Prognostic impact of diabetes mellitus on hepatocellular carcinoma: Special emphasis from the BCLC perspective

Abstract

BackgroundDiabetes mellitus (DM) is associated with higher incidence and poorer prognosis of hepatocellular carcinoma (HCC). The influence of DM on patient survival in different HCC stages is not known.MethodsA prospective dataset of 3,182 HCC patients was collected between 2002 and 2014. Patients were divided into three groups according to BCLC stages (BCLC stage 0 and stage A, BCLC stage B, BCLC stage C and stage D). We compared the cumulative survival rate of diabetic and non-diabetic patients in different BCLC groups. The correlation between DM and overall survival was also analyzed by multivariate Cox regression model within each group.ResultsDM is present in 25.2% of all patients. Diabetic patients had lower cumulative survival in BCLC stage 0 plus BCLC stage A group (log rank p<0.001), and BCLC stage B group (log rank p = 0.012), but not in BCLC stage C plus BCLC stage D group (log rank p = 0.132). Statistically significant differences in overall survival are found between diabetic and non-diabetic patients in BCLC stage 0 plus stage A group (adjusted hazard ratio [HR] = 1.45, 95% confidence interval [CI] 1.08–1.93, p = 0.013), and BCLC stage B (adjusted HR = 1.77, 95% CI 1.24–2.51, p = 0.002). In contrast, the survival difference is not seen in BCLC stage C plus stage D group (adjusted HR = 1.09, 95% CI 0.90–1.30, p = 0.387).ConclusionsDM is prevalent in HCC, and is associated with lower survival rate in HCC patients with BCLC stage 0 plus stage A and B, but not in those with BCLC stage C plus stage D.

Assessment of the Relationship Between the Monitoring Results of Patients With Viral Hepatitis-Related Hepatocellular Carcinoma and Type 2 Diabetes Mellitus.

“…Su et al investigated the effects of DM on survival in 3,182 HCC patients and used the BCLC staging criteria (25). They reported that diabetic patients had a poorer prognosis.…”

Effect of Nonalcoholic Fatty Liver Disease and Metabolic Risk Factors on Waitlist Outcomes in Patients With Hepatocellular Carcinoma

“… 21 , 28 , 29 A recent study showed that diabetes was a predictor of decreased survival in the interferon era but not the direct-acting antiviral era, but the reasons for this are unclear. 30 Finally, it also appears that BCLC stage is important, as Su et al reported lower survival rates in HCC patients with diabetes and BCLC stage 0, A, and B, but no difference in survival seen in stages C and D. 31 , 32 …”

Predictors of failure to detect early hepatocellular carcinoma in patients with chronic hepatitis B who received regular surveillance

“…First assumption was, fatty infiltration in liver, often can be seen in diabetic patients, resulted in poor echogenicity and might have hindered HCC early detection; however, ultrasonographic fatty liver was not a predictor for HCC detection failure. On the other hand, diabetes mellitus is more prevalent in patients with advanced HCC compared to those with early HCC . Therefore, it seems highly probable that increased insulin resistance and hyperinsulinaemia in diabetes might upregulate the production of insulin‐like growth factor‐1 (IGF‐1), which stimulates cell proliferation, inhibits apoptosis and increase tissue turn over .…”

“…The biological , diabetes mellitus status. Cumulative incidence rates of HCC detection failure after 5 years of surveillance were higher in patients with clinical cirrhosis (liver cirrhosis vs nonliver cirrhosis; 3.1% vs 0.6%; P < 0.001), higher AFP levels (AFP ≥ 9 ng/mL vs AFP < 9 ng/mL; 8.7% vs 1.0%, P < 0.001), higher LS values (LS ≥ 11.7 kPa vs LS < 11.7 kPa; 5.7% vs 0.4%; P < 0.001), and diabetes mellitus (diabetes mellitus vs nondiabetes mellitus; 4.3% vs 0.6%; P < 0.001) 51,52 Therefore, it seems highly probable that increased insulin resistance and hyperinsulinaemia in diabetes might upregulate the production of insulin-like growth factor-1 (IGF-1), which stimulates cell proliferation, inhibits apoptosis and increase tissue turn over. 53,54 This leads to hepatocarcinogenesis and accelerated tumour growth.…”