Background Despite the observed association between diabetes mellitus and hepatocellular carcinoma (HCC), little is known about the effect of diabetes duration prior to HCC diagnosis and whether some diabetes medications reduced the risk of HCC development. Aim We aimed at determining the association between HCC risk and diabetes duration and type of diabetes treatment. Methods A total of 420 HCC patients and 1104 healthy controls were enrolled in an ongoing hospital-based case-control study. We used multivariate logistic regression models to adjust for HCC risk factors. Results The prevalence of diabetes mellitus was 33.3% in HCC and 10.4% in the control group, yielding an adjusted odds ratio (AOR) and 95% confidence interval (CI) of 4.2 (3.0-5.9). In 87% of cases, diabetes was present prior to HCC diagnosis yielding an AOR of 4.4 (95%CI, 3.0-6.3). Compared to patients with a diabetes duration of 2-5 years, the estimated AORs (95% CI) for those with a diabetes duration of 6-10 years and those with diabetes duration > 10 years were 1.8 (0.8-4.1) and 2.2 (1.2-4.8) respectively. In respect to diabetes treatment, the AORs (95% CI) were 0.3 (0.2-0.6), 0.3 (0.1-0.7), 7.1 (2.9-16.9), 1.9 (0.8-4.6), and 7.8 (1.5-40.0) for those treated with biguanides, thiazolidinediones, sulfonylureas, insulin, and dietary control respectively. Conclusions Diabetes increases HCC risk, and such risk is correlated with long duration of diabetes. Relying on dietary control and treatment with sulfonylureas or insulin conferred the highest magnitude of HCC risk, while biguanides or thiazolidinediones treatment was associated with 70% HCC risk-reduction among diabetics.

The combination of B + E in patients who had advanced HCC showed significant, clinically meaningful antitumor activity. B + E warrant additional evaluation in randomized controlled trials.

Purpose Hepatitis B virus (HBV) and hepatitis C virus (HCV) are considered to be hepatotropic and are a major cause of hepatocellular carcinoma. However, little is known about the role of HBV and HCV infection in other malignancies. This study aimed to determine whether HBV and HCV infection increase the risk for pancreatic cancer development. Patients and Methods At The University of Texas M.D. Anderson Cancer Center, Houston, we recruited 476 patients with pathologically confirmed adenocarcinoma of the pancreas and 879 age-, sex-, and race-matched healthy controls. Blood samples were tested for the presence of HCV antibodies (anti-HCV), HBV surface antigen (HBsAg), antibodies against HBV core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). The positive samples were retested by two confirmatory tests. An unconditional multivariable logistic regression analysis was used to estimate adjusted odds ratios (AORs). Results Anti-HCV was positive in 7 cases (1.5%) and 9 controls (1%). Anti-HBc was positive in 36 cases (7.6%) and 28 controls (3.2%). The estimated AORs and 95% confidence intervals (CIs) were as follows: anti-HCV+, 0.9 (0.3–2.8), anti-HBc+, 2.5 (1.5–4.2), anti-HBc+/anti-HBs+, 2.3 (1.2–4.2), and anti-HBc+/anti-HBs-, 4 (1.4–11.1). Risk modification by past exposure to HBV was observed among diabetics (AOR, 7.1; 95% CI, 1.7–28.7). Conclusion Past exposure to HBV may be associated with pancreatic cancer development. Should such findings be confirmed by other studies, it may offer important insights on the etiology of the pancreatic cancer and may suggest the need to consider prevention of HBV reactivation among HBV-related pancreatic cancer patients during chemotherapy treatment.

Infections with hepatitis B virus (HBV) or hepatitis C virus (HCV) are associated with significant morbidity and mortality among patients with cancer, especially in patients with hematologic malignancies and those who undergo hematopoietic stem-cell transplantation. Reported rates of HBV reactivation in HBV carriers who undergo chemotherapy range from 14-72%. In these patients, mortality rates range from 5-52%. HCV reactivation seems to be less common than HBV reactivation and is usually associated with a good outcome and low mortality. However, once severe hepatitis develops, as a result of viral reactivation, mortality rates seem to be similar among patients infected with HBV or HCV. Liver damage owing to viral reactivation frequently leads to modifications or interruptions of chemotherapy, which can negatively affect patients' clinical outcome. Risk factors for the development of severe HBV or HCV reactivation need to be better defined to permit identification of patients who may benefit from preventive measures, early diagnosis, and therapy. In this article, we review the epidemiology, pathogenesis, risk factors, and clinical and laboratory manifestations associated with reactivation of HBV and HCV during immunosuppressive therapy. We also discuss strategies for the prevention and treatment of viral reactivation, including the management of reactivation with new antiviral agents.

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