Clinicopathological characteristics of hepatitis B surface antigen-negative and hepatitis C antibody-negative hepatocellular carcinoma

Abstract

Abstract. The present study investigated the clinicopathological characteristics of resected hepatitis B virus surface antigen (HBs-Ag)-negative, hepatitis C virus antibody (HCV-Ab)-negative hepatocellular carcinoma (NBNC HCC). The clinicopathological characteristics of 164 patients with NBNC HCC, 144 patients with HBs-Ag-positive HCC (HBV group) and 550 patients with HCV-Ab-positive HCC (HCV group) were compared. In the NBCN HCC group, 61 patients succumbed after 2 years. Subsequently, NBCN HCC patients were compared according to survival time (<2 years, 39 patients vs. ≥2 years, 64 patients) to identify prognostic factors. Finally, the clinicopathological characteristics of NBNC HCC were compared according to history of alcohol abuse/pathological results: Non-alcoholic steatohepatitis HCC (NASH group, 40 patients), alcohol abuse HCC (AL group, 80 patients) and other HCCs (non-NASH/non-AL group, 44 patients). Age, diabetes prevalence and body mass index were significantly higher for NBNC HCC compared with virus-related HCC. Among stage II cases, the prognosis was significantly better for the NBNC compared with that for the HCV group. A high α-fetoprotein level, poorly differentiated HCC and advanced liver fibrosis were independent risk factors for the prognosis of NBNC HCC. The proportion of female patients was significantly higher among NASH compared with AL HCC patients. The cumulative survival rates following surgery were similar in the NASH, AL and non-NASH/non-AL groups. NBNC HCC is considered to be a lifestyle disease, with better prognosis for stage II patients. The prognostic factors for NBNC HCC patients undergoing hepatectomy were similar to those with virus-related HCC and did not differ according to alcohol abuse history or pathological results.

Epidemiology of non‐alcoholic fatty liver disease and non‐alcoholic steatohepatitis in Japan: A focused literature review

“…15,24,26,27 Moreover, DM was significantly more prevalent in patients with NASH-related cirrhosis compared to non-NASHrelated cirrhosis according to Hashizume et al and Yatsjui et al 27,38 The prevalence of DM in patients with NASH-related HCC was reported in six studies and ranged from 38 to 63%. 20,30,[39][40][41][42] Dyslipidemia. Dyslipidemia and its most common form, hyperlipidemia, are also frequently found in NAFLD and NASH patients.…”

“…48 Fibrosis stage did not significantly change despite 6 of the 10 patients reporting an improvement in fibrosis stage. 48 In three studies reporting the mean fibrosis stage of patients with NASH-related HCC, the score ranged from 2.30 to 3.20 based on Brunt 30,40,49 and New Inuyama scoring. 30,40,49 Iida et al observed the fibrosis stage of HCC patients according to HCC etiology and reported no significant difference in mean fibrosis between NASH (2.30), alcoholic liver disease (ALD) (2.20), and non-NASH non-ALD (2.40).…”

“…48 In three studies reporting the mean fibrosis stage of patients with NASH-related HCC, the score ranged from 2.30 to 3.20 based on Brunt 30,40,49 and New Inuyama scoring. 30,40,49 Iida et al observed the fibrosis stage of HCC patients according to HCC etiology and reported no significant difference in mean fibrosis between NASH (2.30), alcoholic liver disease (ALD) (2.20), and non-NASH non-ALD (2.40). 40 In two studies conducted by Yasui et al, mean fibrosis stage was found to be lower among male patients compared to female patients, with Yasui et al reporting statistical difference between cohorts (P < 0.05).…”

Hepatitis C virus core protein induces hepatic steatosis via Sirt1‐dependent pathway

“…HCV infection alters lipid metabolism and leads to dyslipidemia, hepatic steatosis and advanced fibrosis . Persistent viral infections tend to induce liver dysfunction and may further result in cirrhosis and hepatocellular carcinoma . Hepatic steatosis is one of the primary aetiologies of induced liver diseases.…”

“…3 Persistent viral infections tend to induce liver dysfunction and may further result in cirrhosis and hepatocellular carcinoma. 4,5 Hepatic steatosis is one of the primary aetiologies of induced liver diseases. Compared to other chronic liver diseases, the occurrence of hepatic steatosis is prevalent in patients with chronic hepatitis C. 6 The core protein of HCV localizes to the surface of lipid droplets and contributes to hepatic steatosis by interfering with intracellular lipid metabolism.…”