In this prospective study, we evaluated the feasibility and clinical utility of directly administering iodinated contrast medium into the portal vein following PVE and quantitatively assessing the resulting iodine distribution in the FLR with DECT. We identified a significant positive correlation between FLR iodine content and the KGR, suggesting that the measured iodine distribution in the FLR can serve as an early imaging biomarker of subsequent hypertrophy.

Our initial hypothesis posited that alterations in portal hemodynamics following PVE would primarily dilute the iodine concentration in the FLR due to a simple increase in portal blood flow. Contrary to this expectation, we observed higher iodine levels in the FLR. These unexpected findings suggest that the mechanisms driving hypertrophy extend beyond mere increases in portal blood volume.

Specifically, it is known that following PVE, not only does portal blood flow to the FLR increase, but portal pressure also rises [5]. There is a report that this elevation in portal pressure after PVE dilates the portal veins within the FLR, leading to stretched endothelial cells that secrete interleukin-6 (IL-6), a cytokine that promotes liver regeneration [6]. Additionally, it has been demonstrated in the literature that FLR hypertrophy after PVE correlates significantly with the increase in portal blood flow measured on postoperative day three, rather than immediately after PVE [7]. This temporal association further supports the hypothesis that FLR hypertrophy is driven not merely by increased portal blood flow, but also by the rise in portal pressure after embolisation and subsequent cytokine-mediated mechanisms. The observed iodine content in the FLR in this study may not only directly reflect changes in blood flow but also include contributions from portal blood flow redistribution and cytokine-driven regenerative mechanisms. It may serve as an earlier indicator of FLR hypertrophy than the increase in portal blood flow itself.

This technique offers a novel approach for predicting FLR growth after PVE, enabling earlier identification of patients at risk for inadequate hypertrophy and informing timely additional interventions—such as hepatic vein embolisation—before major hepatectomy [8]. To substantiate these preliminary results and incorporate them into standard practice, further research with larger patient cohorts and refined imaging protocols is warranted.