A 54-year-old man visited the emergency room for aggravated epigastric pain. The patient had chronic hepatitis B since his twenties and received no special treatment. He was previously diagnosed with hepatocellular carcinoma (2 lesions in segments 6 and 8) at the age of 46 and was transferred to our hospital. He received transarterial chemoembolization (TACE) and radiofrequency ablation. The hepatocellular carcinoma recurred in segment 5 after 3 years, and the patient received additional TACE followed by laparoscopic wedge resection. During subsequent follow-up, the patient was found to have recurrent multiple hepatocellular carcinoma with the continued elevation of alpha-fetoprotein, and the lesion continued to progress even after repeated TACEs in the last 1 year. He started 400 mg of sorafenib twice a day 3 weeks ago. At the first outpatient visit after one week of sorafenib treatment, the patient complained of minor pain in the upper abdomen but the general condition was fair. He was instructed to revisit if the pain aggravated. As the pain worsened, the patient returned to the emergency room after discontinuing the medication for 2 days. The abdominal pain was assessed as 3 points on the Visual Analog Scale. The patient complained of nausea and indigestion in addition to abdominal pain, but there was no fever or diarrhea. As the abdominal pain worsened, the Eastern Cooperative Oncology Group Performance Status Scale worsened from 1 point to 3 points. Apart from hepatitis B and hepatocellular carcinoma, the patient had type 2 diabetes for which he was taking glimepiride. The patient was a social drinker, but abstained from alcohol since diagnosis of the hepatocellular carcinoma. Physical examination showed slight tenderness in the right upper abdomen and the epigastrium, but no rebound tenderness or abdominal rigidity was observed. The laboratory findings were as follows: leukocyte 5,480/uL, hemoglobin 15.6 g/dL, platelet 301,000/uL, total protein 7.0 g/dL, albumin 3.7 g/dL, aspartate aminotransferase 25 IU/L, alanine aminotransferase 34 IU/L, total bilirubin 1.65 mg/dL, direct bilirubin 1.00 mg/dL, gamma glutamyl transpeptidase 596 IU/L, alkaline phosphatase 350 IU/L, amylase 35 U/L, lipase 191 U/L, C-reactive protein 10.660 mg/dL, blood urea nitrogen 16.8 mg/dL, and creatinine 0.72 mg/dL. In the coagulation test, the prothrombin time was 16.7 seconds (international normalized ratio 1.45). The creatine kinase-muscle/brain fraction and troponin T levels were normal, and the electrocardiography showed normal sinus rhythm. Abdominal ultrasonography showed a sludge-filled gallbladder and multiple masses with increased echogenicity in the liver, but there were no dilated bile ducts or pancreatic abnormalities.

After the initial examination, the patient’s abdominal pain was suspected to be 1) acute gastritis due to sorafenib administration, 2) acute pancreatitis associated with sorafenib, or 3) acute biliary pancreatitis or cholangitis due to the gallbladder sludge which was either related or unrelated to sorafenib administration. We therefore decided to 1) discontinue sorafenib as a possible cause, 2) fast the patient, keeping in mind the possible aforementioned conditions and administer sufficient intravenous fluids, and 3) observe the improvement in clinical features and results of biochemical tests. We also intended to perform computed tomography (CT) scans in case the patient had fever or the symptoms or test results deteriorated. The patient improved to 1 point on the Visual Analog Scale system from the day after admission, and the levels of lipase, gamma glutamyl transpeptidase, and alkaline phosphatase decreased to 126 U/L, 426 IU/L, and 257 IU/L, respectively. On the 3rd day of admission, the patient no longer complained of abdominal pain and started having meals, while the levels of total bilirubin and C-reactive protein improved to 1.45 mg/dL and 8.620 mg/dL, respectively. The patient remained stable, the abdominal pain resolved, and continued to have meals, but he continued to complain of intermittent nausea and indigestion despite the administration of proton pump inhibitors and prokinetics. Endoscopy was additionally performed, and the endoscopic findings showed no significant changes in the esophageal varices and reflux esophagitis as well as portal hypertensive gastropathy compared to the findings 9 months ago. However, a new large bulging mass, occupying the gastric lumen from the anterior wall of the upper body to the fundus, was observed, and was suspected to cause extrinsic compression (Fig. 1). A CT scan of the abdomen revealed a new cystic lesion, about 8 cm in size, with necrosis of the pancreatic tail parenchyma, which was diagnosed as a pseudocyst of the pancreas (Fig. 2A, B). As the abdominal pain resolved and there were no signs of infection, the lesion was monitored for spontaneous resolution without further interventions.

The patient’s condition improved to 1 point on the Eastern Cooperative Oncology Group Performance Status Scale system, the abdominal pain resolved, and his dietary intake recovered. Sorafenib was discontinued and the treatment was changed to Adriamycin and cisplatin systemic chemotherapy. One month later, the CT scan showed that the size of the pseudocyst in the pancreatic tail decreased to about 7 cm. It was planned that the patient would maintain systemic chemotherapy and follow-up the pancreatic lesion at regular treatment response evaluations (Fig. 2C, D).