Söderström Ann, Norkrans Gunnar, Conradi Nils, Krantz Marie, Horal Peter, Lindh Magnus
Department of Infectious Diseases, Göteborg University, Sweden.
J Pediatr Gastroenterol Nutr. 2002 Oct;35(4):487-94. doi: 10.1097/00005176-200210000-00006.
Despite high viral load, children with chronic hepatitis B virus (HBV) infection may lack significant biochemical signs of liver dysfunction. Failure to develop abnormal liver chemistriesis is probably due to immunologic hyporeactivity. Despite the absence of biochemical abnormalities in these patients, there is still a risk for long-term complications. The pathogenic importance of viral load and genetic variability is less well studied in children than in adults.
We evaluated viremia levels, genotypes, and mutations related to histologic evidence of liver damage in 71 HBV carriers, aged 2 to 18 years, all of non-Swedish origin.
None of the of 22 children who were hepatitis B e antigen (HBeAg) negative had severe liver disease or had HBV DNA levels greater than 10 copies/mL (mean 10 ); 3 (14%) of them had increased alanine aminotransferase (ALT). The 49 HBeAg-positive children had a mean HBV DNA level of 10 copies/mL, and increased ALT was seen in 28 (55%). Core promoter mutations (at nt 1764) or precore mutations (at codon 1, 2, or 28) were rare; they were seen in four and one HBeAg-positive children, and in four and nine HBeAg-negative children, respectively, without association to liver damage. C-1858 was associated with more liver inflammation. Genotype did not significantly influence liver damage. Children with horizontal transmission had a faster rate of seroconversion and more inflammation of the liver.
Severe HBeAg-negative hepatitis with high HBV DNA levels and mutations in the core promoter or precore regions seems to be less common in children than in adults. C-1858 strains may be more pathogenic, but this requires further study. Epidemiologic factors influence the course of infection.
尽管慢性乙型肝炎病毒（HBV）感染儿童的病毒载量很高，但可能缺乏明显的肝功能障碍生化指标。未能出现肝生化指标异常可能是由于免疫反应低下。尽管这些患者没有生化异常，但仍存在长期并发症的风险。与成人相比，病毒载量和基因变异性在儿童中的致病重要性研究较少。
我们评估了71名年龄在2至18岁、均非瑞典裔的HBV携带者的病毒血症水平、基因型以及与肝损伤组织学证据相关的突变。
22名乙肝e抗原（HBeAg）阴性儿童中，无一例患有严重肝病或HBV DNA水平高于10拷贝/毫升（平均10 ）；其中3名（14%）丙氨酸转氨酶（ALT）升高。49名HBeAg阳性儿童的平均HBV DNA水平为10拷贝/毫升，28名（55%）ALT升高。核心启动子突变（位于核苷酸1764处）或前核心突变（位于密码子1、2或28处）很少见；分别在4名和1名HBeAg阳性儿童以及4名和9名HBeAg阴性儿童中发现，与肝损伤无关。C-1858与更多的肝脏炎症相关。基因型对肝损伤没有显著影响。水平传播的儿童血清转换率更快，肝脏炎症更严重。
严重的HBeAg阴性肝炎伴高HBV DNA水平以及核心启动子或前核心区域突变在儿童中似乎比在成人中少见。C-1858毒株可能更具致病性，但这需要进一步研究。流行病学因素影响感染进程。
