ADENOMATOUS HYPERPLASIA IN THE VICINITY OF SMALL HEPATOCELLULAR-CARCINOMA
ADENOMATOUS HYPERPLASIA IN THE VICINITY OF SMALL HEPATOCELLULAR-CARCINOMA
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DOI：
10.1002/hep.1840150516
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发表时间：
1992-05-01
期刊：
影响因子：
13.5
通讯作者：
KOJIRO, M
中科院分区：
文献类型：
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作者：
EGUCHI, A;NAKASHIMA, O;KOJIRO, M
对连续切除的80例伴有肝硬化的小肝癌的非癌区所见的结节性病变进行了病理形态学研究。 共发现51个结节性病变，分为以下四组：大的再生结节（30个结节）、腺瘤性增生（12个结节）、不典型腺瘤性增生（4个结节）和含有癌灶的腺瘤性增生（5个结节）。 大体上，所有大的再生结节界限清楚，但部分腺瘤性增生组呈模糊结节状。 80例切除的16例肝细胞癌（20%）附近发现的腺瘤性增生组中，不典型腺瘤性增生和含有癌灶的腺瘤性增生占43%。 含有癌灶的腺瘤性增生的平均大小（+/- S.D.）为 15.8 +/- 2.2 毫米，显着大于 10.1）。 所有含有癌灶的腺瘤性增生和75%的非典型腺瘤性增生均表现出明显的脂肪变化，但没有一个大的再生结节伴有任何脂肪变化。本研究证明了从腺瘤性增生到肝细胞癌的形态学转变，提示多步肝癌发生。 因此，据预测，大约20%的肝细胞癌可能具有多中心起源的潜力，大约40%的腺瘤性增生可能发生恶变，但很难估计确切的发病数。 不同程度脂肪变化的存在可能是腺瘤性增生向肝细胞癌恶性转化的重要形态学标志之一。 我们还应该意识到，大小超过 1.5 厘米的腺瘤增生可能已经在结节的某处含有癌灶。 因此，腺瘤性增生应作为癌前病变来治疗。
The nodular lesions seen in the noncancerous areas of the 80 consecutively resected small hepatocellular carcinoma associated with cirrhosis were pathomorphologically studied. A total of 51 nodular lesions were found, and they were classified into the following four groups: large regenerative nodule (30 nodules), adenomatous hyperplasia (12 nodules), atypical adenomatous hyperplasia (4 nodules) and adenomatous hyperplasia containing cancerous foci (5 nodules). Grossly, all large regenerative nodules were well demarcated, but some of the adenomatous hyperplasia group were vaguely nodular. Atypical adenomatous hyperplasia and adenomatous hyperplasia containing cancerous foci accounted for 43% of the adenomatous hyperplasia group found in the vicinity of the 16 resected hepatocellular carcinoma (20%) out of 80 cases. The mean size (+/- S.D.) of the adenomatous hyperplasias containing cancerous foci, 15.8 +/- 2.2 mm, was significantly larger than 10.1). All adenomatous hyperplasias containing cancerous foci and 75% of the atypical adenomatous hyperplasias demonstrated a marked fatty change, but none of the large regenerative nodules were accompained by any fatty changes.This study demonstrated the morphological transition from adenomatous hyperplasia to hepatocellular carcinoma that was suggestive of multistep hepatocar-cinogenesis. As a result, it is predicted that approximately 20% of all hepatocellular carcinomas may have the potential for being of multicentric origin and that approximately 40% of adenomatous hyperplasias may undergo malignant transformation, but it is difficult to estimate the exact number of incidences. The presence of varying degrees of fatty change may be one of the significant morphological markers for a malignant transformation from adenomatous hyperplasia to hepatocellular carcinoma. We should also be aware that adenomatous hyperplasias larger than 1.5 cm in size might already contain cancerous foci somewhere in the nodule. Accordingly, adenomatous hyperplasia should be treated as a premalignant lesion.