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Journal Watch - May 2021 (2)

LI-RADS v2018 major criteria: Do hepatocellular carcinomas in non-alcoholic steatohepatitis differ from those in virus-induced chronic liver disease on MRI?

Barat M, Nguyen TTL, Hollande C, Coty JB, Hoeffel C, Terris B, Dohan A, Mallet V, Pol S, Soyer P.

Eur J Radiol. 2021 May; 138:109651.

DOI: 10.1016/j.ejrad.2021.109651. PMID: 33740627

 

Currently, the diagnosis of hepatocellular carcinoma (HCC) is based on cross-sectional imaging, namely contrast-enhanced computed tomography (CECT) and magnetic resonance imaging (MRI), setting the primary endpoint in the identification of the tumor in the early stage, when patient's condition and liver function can lead to surgical treatment. The main risk factors for developing HCC are virus- and alcohol-induced cirrhosis (1). Patients with nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), especially in the Western countries, also have a mild risk for developing HCC (2). Contrast-enhanced CT and MR imaging features of HCC, i.e. enhancement during the arterial phase and wash-out in the portal-venous phase, are worldwide accepted and endorsed by the LI-RADS (3). However, LI-RADS can't be applied to NASH patients, which have a twofold increased risk of HCC-related mortality (4).

In this setting the Authors of the present paper have retrospectively validated MRI LI-RADS major features in patients affected by NASH, enrolling a total of 82 patients (41 HCC with virus-induced cirrhosis and 41 with NASH) from two centers. The final diagnosis was obtained according to the histopathological results. All patients underwent liver MRI examination on a 1.5T scanner before and after intravenous administration of a gadolinium-based extracellular contrast agent (gadoterate meglumine and gadobenate dimeglumine in 32 and 9 patients with NASH and in 33 and 8 patients with virus-induced cirrhosis, respectively). MRI examinations of the two groups were compared for imaging presentation, LI-RADS major criteria, and LI-RADS categorization (5) by two independent readers, blinded to clinical and histopathological data.

Authors reported no statistically significant differences regarding tumor longest diameter (30.3 ± 20.9 in NASH vs 38.0 ± 26.3 mm in virus group, respectively, p=0.121), signal drop on IP/OP T1W imaging (11.8 ± 18.5 vs 6.0 ± 9.7%, p=0.464) and ADC value (975 ± 257 vs 1048 ± 253 ×10-3 mm2/s, p=0.197). Moreover, no significant differences were found regarding qualitative variables, in particular location (right liver lobe 76 vs 63%, p=0.337), arterial phase hyperenhancement (93 vs 98%, p=0.616), wash-out (63 vs 83%, p=0.502), tumor capsule (68 vs 61%, p=0.488), and portal vein invasion (12 vs 24%, p=0.253), with an overall good agreement for all features, except for tumor capsule in NASH patients (k=0.367).

In both groups, the most represented LI-RADS category was 5 (63 vs 80%), followed by 4 (22 vs 12%) and 3 (15 vs 7%), with no significant difference between groups (p=0.303) and a good agreement between the two readers (k=0.802 for NASH patients and k=0.720 for virus-induced cirrhotic patients).

Two important previous studies published in literature examined the importance of imaging features of HCC in NASH patients: Alsharan et al. (6) and Thompson et al. (7) reported the non-rim like hyperenhancement during the arterial phase in the majority of patients (100% and 93%, respectively).  Same results were reported by the three groups regarding tumor capsule, observed in 63% of patients enrolled by the present study, 60% by Alsharan et al., and 71% by Thompson et al. However, similar results were not reported for the wash-out appearance on the portal-venous phase, observed in 40% and 21% (lsharan et al., and Thompson et al) respectively).

Some limitations should be reported: firstly, the small sample size and the population analyzed including patients with S4 or F4 underlying chronic liver disease. Second, a not negligible percentage of patients received an hepatocyte selective contrast agent even if the risk of bias was limited to the lack of analysis of the hepatobiliary phase. Third, the retrospective design did not allow the evaluation of LI-RADS 1, 2, and 3 because only histopathologically proven HCC were included.

In conclusion, the Authors provided original data regarding HCC in NASH patients showing that MRI features are similar to those of HCC in virus-induced chronic liver disease and resulting in similar LI-RADS categorization. In this setting, additional studies are needed to further validate LI-RADS applicability to NASH patients.

 

References:

  1. Ayuso C, Rimola J, Vilana R, et al (2018) Diagnosis and staging of hepatocellular carcinoma (HCC): current guidelines. European Journal of Radiology 101:72–8 doi.org/10.1016/j.ejrad.2018.01.025
  2. Anstee QM, Reeves HL, Kotsiliti E, et al (2019) From NASH to HCC: current concepts and future challenges. Nat Rev Gastroenterol Hepatol 16:411–428. doi.org/10.1038/s41575-019-0145-7
  3. Chernyak V, Fowler KJ, Kamaya A, et al (2018) Liver Imaging Reporting and Data System (LI-RADS) Version 2018: Imaging of Hepatocellular Carcinoma in At-Risk Patients. Radiology 289:816–830. doi.org/10.1148/radiol.2018181494
  4. Gupta A, Das A, Majumder K, et al (2018) Obesity is Independently Associated With Increased Risk of Hepatocellular Cancer-related Mortality: A Systematic Review and Meta-Analysis. Am J Clin Oncol 41:874–88 doi.org/10.1097/COC.0000000000000388
  5. Elsayes KM, Kielar AZ, Elmohr MM, et al (2018) White paper of the Society of Abdominal Radiology hepatocellular carcinoma diagnosis disease-focused panel on LI-RADS v2018 for CT and MRI. Abdom Radiol (NY) 43:2625–2642. doi.org/10.1007/s00261-018-1744-4
  6. Al-Sharhan F, Dohan A, Barat M, et al (2019) MRI presentation of hepatocellular carcinoma in non-alcoholic steatohepatitis (NASH). Eur J Radiol 119:108648. doi.org/10.1016/j.ejrad.2019.108648
  7. Thompson SM, Garg I, Ehman EC, et al (2018) Non-alcoholic fatty liver disease-associated hepatocellular carcinoma: effect of hepatic steatosis on major hepatocellular carcinoma features at MRI. Br J Radiol 91:20180345. doi.org/10.1259/bjr.20180345

 

Dr. Cesare Maino is a young attending radiologist working at San Gerardo Hospital in Monza, Lombardy, Italy, graduated at the Vita-Salute San Raffaele University of Milan in July 2015 and post-graduated at the University of Milano Bicocca in November 2020. He attends ESGAR annual meetings since 2017 and is a mentee of the ESGAR mentorship program.

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