Igaki Naoya, Nakaji Miyuki, Moriguchi Rintarou, Akiyama Hiroyuki, Tamada Fumihiko, Oimomi Munetada, Goto Takeo
Department of Internal Medicine, Takasago Municipal Hospital, 33-1 Kamimachi, Arai-cho, 676-8585, Takasago, Japan.
J Gastroenterol. 2003;38(10):968-76. doi: 10.1007/s00535-003-1180-1.
We aimed to clarify the pathogenesis of an outbreak of fulminant hepatitis B in hemodialysis (HD) patients whose compromised cell-mediated immunity in turn contributed to chronic hepatitis B virus (HBV) carriage.
Five consecutive adult HD patients with acute hepatitis B were evaluated. Viral genotype, mutations, and HBV-DNA levels were studied in relation to viral clearance, liver disease severity, and liver histology by immunostaining.
All five patients had hepatitis B surface antigen (HBsAg) genotype C, a G-to-A stop codon mutation at nucleotide (nt) 1896 in the precore region, an A-to-T mutation at nt 1762 and an G-to-A mutation at nt 1764 in the basal core promoter. The possible index patient, who suffered from liver cirrhosis, had HBsAg genotype C, anti-hepatitis B envelope (HBe), and these mutations. The level of HBV-DNA declined by about 10 percent per week and no difference in viral kinetics between the patients who died and the survivor was found, irrespective of therapies. The amount of liver cell apoptosis, as assessed by single-stranded DNA, was scarce. The risk of fulminant hepatic failure did not correlate with the preexistent liver histopathological changes. Acute HBV superinfection was associated with hepatitis C virus (HCV) elimination and increased mortality.
This outbreak of fulminant hepatitis B suggests that HD patients can foster highly virulent HBV strains (possibly owing to their compromised immune responses), which may place others at risk of severe, life-threatening acute liver damage and at increased risk of mortality if chronic carriers of HCV should be infected. We aimed to clarify the pathogenesis of an outbreak of fulminant hepatitis B in hemodialysis (HD) patients whose compromised cell-mediated immunity in turn contributed to chronic hepatitis B virus (HBV) carriage.
我们旨在阐明血液透析（HD）患者中暴发性乙型肝炎暴发的发病机制，这些患者细胞介导的免疫功能受损，进而导致慢性乙型肝炎病毒（HBV）携带。
对连续5例成年急性乙型肝炎HD患者进行评估。通过免疫染色研究病毒基因型、突变和HBV-DNA水平与病毒清除、肝病严重程度及肝脏组织学的关系。
所有5例患者的乙型肝炎表面抗原（HBsAg）均为C基因型，前核心区核苷酸（nt）1896处存在G到A的终止密码子突变，基本核心启动子区nt1762处有A到T突变以及nt1764处有G到A突变。可能的索引患者患有肝硬化，具有HBsAg C基因型、抗乙型肝炎e抗原（HBe）以及这些突变。HBV-DNA水平每周下降约10%，无论采用何种治疗方法，死亡患者与存活患者之间的病毒动力学均无差异。通过单链DNA评估的肝细胞凋亡量很少。暴发性肝衰竭的风险与既往肝脏组织病理学改变无关。急性HBV重叠感染与丙型肝炎病毒（HCV）清除及死亡率增加相关。
此次暴发性乙型肝炎的暴发表明，HD患者可能会携带高毒力的HBV毒株（可能由于其免疫反应受损），这可能使其他人面临严重的、危及生命的急性肝损伤风险，并且如果HCV慢性携带者受到感染，死亡率会增加。我们旨在阐明血液透析（HD）患者中暴发性乙型肝炎暴发的发病机制，这些患者细胞介导的免疫功能受损，进而导致慢性乙型肝炎病毒（HBV）携带。
