A 36-year-old man was admitted to Yong Dong Severance Hospital because of a 10-day history of jaundice and epigastric discomfort. He had suffered from pulmonary tuberculosis about 15 years and 6 years before. On admission, he had pruritus, icteric sclerae and skin. The breathing sound was decreased on the right lower lung field. Direct tenderness was noted on the epigastrium, but liver and spleen were not palpable.
Abnormal laboratory findings were as follows: platelets 101,000/mm3, total bilirubin 19.6 mg/dl, direct bilirubin 13.4 mg/dl, alkaline phosphatase 188 IU/L, gamma-GTP 133 IU/L, alpha-fetoprotein 22.1 ng/ml, urine bilirubin  , urobilinogen +/-. Serum HBsAg, anti-HBc Ab and anti-HBeAb were positive.
An ultrasound examination disclosed a mass at the hepatic hilus, dilatation of the intrahepatic bile duct and cirrhotic change of the liver. A dynamic abdominal CT scan showed an enhancing mass at the hepatic hilus, liver cirrhosis and splenomegaly without focal lesion in hepatic parenchyma (Fig. 1). An endoscopic retrograde cholangiography (ERC) revealed a 3x2 cm sized oval shaped filling defect at the upper common hepatic duct, including the porta hepatis. The surface of the mass was smooth and the upstream intrahepatic bile ducts were slightly dilated (Fig. 2A). An endoscopic nasobiliary drainage was attempted, but failed because a hydrophilic guidewire could not be passed over the obstructing mass. On a percutaneous transhepatic cholangiography (PTC) (Fig. 2B), through a percutaneous transhepatic biliary drainage (PTBD) tube, dye was well passed over the obstructing mass. The mass seemed slightly lobulated and the surface was shallowly grooved. A sono-guided fine needle aspiration cytology revealed no malignant cells. On the 24th hospital day, hepatic angiography was performed and did not show any tumor staining.
On the 28th hospital day, an explorative laparotomy was performed. Grossly, the liver showed macronodular cirrhosis without any palpable masses. An irregular shaped soft tissue mass admixed with bile was found at the hepatic hilus after the distended commom hepatic duct was opened. The mass was yellowish to grayish in color and very friable. These findings were consistent with a so-called "chicken fat" appearance. Cholecystectomy, segmental resection of the intrahepatic ducts and common hepatic duct, septoplasty of the intrahepatic duct and hepaticojejunostomy were performed.
Microscopically, tumor cells appeared as nests in pseudoacinus patterns, and bile pigment was found in the cytoplasm (Fig. 3A, 3B, 3C). The immunohistochemical stain demonstrated positive reaction for alpha-fetoprotein but negative reaction for carinoembryonic antigen (Fig. 4A, 4B). The final diagnosis was hepatocellular carcinoma.
The patient was recommended to have adjuvant therapy such as external radiotherapy or systemic chemotherapy, but refused. Three months after the operation, a hepatic angiography with CT arterioportography and lipiodol-CT were performed, which gave no definite mass lesion in the hepatic parenchyma. About 6 months after the operation, a follow-up ultrasound examination disclosed two small hypoechoic lesions (1.2-1.5 cm in diameter) at the segment 8 and the segment 5 (Fig. 5A, 5B). A repeat hepatic angiography with CT arterioportography was performed. Tumor staining was not found on hepatic angiography, but two low density lesions were suspected at the segment 8 and the segment 5 on CT arterioportography (Fig. 6A, 6B). However, no lipiodol remained on lipiodol-CT taken 3 weeks later (Fig. 7A, 7B). The patient has been closely followed up with ultrasonography every 2 months until now (1 year after the operation) and there was no evidence of the growth of two hypoechoic lesions seen on ultrasonography or development of new lesions.