Portal venous tumor growth-type of hepatocellular carcinoma without liver parenchyma tumor nodules: a case report
Portal venous tumor growth-type of hepatocellular carcinoma without liver parenchyma tumor nodules: a case report
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DOI：
10.1016/s1665-2681(19)31304-3
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发表时间：
2013-11-01
影响因子：
3.8
通讯作者：
Azuma, Takeshi
中科院分区：
文献类型：
--
作者：
Saito, Masaya;Seo, Yasushi;Azuma, Takeshi
患者为43岁男性，患有慢性乙型肝炎，无肝细胞癌病史，2011年10月首次诊断为右门静脉主干及门静脉分支血栓，食管静脉曲张破裂，行内镜下静脉曲张结扎术，但多次破裂。尽管进行了抗凝治疗，2012年3月血栓仍从门静脉右干扩展到肠系膜上静脉。CT扫描显示门静脉血栓从早期到晚期呈低密度。 CT扫描或超声检查未发现肝脏局灶性病变，甲胎蛋白（AFP）在正常范围内。 2012年4月因顽固性食管静脉曲张出血死亡。尸检标本病理检查显示门静脉血栓形成符合低分化肝癌。门静脉肿瘤血栓形成（PVTT）仅有少量肿瘤血管，由于HCC形成引起的纤维瘤变而受到压迫，因此CT上表现为动脉期至门静脉期的低密度病灶。另外，PVTT对AFP呈阴性，因此代表AFP血清值在正常范围内。 PVTT 的 c-kit 染色呈阳性，c-kit 是一种肝干细胞标记物。病理学未发现全肝实质肿瘤。 PVTT可能具有推测的肝癌干细胞的特征。我们经历了第一例仅发生在门静脉的 HCC，无肝实质肿瘤结节，与非恶性门静脉血栓形成的鉴别诊断很困难。我们还报道了 HCC 门静脉肿瘤生长型的新肿瘤特征。
The patient was a 43-year-old man with chronic hepatitis B without history of hepatocellular carcinoma (HCC), who was first diagnosed with thrombosis in right portal vein trunk and portal vein branches and ruptured esophageal varices in October 2011. He underwent endoscopic variceal ligation, but ruptured repeatedly. Despite anti-coagulant therapy, the thrombosis expanded from right portal vein trunk to upper mesenteric vein in March 2012. Computed tomography (CT) scan showed that portal vein thrombosis had low density from early to late phase. No focal liver lesions were identified by CT scan or ultrasound, and alpha-fetoprotein (AFP) was within normal range. He died by intractable esophageal variceal bleeding in April 2012. Pathological examination of autopsy specimen showed that portal vein thrombosis was consistent with poorly-differentiated HCC. The portal vein tumor thrombosis (PVTT) had only a few tumor vessels, which were compressed by fibromatous change originating from HCC formation, so were represented as low-density lesions from arterial to portal phase of CT. In addition, PVTT was negative for AFP, so representing serum value of AFP within normal range. PVTT had positive staining for c-kit, which is a liver stem cell marker. Liver tumors in the whole liver parenchyma were not found pathologically. PVTT might have the characteristics of presumed liver cancer stem cells. We experienced the first case of HCC only in portal vein without liver parenchyma tumor nodules, with difficult differential diagnosis from a non-malignant portal vein thrombosis. We also reported new tumor profiles of the portal venous tumor growth- type of HCC.