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我们从上海甲型肝炎疫情中学到了什么?

What did we learn from the Shanghai hepatitis A epidemic?

作者信息

Cooksley W G

机构信息

Royal Brisbane Hospital Research Foundation and University of Queensland, Brisbane, Australia.

出版信息

J Viral Hepat. 2000 May;7 Suppl 1:1-3. doi: 10.1046/j.1365-2893.2000.00021.x.

DOI:10.1046/j.1365-2893.2000.00021.x
PMID:10870174
Abstract

A major outbreak of hepatitis A (HAV), associated with consumption of raw clams, occurred in Shanghai, China in 1988. Over 300 000 cases were reported, of which 47 (0.015%) were fatal. An elevated mortality rate was observed in hepatitis B surface antigen (HBsAg)-positive patients (0.05%). The majority of these patients were also hepatitis B e antigen (HBeAg)-positive, indicating active liver disease and high viral replication rates. The increased mortality in hepatitis B virus (HBV)/HAV coinfected individuals is hypothesized to be the result of T-cell-mediated destruction of HBV-infected hepatocytes, enhanced by acute HAV infection. Following recovery from HAV there is an increase in HBV expression and activated cytotoxic cells and subsequent cytolysis. Patients with chronic HBV infection are clearly at considerable risk of severe disease and increased mortality in the event of HAV infection. The period of greatest risk is during the immunoeliminative phase of HBV infection, which generally occurs in early adulthood. With the prevalence of HBV approaching 10% in this group, there is a clear opportunity for benefit from vaccination.

摘要

1988年,中国上海发生了一起与食用生蛤蜊相关的甲型肝炎(HAV)大暴发。报告的病例超过30万例,其中47例(0.015%)死亡。在乙型肝炎表面抗原(HBsAg)阳性患者中观察到死亡率升高(0.05%)。这些患者中的大多数也是乙型肝炎e抗原(HBeAg)阳性,表明存在活动性肝病且病毒复制率高。据推测,乙型肝炎病毒(HBV)/HAV合并感染个体死亡率增加是急性HAV感染增强T细胞介导的HBV感染肝细胞破坏的结果。HAV感染恢复后,HBV表达增加,细胞毒性细胞活化并随后发生细胞溶解。慢性HBV感染患者在发生HAV感染时显然有患严重疾病和死亡率增加的相当大风险。最大风险期是在HBV感染的免疫清除阶段,这通常发生在成年早期。鉴于该群体中HBV流行率接近10%,显然有机会从疫苗接种中获益。

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