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Aim: To review the usefulness of endoscopic biliary stenting for obstructive jaundice caused by hepatocellular carcinoma and identify problems that may need to be addressed., Methods: The study population consisted of 36 patients with obstructive jaundice caused by hepatocellular carcinoma (HCC) who underwent endoscopic biliary stenting (EBS) as the initial drainage procedure at our hospital. The EBS technical success rate and drainage success rate were assessed. Drainage was considered effective when the serum total bilirubin level decreased by 50% or more following the procedure compared to the pre-drainage value. Survival time after the procedure and patient background characteristics were assessed comparatively between the successful drainage group (group A) and the non-successful drainage group (group B). The EBS stent patency duration in the successful drainage group (group A) was also assessed., Results: The technical success rate was 100% for both the initial endoscopic nasobiliary drainage and EBS in all patients. Single stenting was placed in 21 patients and multiple stenting in the remaining 15 patients. The drainage successful rate was 75% and the median interval to successful drainage was 40 d (2-295 d). The median survival time was 150 d in group A and 22 d in group B, with the difference between the two groups being statistically significant (P < 0.0001). There were no statistically significant differences between the two groups with respect to patient background characteristics, background liver condition, or tumor factors; on the other hand, the two groups showed statistically significant differences in patients without a history of hepatectomy (P = 0.009) and those that received multiple stenting (P = 0.036). The median duration of stent patency was 43 d in group A (2-757 d). No early complications related to the EBS technique were encountered. Late complications occurred in 13 patients (36.1%), including stent occlusion in 7, infection in 3, and distal migration in 3., Conclusion: EBS is recommended as the initial drainage procedure for obstructive jaundice caused by HCC, as it appears to contribute to prolongation of survival time.

Increased insulin resistance is frequently associated with chronic liver disease and is a pathophysiological feature of hepatogenous diabetes. Distinctive factors including hepatic parenchymal cell damage, portal-systemic shunting and hepatitis C virus are responsible for the development of hepatogenous insulin resistance/diabetes. Although it remains unclear whether insulin secretion from pancreatic beta cells is impaired as it is in type 2 diabetes, retinopathic and cardiovascular risk is low and major causes of death in cirrhotic patients with diabetes are liver failure, hepatocellular carcinoma and gastrointestinal hemorrhage. Hemoglobin A1c is an inaccurate marker for the assessment and management of hepatogenous diabetes. Moreover, exogenous insulin or sulfonylureas may be harmful because these agents may promote hepatocarcinogenesis. Thus, pathogenesis, cause of death, assessment and therapeutic strategy for hepatogenous insulin resistance/diabetes differ from those for lifestyle-related type 2 diabetes. In this article, we review features of insulin resistance in relationship to chronic liver disease. We also discuss the impact of anti-diabetic agents on interferon treatment and hepatocarcinogenesis.