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非肝硬化肝脏中的肝细胞癌

[Hepatocellular carcinoma in the non-cirrhotic liver].

作者信息

Evert M, Dombrowski F

机构信息

Institut für Pathologie, Ernst-Moritz-Arndt-Universität, Greifswald.

出版信息

Pathologe. 2008 Feb;29(1):47-52. doi: 10.1007/s00292-007-0953-3.

Abstract

Of hepatocellular carcinomas (HCC), 15-20% occur in the non-cirrhotic liver. All factors which cause HCC when liver cirrhosis (LC) is present, can also lead to HCC without LC. On the basis of the relative frequency, HCC can be roughly differentiated into 3 groups: 1) HCC, rarely occurring without cirrhosis (e.g. virus hepatitis, alcohol abuse). 2) HCC, frequently occurring without LC (alpha1-antitrypsin deficiency, hemochromatosis, non-alcoholic fatty liver disease). 3) HCC, consistently occurring without LC (glycogen storage disease type 1, consumption of oral contraceptives/anabolic steroids). In groups 1 and 2 the level of hepatocellular toxicity necessary to reach LC is not yet achieved but the carcinogenic effect is already strong enough to induce HCC, possibly owing to the influence of additional carcinogens or host factors. In group 3, the carcinogenic effect is mediated by a long-standing alteration of the hepatocellular metabolism that is of low toxic effect and does not lead to cell death, but is nevertheless carcinogenic. In these cases, the initial formation of hepatocellular adenomas that subsequently transform into HCC is a common finding (adenoma-carcinoma sequence).

摘要

在肝细胞癌(HCC)中,15% - 20%发生于非肝硬化肝脏。所有在存在肝硬化(LC)时导致HCC的因素,在无LC的情况下也可导致HCC。根据相对发生率,HCC可大致分为3组:1)极少在无肝硬化时发生的HCC(如病毒性肝炎、酒精滥用)。2)常无LC发生的HCC(α1 - 抗胰蛋白酶缺乏症、血色素沉着症、非酒精性脂肪性肝病)。3)始终无LC发生的HCC(1型糖原贮积病、口服避孕药/合成代谢类固醇的使用)。在第1组和第2组中,达到LC所需的肝细胞毒性水平尚未达到,但致癌作用已经足够强大以诱发HCC,这可能是由于其他致癌物或宿主因素的影响。在第3组中,致癌作用是由肝细胞代谢的长期改变介导的,这种改变毒性作用低,不会导致细胞死亡,但仍具有致癌性。在这些情况下,最初形成肝细胞腺瘤随后转变为HCC是常见现象(腺瘤 - 癌序列)。

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