Hepatic metastases from hepatoid adenocarcinoma of stomach mimicking hepatocellular carcinoma
A 65-year-old man was admitted to our hospital for evaluation of a huge hepatic tumor that was incidentally detected during an abdominal sonographic screening examination. He complained of mild abdominal discomfort. He had a medical history of hypertension and a social history of alcohol for several decades. The laboratory tests at the time of admission showed an aspartate aminotransferase (AST) level of 90 U/L, alanine aminotransferase level (ALT) of 17 U/L, total bilirubin level of 0.9 mg/dL, alkaline phosphatase level of 67 U/L. The serum level of AFP (5,714 IU/mL) and protein induced by vitamin K absence or antagonist-II (PIVKA-II; 1,005 mAU/mL) were markedly elevated. The CEA level was within normal limits. His serum was positive for hepatitis B surface antibody, but negative for hepatitis B surface antigen and anti-HCV.\nThe ultrasonographic images showed a 9 cm sized hyperechoic mass with internal anechoic portion in right hepatic lobe with adjacent small hypoechoic nodules (). We then performed contrast-enhanced multidetector-row CT. The contrast-enhanced dynamic CT images revealed a 9.5×7 cm sized mass in the liver, comprised of a central necrotic portion and a peripheral solid enhancing portion. Liver cirrhotic changes were not observed on CT or ultrasonographic images. After contrast enhancement, the peripheral solid portion of the huge hepatic mass showed heterogeneous enhancement on arterial phase image and washout of contrast enhancement on delayed phase image. The tumor thrombus was visualized in adjacent right portal vein and a 1.3 cm sized mass was observed in inferior aspect of huge hepatic mass. The tumor thrombi were observed in proximal main portal vein to superior mesenteric vein. The multiple enlarged, conglomerate lymph nodes were observed along the left gastric artery, gastroduodenal artery and right gastroepiploic artery. The CT images also revealed irregular wall thickening of gastric antrum (). For evaluation of gastric abnormality, an endoscopic biopsy was performed. An infiltrative mass with ulceration at the gastric antrum was detected on the endoscopic image and endoscopic specimens were obtained in the gastric lesion. The specimen was pathologically confirmed as poorly differentiated adenocarcinoma. For further evaluation of the hepatic tumors, contrast enhanced liver magnetic resonance imaging (MRI) using gadoxetic-acid was performed. The huge hepatic mass consisted of a central necrotic portion and a peripheral solid portion. The peripheral solid portion showed low signal intensity on T1WI and high signal intensity on T2WI. After contrast enhancement, the peripheral solid portion of the huge hepatic mass showed heterogeneous enhancement on arterial phase image, low signal intensity on portal venous, late dynamic and hepatobiliary phase images (). Dynamic MRI revealed several small nodules that were unclear on abdominal CT. These lesions showed typical enhancement pattern of HCC such as early enhancement on arterial phase and delayed washout on late dynamic and hepatobiliary phases.\nBased on laboratory tests showing marked elevated AFP and PIVKA-II, existence of pathologic proven gastric adenocarcinoma, and typical enhancement pattern of HCC of huge and small hepatic tumors on CT and MRI, we thought two possible diagnoses; the one was double primary malignancy as primary advanced gastric malignancy and primary HCC in the liver. The other was AFP producing gastric malignancy and its hepatic metastases. The ultrasonography-guided biopsy of the hepatic tumors was performed. Microscopic examination revealed that the histology of the hepatic tumor was similar to that of specimens from the gastric cancer. The results of immunohistochemical stains were positive for AFP, Glypican-3, Glutamine synthase, Cytokeratin, and CK8/18. But CK20, CK7, and human serum albumin were negative. These histologic features resulted in the diagnosis of this case as a gastric hepatoid adenocarcinoma with hepatic metastases. He had eight cycles of chemotherapy with FOLFOX and he remains alive for five months after diagnosis.