Prevalence, incidence, and prognosis of hepatobiliary disease in community-based patients with type 2 diabetes: the Fremantle Diabetes Study.

Abstract

Few studies have examined morbidity and mortality associated with hepatobiliary disease in diabetes. Most have used administrative databases and/or have had limited/incomplete data including recognized risk factors for hepatobiliary disease. The objective of the study was to explore the relationship between type 2 diabetes and hepatobiliary disease in well-characterized patients with detailed risk factor data including viral hepatitis status and hemochromatosis genotype. This was a community-based longitudinal observational study. The study was conducted in an urban Australian community. The study included 1294 patients of mean ± SD aged 64.1 ± 11.3 yr and 5156 age-, gender-, and ZIP code-matched nondiabetic controls. Prevalent and incident hepatobiliary disease and hepatobiliary disease-related death were measured. Competing risks proportional hazard models provided independent associates of these end points. During 13,705 patient-years (mean 11.5 yr), 144 patients had an initial hepatobiliary disease-related hospitalization/cancer registration vs. 403 controls during 63,937 person-years of follow-up, an incidence rate ratio of 1.66 (95% confidence interval 1.37-2.02). Incident hepatobiliary disease was associated with a lower glycosylated hemoglobin and higher urinary albumin to creatinine ratio. Nearly half of the patients (49.9%) died during follow-up [crude mortality ratio vs. nondiabetic controls 1.97 (1.16-3.32)], and 21 (3.3%) from hepatobiliary disease including two cases of cirrhosis attributable to nonalcoholic steatohepatitis. Hepatobiliary disease-related death was independently predicted by prior hepatobiliary disease, hepatitis C seropositivity, retinopathy, and peripheral neuropathy; higher educational level and higher fasting serum glucose were protective. Hepatobiliary disease and associated mortality are increased in type 2 diabetes. Multiple factors including fatty infiltration, microangiopathy, and direct glucotoxicity are likely to contribute, but hospitalization and death due to cirrhosis from nonalcoholic steatohepatitis appear uncommon.