Hepatocellular carcinoma and nodular regenerative hyperplasia: possible pathogenetic relationship.
Hepatocellular carcinoma and nodular regenerative hyperplasia: possible pathogenetic relationship.
复制标题
肝细胞癌与结节性再生性增生：可能的发病关系。
DOI：
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发表时间：
1996
期刊：
影响因子：
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通讯作者：
Ishak Kg
中科院分区：
文献类型：
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作者：
U. Nzeako;Z. Goodman;Ishak Kg
目标
在最近对北美居民肝细胞癌（HCC）的回顾中，我们惊讶地发现，在武装部队病理研究所 1980-1993 年的咨询档案中，42.6% 的肿瘤出现在非肝硬化肝脏中。我们随后注意到其中许多的非肿瘤性肝脏患有结节性再生性增生（NRH），这种情况与肝细胞发育不良（一种假定的癌前病变）有关。为了调查 NRH 可能是 HCC 前兆的可能性，我们研究了 HCC 和 NRH 相关的病例，并检查了门静脉阻塞在 HCC 肝脏中发生的 NRH 中的可能作用。
方法
根据研究标准和组织学切片选择受试者，审查临床/尸检记录，并记录肿瘤性和非肿瘤性肝脏的特征。在有和没有 NRH 的组之间就定义的变量进行简单的统计比较。
结果
在 804 名适合研究的患者中，342 名是非肝硬化患者，其中 23 名患有 NRH。 NRH 患者的平均年龄为 65 +/- 13.6 (SD) 岁。其中17例（73.9%）有肝细胞发育不良，16例（69.6%）有门静脉侵犯。患有NRH的患者发生肝细胞发育不良的比例显着高于不患有NRH的患者（p < 0.01），但两组之间在门静脉侵犯方面没有显着差异。 3 名患者 (13%) 在诊断 NRH 之前接受过化疗和/或放疗。
结论
这些发现可能是由于 NRH 肝脏中发生的发育不良病灶内发生 HCC，但这些结果并不排除相反的可能性，即 NRH 也可能在患有 HCC 的非肝硬化肝脏中发生，继发于门静脉侵入伴门静脉闭塞。 HCC 和 NRH 之间的时间关系可能是由多种致病因素的特定相互作用决定的。在 HCC 患者中，除肿瘤侵袭导致的门静脉阻塞外，其他因素也可能在 NRH 的发病机制中发挥作用。
OBJECTIVE
In a recent review of hepatocellular carcinoma (HCC) in North American residents, we were surprised to learn that 42.6% of these tumors in the 1980-1993 consultation files of the Armed Forces Institute of Pathology had arisen in noncirrhotic livers. We subsequently noted that the nonneoplastic livers of a number of these had nodular regenerative hyperplasia (NRH), a condition that has been associated with liver cell dysplasia, a putative premalignant lesion. To investigate the possibility that NRH might be a precursor of HCC, we studied those cases in which there was an association of HCC and NRH and examined the possible role of portal vein obstruction in NRH occurring in livers with HCC.
METHODS
Subjects were selected based on study criteria and histological slides, clinical/autopsy records were reviewed, and features of neoplastic and nonneoplastic liver were noted. Simple statistical comparisons were made between the groups with and without NRH with respect to defined variables.
RESULTS
Of 804 patients suitable for study, 342 were noncirrhotic, and 23 of these had NRH. Mean age of patients with NRH was 65 +/- 13.6 (SD) yr. Seventeen of these (73.9%) had liver cell dysplasia, and 16 (69.6%) had portal venous invasion. Liver cell dysplasia occurred in a significantly greater proportion of those with NRH than those without (p < 0.01), but there was no significant difference between both groups with regard to portal venous invasion. Three patients (13%) had received chemotherapy and/or radiotherapy before diagnosis of NRH.
CONCLUSIONS
These findings may be due to the development of HCC within the dysplastic foci that occur in livers with NRH, but the findings do not exclude the converse possibility that NRH may also develop in a noncirrhotic liver with HCC, secondary to portal venous invasion with portal vein occlusion. The temporal relationship between HCC and NRH is probably determined in each case by the particular interaction of multiple pathogenetic factors. Among patients with HCC, factors other than the portal vein obstruction by tumor invasion may play a role in the pathogenesis of NRH.