A 54-year-old man with type 2 diabetes mellitus and liver cirrhosis secondary to hepatitis B virus infection was admitted to the Department of Gastroenterology at Clinical Medical College of Yangzhou University, Jiangsu Province, China, on 21 February 2011 because of abdominal pain. The patient had a 3-day history of yellow conjunctivae and urine. On 22 February 2011, abdominal magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) showed a maximum common bile duct (CBD) diameter of 13 mm with an area of heterogeneous intensity signals in the distal portion of the CBD suggestive of CBD stones (Figure 1A), and normal intrahepatic bile ducts. There was mild obstruction at the duodenal ampulla (Figure 1B), liver cirrhosis, and enlargement of the spleen. Routine laboratory tests showed high serum levels of direct bilirubin (DBIL) (42.5 mumol/l, normal range 1.7 to 7.8 mumol/l), total bilirubin (TBIL) (62.7 mumol/l, normal range 5.7 to 23.5 mumol/l), aspartate aminotransferase (AST) (91 U/l, normal range 0 to 50 U/l), alanine aminotransferase (ALT) (206 U/l, normal range 0 to 50 U/l), and CA19-9 (821.03 U/ml, normal range <35 U/l); normal serum levels of amylase (62 U/l, normal range 30 to 110 U/l) and alpha-fetoprotein (AFP) (6.17 ng/ml, normal range 0 to 7 ng/ml); and a normal urinary amylase level (326 U/l, normal range 32 to 641 U/l). Endoscopic papillary balloon dilation (EPBD) was performed on 23 February 2011, and the procedure report described extraction of a muddy stone from the CBD. Eight days after EPBD, the plasma CA19-9 level was 469.56 U/ml, and hepatic function had improved with DBIL 10.6 mumol/l, TBIL 16.4 mumol/l, AST 36 U/l, and ALT (70 U/l). The report of a follow-up MRCP performed at another hospital, at a time when the patient was asymptomatic, described nodular cirrhosis, enlargement of the gallbladder, mild dilation of the intra- and extrahepatic bile ducts, irregular areas of low signal intensity in the CBD that were interpreted as CBD stones (Figure 2), and a 1.1 cm diameter mass with clear borders in the lateral portion of the left lobe of the liver that was hypointense on T1-weighted images and slightly hyperintense on T2-weighted images. The consulted team (surgeon, radiation oncologist, medical oncologist, and radiologist) considered that the hepatic mass might be a benign nodule, and should be monitored.
The patient did not return to hospital until recurrence of pancreatitis 5 months later. He was hospitalized for AP and obstructive jaundice on 21 September 2011. On admission, abdominal ultrasonography showed liver cirrhosis with a 27 x 38 mm area of heterogeneous echogenicity in the left lobe and a thickened, uneven gallbladder containing muddy stones. The CBD was dilated (9 to 16 mm in diameter), with areas of dense, spotty echoes referred to as muddy stones, and the left intrahepatic bile duct was also slightly dilated. Abdominal MRI and MRCP on the day after admission showed cholecystitis, gallbladder stones, a mass in the left lobe of the liver with unclear margins that was isointense on short inversion time inversion recovery sequences (Figure 3A), filling defects in the CBD suggestive of stones (Figure 3B), dilation of the intra- and extrahepatic bile ducts, pancreatitis, and liver cirrhosis. On 5 October 2011, abdominal computed tomography (CT) showed an irregular, low-density mass measuring 27 x 38 mm in the left lobe of the liver, and a dilated CBD with muddy stones. Contrast-enhanced CT showed inhomogeneous enhancement of the liver mass and dilation of the intrahepatic bile ducts. The contrast density of the CBD stones was similar in the arterial and portal venous phases, ranging from 15 to 22 Hounsfield units (HU).
Routine laboratory tests showed high serum levels of amylase (1,423 U/l), DBIL (136.1 mumol/l), TBIL (141.2 mumol/l), AST (223 U/l), ALT (366 U/l), and CA19-9 (2041 U/ml); a high urinary amylase level (6,826 U/l); and a normal serum AFP level (6.36 ng/ml). The patient had acute epigastric pain, fever, and jaundice. The high serum amylase level and abdominal CT findings indicated a diagnosis of AP.
Because the pancreatitis was not severe and the patient's condition gradually improved, emergency endoscopic retrograde cholangiopancreatography (ERCP) was not performed. After the pancreatitis was stabilized, surgical exploration of the abdomen was performed on 10 October 2011. Because of the patient's history of liver cirrhosis secondary to hepatitis B virus infection, there was a high probability that the liver mass was hepatocellular carcinoma. We planned to perform cholecystectomy and bile duct exploration, with intraoperative diagnosis of the nature of the liver mass. Intraoperative exploration showed nodular cirrhosis of the liver, an edematous gallbladder, a large number of muddy gallbladder stones, and an unencapsulated tumor in the left lobe of the liver measuring 45 x 35 x 25 mm. A soft grayish-white embolus (45 x 11 x 9 mm) was extracted from the distal CBD, and grayish-white tumor debris was observed in the left intrahepatic bile duct. Intraoperative biopsy and frozen section examination showed HCC with tumor CBDE. Left hemihepatectomy, cholecystectomy, and bile duct exploration were performed. Postoperative pathological examination of the surgical specimen confirmed moderately differentiated HCC in the left lobe of the liver and the CBDE. The surgical margins were free of tumor cells.
The serum CA19-9 level decreased to 81.20 U/ml by the 13th day after surgery, and the patient was discharged from hospital on the 35th day after surgery. The patient subsequently died of liver failure in another hospital on 12 February 2012.