Percutaneous transvenous shunt occlusion for portosystemic encephalopathy due to lenvatinib administration to a patient with hepatocellular carcinoma and portosystemic shunt.

We report a 74-year-old male patient with compensated cirrhosis after hepatic C virus eradication. After the patient underwent hepatectomy for hepatocellular carcinoma, multiple lung and lymph node metastases were detected by computed tomography. Computed tomography also revealed a portosystemic shunt from the superior mesenteric vein to the right testicular vein. He was administered lenvatinib (12 mg). Five days after the initiation of lenvatinib, he developed grade 3 hepatic encephalopathy, and his ammonia level increased. Lenvatinib was stopped, with improvement of the encephalopathy and decrease in ammonia level. When lenvatinib was restarted, grade 2 encephalopathy recurred which then improved upon stopping the drug. We thought that the encephalopathy was due to the portosystemic shunt, and occlusion of the shunt was performed. The day after shunt occlusion, lenvatinib (8 mg) was restarted, and the lenvatinib dose was increased to 12 mg at 2 days after shunt occlusion. Subsequently, the ammonia level remained stable and the patient remained alert and conscious. Lenvatinib was continued until the time of this report (40 days after shunt occlusion), and after 1 month of lenvatinib therapy, the computed tomography verified absence of the portosystemic shunt and stable disease of hepatocellular carcinoma.