Arslanoglu Atilla, Chalian Hamid, Sodagari Faezeh, Seyal Adeel R, Töre Hüseyin Gürkan, Salem Riad, Yaghmai Vahid
1 All authors: Department of Radiology, Northwestern Memorial Hospital, Northwestern University Feinberg School of Medicine, 676 N Saint Clair St, Ste 800, Chicago, IL 60611.
AJR Am J Roentgenol. 2016 Mar;206(3):536-43. doi: 10.2214/AJR.15.15339.
The objective of our study was to determine whether the conventionally used enhancement threshold of 10 HU for assessing tumor viability in treated hepatocellular carcinoma (HCC) lesions is valid.
To distinguish pseudoenhancement from enhancement in a tumor, we used an in vivo model: The attenuation of 54 hepatic cysts during the unenhanced and portal venous phases of MDCT, similar to what may be observed in HCC with central necrosis, was used to determine the threshold for pseudoenhancement. To validate this model, we compared the attenuation value of liver parenchyma in this cohort with that of 22 HCCs during the late arterial phase of enhancement. We tested the effect of this pseudoenhancement on quantifying necrosis in HCC compared with the conventionally used threshold of 10 HU.
Values of enhancing HCC tissue on arterial phase MDCT (mean, 121.3 HU) were comparable with normal liver parenchyma on venous phase MDCT (117.3 HU) (p = 0.27). The threshold of 17.1 HU was the best threshold for the detection of pseudoenhancement in cysts (99% accuracy, 100% sensitivity, and 98% specificity). When this threshold was used instead of the conventional threshold of 10 HU, the mean necrosis proportion of treated HCC increased from 34.0% to 42.6% and the mean viable tumor proportion decreased from 66.0% to 57.4%. The quantification of viable HCC tissue based on 10 HU and the quantification of viable HCC tissue based on 17.1 HU were found to be significantly different (p < 0.0001).
The threshold of 17.1 HU may be the appropriate cutoff for nonenhancement in a necrotic HCC. Use of this threshold may potentially affect how response to therapy is quantified and categorized.
本研究的目的是确定在评估经治疗的肝细胞癌（HCC）病灶中肿瘤活性时，传统使用的10 HU增强阈值是否有效。
为区分肿瘤中的假性增强与真正增强，我们使用了一种体内模型：利用54个肝囊肿在MDCT平扫期和门静脉期的衰减情况（类似于在伴有中央坏死的HCC中可能观察到的情况）来确定假性增强的阈值。为验证该模型，我们将该队列中肝实质的衰减值与22个HCC在增强晚期动脉期的衰减值进行了比较。我们测试了与传统的10 HU阈值相比，这种假性增强对HCC坏死定量的影响。
动脉期MDCT上增强的HCC组织值（平均121.3 HU）与静脉期MDCT上的正常肝实质值（117.3 HU）相当（p = 0.27）。17.1 HU的阈值是检测囊肿假性增强的最佳阈值（准确率99%，灵敏度100%，特异性98%）。当使用该阈值而非传统的10 HU阈值时，经治疗的HCC的平均坏死比例从34.0%增加到42.6%，平均存活肿瘤比例从66.0%降至57.4%。发现基于10 HU的存活HCC组织定量与基于17.1 HU的存活HCC组织定量存在显著差异（p < 0.0001）。
17.1 HU的阈值可能是坏死性HCC中非增强的合适截断值。使用该阈值可能会潜在影响对治疗反应的定量和分类方式。
