A serum amyloid A-positive hepatocellular neoplasm arising in alcoholic cirrhosis: a previously unrecognized type of inflammatory hepatocellular tumor

A serum amyloid A-positive hepatocellular neoplasm arising in alcoholic cirrhosis: a previously unrecognized type of inflammatory hepatocellular tumor
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DOI:
10.1038/modpathol.2012.114
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发表时间:
2012-12-01
期刊:
影响因子:
7.5
通讯作者:
Nakanuma, Yasuni
Nakanuma, Yasuni
中科院分区:
医学1区
文献类型:
--
作者:
Sasaki, Motoko;Yoneda, Norihide;Nakanuma, Yasuni

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肝细胞腺瘤通常发生在没有明显纤维化的情况下。在此,我们报告了7例血清淀粉样蛋白A阳性肝细胞肿瘤患者,其特征与酒精性肝硬化引起的炎性肝细胞腺瘤相同。从我们的病理档案(1997-2011年)中检索到7例(2例女性和5例男性,年龄范围41-67岁)与酒精性肝硬化相关的富血管肝细胞结节患者。所有患者肝细胞结节为多发性(43个),17个结节进行了组织学检查。我们调查了血清淀粉样蛋白A,谷氨酰胺合成酶和磷脂酰肌醇蛋白聚糖-3在肝细胞结节和对照病变,包括5个局灶性结节增生,18个异型增生结节,和54个肝细胞癌的各种背景疾病的免疫反应。总之,17个结节中有15个表现出强烈和明显的血清淀粉样蛋白A免疫反应性,与炎性肝细胞腺瘤的特征相同。血清淀粉样蛋白A阳性的肝细胞肿瘤表现为不同程度的细胞密度增加、炎性浸润、肝窦扩张和小管反应。虽然大约一半的不典型增生结节和肝细胞癌表现出局灶性血清淀粉样蛋白A的免疫反应性,血清淀粉样蛋白A阳性肝细胞肿瘤的血清淀粉样蛋白A表达的程度显着高于对照结节。血清淀粉样蛋白A阳性肝细胞肿瘤没有表现出谷氨酰胺合成酶的过度表达或磷脂酰肌醇蛋白聚糖-3的免疫反应性。相反,大多数肝细胞癌表现出谷氨酰胺合成酶的过度表达和磷脂酰肌醇蛋白聚糖-3的免疫反应性,无论背景疾病。总之,这项研究突出了一组特征性的肝细胞肿瘤发生在酒精性肝硬化,这与炎性肝细胞腺瘤的特点。这些血清淀粉样蛋白A阳性的肝细胞肿瘤可能是酒精中毒患者中一种新的炎性肝细胞肿瘤。Modern Pathology(2012)25,1584-1593; doi:10.1038/modpathol.2012.114; 2012年7月6日在线发表
Hepatocellular adenoma usually arises in the absence of significant fibrosis. Herein, we report seven patients with serum amyloid A-positive hepatocellular neoplasm, which shares features with inflammatory hepatocellular adenoma arising in alcoholic cirrhosis. Seven patients (two women and five men, age range 41-67 years) with hypervascular hepatocellular nodules associated with alcoholic cirrhosis were retrieved from our pathological files (1997-2011). The hepatocellular nodules were multiple (43) in all patients and 17 nodules were histologically examined. We surveyed the immunoreactivity for serum amyloid A, glutamine synthetase, and glypican-3 in the hepatocellular nodules and control lesions, including 5 focal nodular hyperplasia, 18 dysplastic nodules, and 54 hepatocellular carcinomas in various background diseases. In all, 15 of 17 nodules showed strong and distinct immunoreactivity for serum amyloid A, sharing features with inflammatory hepatocellular adenoma. The serum amyloid A-positive hepatocellular neoplasms showed increased cellular density, inflammatory infiltrate, sinusoidal dilatation, and ductular reaction to various degrees. Although about a half of dysplastic nodules and hepatocellular carcinomas showed focal immunoreactivity for serum amyloid A, the extent of serum amyloid A expression was significantly higher in serum amyloid A-positive hepatocellular neoplasms, than in control nodules. The serum amyloid A-positive hepatocellular neoplasms did not show the overexpression of glutamine synthetase or immunoreactivity for glypican-3. In contrast, most hepatocellular carcinomas showed the overexpression of glutamine synthetase and immunoreactivity for glypican-3, irrespective of background diseases. In conclusion, this study highlights a characteristic group of hepatocellular neoplasms arising in alcoholic cirrhosis, which share features with inflammatory hepatocellular adenomas. These serum amyloid A-positive hepatocellular neoplasms may be a new type of inflammatory hepatocellular tumors in alcoholic patients. Modern Pathology (2012) 25, 1584-1593; doi:10.1038/modpathol.2012.114; published online 6 July 2012