岁，p<0.05）。前核心区突变患者的病程比表面基因突变患者（p<0.01）和野生型患者（p<0.05）短。组织学上，前核心区突变型患者的肝病比野生型更活跃（39%对15%，p<0.05）。前核心区突变患者总是有症状，常表现为腹水（67%）和黄疸（55%）。表面基因突变型患者常表现为静止性肝硬化（77%）或伴有肝癌的肝硬化（15%）。
亚洲印度人中四分之一的HBV相关慢性肝病归因于突变型HBV形式。与野生型相比，变异病毒的存在改变了疾病的自然史，前核心区变异病程更具侵袭性，表面基因突变型病程更静止但预后不良。
