HAIC-Based Combination Therapy for Advanced Hepatocellular Carcinoma with Vp4 Portal Vein Tumor Thrombus and...

Advanced hepatocellular carcinoma (HCC) with Vp4/main portal vein tumor thrombus (PVTT) and Child-Pugh B liver function remains difficult to manage because patients with impaired hepatic reserve are vulnerable to hepatic decompensation and are underrepresented in pivotal systemic therapy trials. We report a 57-year-old man with hepatitis B virus-related cirrhosis, advanced HCC, Vp4 PVTT, BCLC stage C/CNLC stage IIIa disease, Child-Pugh B7 liver function, and ECOG performance status 1. Baseline contrast-enhanced computed tomography (CT) showed multifocal confluent intrahepatic tumors forming a measurable target mass of 91 mm × 71 mm. After multidisciplinary evaluation, the patient received modified FOLFOX-based hepatic arterial infusion chemotherapy (HAIC) every 3 weeks for four cycles, combined with lenvatinib (8 mg once daily), camrelizumab (200 mg every 3 weeks), and entecavir. After four cycles, the confluent target lesion decreased to 46 mm × 45 mm, alpha-fetoprotein (AFP) decreased from 656 ng/mL to 3.58 ng/mL (normal range, 0-7 ng/mL), and PVTT burden decreased radiologically. Ascites present at baseline resolved during treatment. At 34 months, the residual lesion measured 41 mm × 28 mm, AFP remained within the normal range, no new intrahepatic lesions were detected, and PVTT remained controlled, although a small amount of ascites was again detected. A retrospective RECIST version 1.1 assessment classified the best overall response as partial response, which was sustained at the 34-month follow-up. The Child-Pugh score was B7 at baseline, improved to A5 after ascites resolution, and was A6 at the 34-month follow-up. No grade 3 or higher treatment-related adverse events were documented. This case does not establish treatment efficacy but illustrates a hypothesis-generating approach to patient selection, non-embolization-based locoregional therapy, antiviral treatment, and longitudinal safety monitoring in a high-risk HCC subgroup for whom prospective evidence is limited.