Impacts of development of acute-on-chronic liver failure and bacteria infections on pancreatic β-cell function and glucose homeostasis in patients with liver cirrhosis

Abstract

AbstractBackground/PurposeGlucose metabolism disorders (GMDs), including diabetes and impaired glucose tolerance, is a common complication and associated with poor prognosis in patients with liver cirrhosis. The aim of this study was to investigate the impacts of development of acute-on-chronic liver failure (ACLF) and bacteria infections (BIs) on pancreatic β-cell function and glucose homeostasis in patients with acute deterioration of liver cirrhosis.MethodsThree hundred and twenty seven patients with acute deterioration of liver cirrhosis were retrospectively included. Oral glucose tolerance test (OGTT) and OGTT-based β cell function indices were used to evaluate pancreatic β-cell function and disturbance in glucose homeostasis. Univariate and multivariate logistic regression were used to identify independent risk factors associated with GMDs.ResultsDevelopment of ACLF or BIs significantly increased the prevalence of GMDs. ACLF or BIs also significantly increased level of homeostasis model of assessment 2-insulin resistance (HOMA2-IR). ACLF but not BIs significantly impaired the glucose-stimulated insulin secretion as assessed using insulinogenic index (IGI). Patients with GMDs had a significantly lower level of IGI than that in patients without GMDs. Prothrombin activity (OR=0.981, 95% CI: 0.960~0.995), HOMA2-IR (OR=1.749, 95% CI: 1.130~2.707) and IGI (OR=0.963, 95% CI: 0.947~0.978) were the independent risk factors associated with GMDs in patients with acute deterioration of liver cirrhosis.ConclusionsIn patients with liver cirrhosis, development of ACLF impairs glucose-stimulated insulin secretion of pancreatic β-cell, both liver impairment and BIs increase insulin resistance and contribute to aggravation of disturbance in glucose