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. 2021 May 27;11:11127. doi: 10.1038/s41598-021-90508-9

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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DECT images of a 58-year-old man with HCC undergoing DEM-TACE 6 weeks ago, showed that no lipiodol deposition in the original tumor lesions, but TAA and TNA were present. The right hepatic lobe showed a low-attenuation lesion on unenhanced CT image (A), significant enhancement at arterial phase (B), and persistent enhancement at the portal venous phase(C). TNA had no enhancement. ROIs of TAA, ANHP, and TNA placed on arterial and portal iodine map (D and E) showed IC and NIC of TAA to be 1.5 mg/ml and 20.1% at arterial phase and 1.8 mg/ml and 48.5% at portal venous phase, respectively. The IC and NIC of ANHP was 0.3 mg/ml and 4.1% at arterial phase, and 1.1 mg/ml and 30.2% at portal venous phase, respectively. The IC and NIC of TNA was 0.1 mg/ml and 0.9% at arterial phase and 0.5 mg/ml and 11.9% at portal venous phase, respectively. The λHu of TAA, ANHP and TNA were 2.86, 0.53 and 0.23, respectively (F).