A 74-year-old man presented to our hospital with nausea and vomiting for 2 weeks, without any history of gastrointestinal disorders. He had a history of alcoholism for over 20 years. An enlarged liver was palpable from the right hypochondrium without obvious jaundice or anemia. Contrast-enhanced computed tomography (CT) scans revealed a mass located in the right lobe of the liver (Figure 1A), measuring approximately 19.3 x 14.6 x 13.2 cm, with enhancement in the arterial phase and rapid washout in the portal phase, suggesting a diagnosis of primary liver cancer. No evidence of significant macrovascular invasion or intra- or extrahepatic metastases was observed on the CT scan. The patient was negative for both hepatitis B surface antigen and hepatitis C virus antibody. Des-gamma-carboxy prothrombin (DCP) was markedly elevated, whereas alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), and carbohydrate antigen 199 (CA 199) were normal. The Child-Pugh score was 5. To obtain definite histological evidence of the tumor and assess the extent of liver cirrhosis, a biopsy was performed. Finally, the patient was diagnosed as HCC with mild liver cirrhosis and staged as BCLC-A in the Barcelona Clinic Liver Cancer (BCLC) staging system. The etiology of HCC was chronic alcoholic hepatitis.
The ratio of FLR to standard liver volume (SLV) after anatomical right hemi-hepatectomy was 51.47% (Figure 1B), which was well-tolerated for hepatectomy (>40%). However, the middle hepatic vein ran almost along the edge of the lesion (Figure 1A). If a right hemi-hepatectomy were to be performed, it would be hard to ensure an adequate surgical margin. A narrow surgical margin has been proved to be an unfavorable prognostic factor. By contrast, an extended right hemi-hepatectomy would probably result in insufficient FLR (Figure 1C, FLR/SLV = 25.78%, far <40%), with a high risk of PHLF. Nevertheless, the patient wished to undergo surgical treatment. After discussion among the multidisciplinary team (MDT), a combination of PVE and multimodality therapies, comprising HAIC, Lenvatinib, and Sintilimab, was considered the optimal choice in the circumstances.
HAIC with the mFOLFOX regimen (oxaliplatin, 85 mg/m2 intra-arterial infusion; leucovorin, 400 mg/m2 intra-arterial infusion; and fluorouracil, 400 mg/m2 bolus infusion and 2,400 mg/m2 continuous infusion) was performed initially. The infusion microcatheter was selectively placed into the common hepatic artery, which was the main feeding artery to the tumor (Figure 2A). After 3 days of HAIC, biological glue was utilized to embolize the right branch of the portal vein (Figures 2B,C), resulting in a brief increase in alanine transaminase (ALT) to 338.6 U/L, aspartate aminotransferase (AST) to 632. U/L, and total bilirubin (TBIL) to 32.4 umol/L. Liver function normalized with medication within 3 days, and Lenvatinib (8 mg per day) plus Sintilimab (200 mg per 3 weeks) were administered subsequently, causing no significant adverse events. After 5 weeks of multimodality therapy, follow-up CT scans showed remarkable regression of the tumor with complete disappearance of intratumoral enhancement on the artery phase (Figure 3A) and increased distance between the tumor and the middle hepatic vein (Figure 3B). The FLR/SLV reached 67.74% (Figure 3C), and the Child-Pugh score was 5, which met the requirements of the surgery. One week later, laparoscopic right hemi-hepatectomy was successfully performed with a >1-cm surgical margin. The gross of the resected specimen showed obvious hemorrhage and necrosis of the tumor (Figures 4A,B). Postoperative pathology revealed an encapsulated tumor with massive hyalinization, necrosis, lymphocyte, and granulocyte infiltration, and no viable tumor cells (Figure 4C). The patient was discharged at the 7th day after the operation without any complications. He was advised to stop drinking and follow up regularly. At the 3-month follow-up, no significant evidence of recurrence on imaging or laboratory tests was observed. The timeline of clinical events is shown in Figure 5.