Steatohepatitic Hepatocellular Carcinoma Did Not Increase in the Last Decade: Metabolic Syndrome May Not Be the Only Contributing Factor
Jacob Alexander, Michael Torbenson, Tsung-Teh Wu, Matthew M Yeh. University of Washington, Seattle, WA; Johns Hopkins University, Baltimore, MD; Mayo Clinic, Rochester, MN
Background: Steatohepatitic hepatocellular carcinoma (SH-HCC) is a recently described HCC variant in which the tumor cells have histological changes that resemble steatohepatitis. Several studies have found an association between the SH-HCC morphology and the metabolic syndrome. Since the prevalence of the metabolic syndrome has steadily increased in recent years, we hypothesized that the prevalence of SH-HCC may have also increased in the past decade.
Design: We studied all surgically resected or explanted HCC cases from 3 tertiary centers in two separate 2-year intervals a decade apart (2000-2001 and 2010-2011,respectively). Pathology slides and clinical data were reviewed. Slides of liver distant from tumor were also reviewed and steatosis was scored according to NASH-CRN. We studied the frequency and clinicopathological correlates of HCC with the described SH-HCC features (steatosis, ballooning of HCC cells, inflammation, Mallory-Denk bodies, and pericellular fibrosis).
Results: SH-HCC was present in 80 of 298 (27%) cases. In the first time interval (2000-2001), 100 HCC cases were identified, of which 23 (23%) had the SH-HCC morphology. 10 years later, the second two year time interval (2010-2011) had a total of 198 HCC cases, of which 57 (28%) had a SH-HCC morphology. There was no significant difference in the prevalence of SH-HCC in these two periods (p=0.28). Background steatosis was significantly more common in 2010-2011, when each grade was analysed separately (p=0.0008), and when grades 1-3 were grouped together and compared with grade 0 (p=0.0002). Overall, those with SH-HCC morphology had a higher BMI when compared to those without (29.7 vs. 27.3; p=0.005), but the prevalence of metabolic syndrome was similar among the two groups. There was a significant association between SH-HCC and background steatosis when grades 1-3 were grouped together and compared with grade 0 (p=0.03), and there was a trend when each grade was analysed separately (p=0.09).
Conclusions: Our findings confirm the association between SH-HCC and some aspects of the metabolic syndrome. However, our data also suggests the metabolic syndrome/fatty liver may not entirely explain the carcinogenesis of SH-HCC in all cases and other pathways and genetic alterations should be further investigated. These results also indicate that the frequency of this morphology has been stable over a 10 year time interval. Longer time intervals may be needed to identify changing patterns in HCC morphology.
Tuesday, March 5, 2013 9:30 AM
Poster Session III # 193, Tuesday Morning