Abstract No. 111: Hepatocellular carcinoma tumor response after portal vein embolization

Abstract

PurposePrevious studies have reported that portal vein embolization (PVE) performed to induce hypertrophy of the future liver remnant (FLR) prior to major hepatectomy can lead to acceleration of tumor growth in the embolized lobe. As these reports predominantly examined metastatic disease, less is known about hepatocellular carcinoma (HCC). We thus studied the effect of preoperative PVE on HCC tumor growth.Materials and MethodsRecords of 12 patients with 16 HCC tumors who underwent preoperative PVE were retrospectively reviewed. Patients receiving other forms of liver-directed therapy such as transcatheter arterial chemo-embolization were excluded from the study. Measurements of total tumor volume were obtained from cross-sectional imaging studies performed before and after PVE utilizing a semi-automated three-dimensional technique, also used to measure FLR volume. Correlation with degree of tumor necrosis from surgical pathology reports was made when available.ResultsSix of the twelve patients (50%) demonstrated a decrease in total tumor volume following PVE, with a relative decrease ranging from 13-87% (mean 49%). Increase in tumor volume was demonstrated in four patients (33%) ranging from 19-37% (mean 29%). The tumor volume in the remaining two patients (17%) did not significantly change. PVE successfully induced contralateral lobe hypertrophy in all twelve patients, eleven of whom went on to major hepatic resection. On pathologic evaluation, complete necrosis was reported in 3 lesions, 33% necrosis in 1 lesion, <30% necrosis in 6 lesions, and no necrosis in 5 lesions. All patients with tumor volume reduction on imaging studies exhibited some level of necrosis, with two demonstrating complete necrosis; however, no correlation between the extent of necrosis and change in tumor volume was apparent.ConclusionOur study demonstrates that PVE may result in a reduction in HCC tumor volume, suggesting a significant contribution of portal venous blood flow to the viability of some hepatocellular tumors. PurposePrevious studies have reported that portal vein embolization (PVE) performed to induce hypertrophy of the future liver remnant (FLR) prior to major hepatectomy can lead to acceleration of tumor growth in the embolized lobe. As these reports predominantly examined metastatic disease, less is known about hepatocellular carcinoma (HCC). We thus studied the effect of preoperative PVE on HCC tumor growth. Previous studies have reported that portal vein embolization (PVE) performed to induce hypertrophy of the future liver remnant (FLR) prior to major hepatectomy can lead to acceleration of tumor growth in the embolized lobe. As these reports predominantly examined metastatic disease, less is known about hepatocellular carcinoma (HCC). We thus studied the effect of preoperative PVE on HCC tumor growth. Materials and MethodsRecords of 12 patients with 16 HCC tumors who underwent preoperative PVE were retrospectively reviewed. Patients receiving other forms of liver-directed therapy such as transcatheter arterial chemo-embolization were excluded from the study. Measurements of total tumor volume were obtained from cross-sectional imaging studies performed before and after PVE utilizing a semi-automated three-dimensional technique, also used to measure FLR volume. Correlation with degree of tumor necrosis from surgical pathology reports was made when available. Records of 12 patients with 16 HCC tumors who underwent preoperative PVE were retrospectively reviewed. Patients receiving other forms of liver-directed therapy such as transcatheter arterial chemo-embolization were excluded from the study. Measurements of total tumor volume were obtained from cross-sectional imaging studies performed before and after PVE utilizing a semi-automated three-dimensional technique, also used to measure FLR volume. Correlation with degree of tumor necrosis from surgical pathology reports was made when available. ResultsSix of the twelve patients (50%) demonstrated a decrease in total tumor volume following PVE, with a relative decrease ranging from 13-87% (mean 49%). Increase in tumor volume was demonstrated in four patients (33%) ranging from 19-37% (mean 29%). The tumor volume in the remaining two patients (17%) did not significantly change. PVE successfully induced contralateral lobe hypertrophy in all twelve patients, eleven of whom went on to major hepatic resection. On pathologic evaluation, complete necrosis was reported in 3 lesions, 33% necrosis in 1 lesion, <30% necrosis in 6 lesions, and no necrosis in 5 lesions. All patients with tumor volume reduction on imaging studies exhibited some level of necrosis, with two demonstrating complete necrosis; however, no correlation between the extent of necrosis and change in tumor volume was apparent. Six of the twelve patients (50%) demonstrated a decrease in total tumor volume following PVE, with a relative decrease ranging from 13-87% (mean 49%). Increase in tumor volume was demonstrated in four patients (33%) ranging from 19-37% (mean 29%). The tumor volume in the remaining two patients (17%) did not significantly change. PVE successfully induced contralateral lobe hypertrophy in all twelve patients, eleven of whom went on to major hepatic resection. On pathologic evaluation, complete necrosis was reported in 3 lesions, 33% necrosis in 1 lesion, <30% necrosis in 6 lesions, and no necrosis in 5 lesions. All patients with tumor volume reduction on imaging studies exhibited some level of necrosis, with two demonstrating complete necrosis; however, no correlation between the extent of necrosis and change in tumor volume was apparent. ConclusionOur study demonstrates that PVE may result in a reduction in HCC tumor volume, suggesting a significant contribution of portal venous blood flow to the viability of some hepatocellular tumors. Our study demonstrates that PVE may result in a reduction in HCC tumor volume, suggesting a significant contribution of portal venous blood flow to the viability of some hepatocellular tumors.