Yong Zhu1, Jun Chen2, Weiwei Kong3, Liang Mao4, Wentao Kong5, Qun Zhou6, Zhengyang Zhou7, Bin Zhu7, Zhongqiu Wang8, Jian He9, Yudong Qiu10. 1. Department of Radiology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 2. Department of Pathology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 3. Department of Oncology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 4. Department of Hepatopancreatobiliary Surgery, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 5. Department of Ultrasonography, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 6. Department of Radiology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 7. Department of Radiology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. 8. Department of Radiology, Jiangsu Province Hospital of Traditional Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, No. 2 Guangzhou Road, Nanjing, Jiangsu Province, China, 210008. 9. Department of Radiology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. hjxueren@126.com. 10. Department of Hepatopancreatobiliary Surgery, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, Jiangsu Province, China, 210008. yudongqiu510@163.com.
Abstract
OBJECTIVES: To explore the difference in contrast-enhanced computed tomography (CT) features of intrahepatic cholangiocarcinomas (ICCs) with different isocitrate dehydrogenase (IDH) mutation status. METHODS: Clinicopathological and contrast-enhanced CT features of 78 patients with 78 ICCs were retrospectively analysed and compared based on IDH mutation status. RESULTS: There were 11 ICCs with IDH mutation (11/78, 14.1%) and 67 ICCs without IDH mutation (67/78, 85.9%). IDH-mutated ICCs showed intratumoral artery more often than IDH-wild ICCs (p = 0.023). Most ICCs with IDH mutation showed rim and internal enhancement (10/11, 90.9%), while ICCs without IDH mutation often appeared diffuse (26/67, 38.8%) or with no enhancement (4/67, 6.0%) in the arterial phase (p = 0.009). IDH-mutated ICCs showed significantly higher CT values, enhancement degrees and enhancement ratios in arterial and portal venous phases than IDH-wild ICCs (all p < 0.05). The CT value of tumours in the portal venous phase performed best in distinguishing ICCs with and without IDH mutation, with an area under the curve of 0.798 (p = 0.002). CONCLUSIONS: ICCs with and without IDH mutation differed significantly in arterial enhancement mode, and the tumour enhancement degree on multiphase contrast-enhanced CT was helpful in predicting IDH mutation status. KEY POINTS: • IDH mutation occurred frequently in ICCs. • ICCs with and without IDH mutation differed significantly in arterial enhancement mode. • ICCs with IDH mutation enhanced more than those without IDH mutation. • Enhancement ratio and tumour CT value can predict IDH mutation status.
OBJECTIVES: To explore the difference in contrast-enhanced computed tomography (CT) features of intrahepatic cholangiocarcinomas (ICCs) with different isocitrate dehydrogenase (IDH) mutation status. METHODS: Clinicopathological and contrast-enhanced CT features of 78 patients with 78 ICCs were retrospectively analysed and compared based on IDH mutation status. RESULTS: There were 11 ICCs with IDH mutation (11/78, 14.1%) and 67 ICCs without IDH mutation (67/78, 85.9%). IDH-mutated ICCs showed intratumoral artery more often than IDH-wild ICCs (p = 0.023). Most ICCs with IDH mutation showed rim and internal enhancement (10/11, 90.9%), while ICCs without IDH mutation often appeared diffuse (26/67, 38.8%) or with no enhancement (4/67, 6.0%) in the arterial phase (p = 0.009). IDH-mutated ICCs showed significantly higher CT values, enhancement degrees and enhancement ratios in arterial and portal venous phases than IDH-wild ICCs (all p < 0.05). The CT value of tumours in the portal venous phase performed best in distinguishing ICCs with and without IDH mutation, with an area under the curve of 0.798 (p = 0.002). CONCLUSIONS: ICCs with and without IDH mutation differed significantly in arterial enhancement mode, and the tumour enhancement degree on multiphase contrast-enhanced CT was helpful in predicting IDH mutation status. KEY POINTS: • IDH mutation occurred frequently in ICCs. • ICCs with and without IDH mutation differed significantly in arterial enhancement mode. • ICCs with IDH mutation enhanced more than those without IDH mutation. • Enhancement ratio and tumour CT value can predict IDH mutation status.
Authors: K Yamashita; A Hiwatashi; O Togao; K Kikuchi; R Hatae; K Yoshimoto; M Mizoguchi; S O Suzuki; T Yoshiura; H Honda Journal: AJNR Am J Neuroradiol Date: 2015-09-24 Impact factor: 3.825
Authors: M Ciresa; A M De Gaetano; M Pompili; A Saviano; A Infante; M Montagna; A Guerra; M Giuga; M Vellone; F Ardito; A De Rose; F Giuliante; F M Vecchio; A Gasbarrini; L Bonomo Journal: Eur Rev Med Pharmacol Sci Date: 2015-08 Impact factor: 3.507