Hepatocellular carcinomas in patients with metabolic syndrome often develop without significant liver fibrosis: A pathological analysis

Abstract

This study shows that HCCs in patients with features of MS as the only risk factor for liver disease have distinct morphological characteristics and mainly occur in the absence of significant fibrosis in the background liver. In addition, some of them arise through malignant transformation of a preexisting liver cell adenoma.

Oxidative stress promotes pathologic polyploidization in nonalcoholic fatty liver disease

“…Importantly, we observed that highly polyploid mononuclear hepatocytes (≥8n) were also enriched in livers of tumoral KO mice compared with those in control animals spectrum of hepatic lesions, ranging from simple reversible steatosis (intrahepatic accumulation of triglycerides) and nonalcoholic steatohepatitis (NASH) to more severe lesions, such as cirrhosis and hepatocellular carcinoma (HCC) (23)(24)(25). There is growing evidence that HCC can occur during NALFD in noncirrhotic livers (26)(27)(28)(29). A "2-hit" model has been proposed to explain the progression of simple fatty liver disease to NASH (30).…”

Progression and Natural History of Nonalcoholic Fatty Liver Disease in Adults

“…A French study analyzed a cohort of 31 patients with HCC with MetS as the only risk factor for liver disease and found mild or no fibrosis in most cases, compared with those harboring HCC associated with an overt cause of liver disease (65% vs 26%, P<.0001). 38 The absence of cirrhosis was further confirmed in 38% of Japanese patients 41 and in one-third of patients from North East England with NAFLD-related HCC. 41 As patients without cirrhosis are not in surveillance programs, most (62.3%) presented symptomatically with larger tumors, and their median survival was just 7.2 months.…”

Hepatic expression of the Sptlc3 subunit of serine palmitoyltransferase is associated with the development of hepatocellular carcinoma in a mouse model of nonalcoholic steatohepatitis

“…However, STAM-F mice did not develop LC within the period when HCC was observed. Although LC is a risk factor for HCC development, HCC in patients with metabolic syndrome often develops without advanced hepatic fibrosis (20). Thus, development of HCC in STAM-F mice with mild fibrosis may be similar to that in human NASH, although the mechanism of the decrease in hepatic steatosis in STAM-F has not been elucidated.…”