Impaired brain glucose metabolism in cirrhosis without overt hepatic encephalopathy: a retrospective 18F-FDG PET/CT study.

There are subclinical neurologic deficits in cirrhotic patients without overt hepatic encephalopathy. We aimed to use F-fluorodeoxyglucose PET/computed tomography to explore the impaired brain glucose metabolism of subclinical hepatic encephalopathy in cirrhosis.Thirty-seven patients with hepatitis B virus-related cirrhosis without overt hepatic encephalopathy and 49 controls were enrolled in the study. The patients' Model for End-Stage Liver Disease scores were calculated. All participants underwent resting state F-fluorodeoxyglucose PET/computed tomography. Between-group comparisons of brain PET/computed tomography data were conducted with two-sample t-tests and multivariate tests with Statistical Parametric Mapping 8 software.Most of the patients (30/37) had a Model for End-Stage Liver Disease score of less than 20. The patients and controls did not significantly differ in baseline characteristics, such as sex, age, plasma glucose level, smoking history or BMI, but they did significantly differ in blood uric acid level and serum levels of bilirubin, albumin, total protein, alkaline phosphatase, alanine aminotransferase and aspartate aminotransferase (P < 0.0001). Relative to brain glucose metabolism in the controls, that in the patients involved both hyper- and hypometabolic regions (P < 0.001). The relative hypometabolic regions included the parietal, occipital and limbic lobes, and the hypermetabolic regions included the hippocampus, parahippocampal gyri, right basal ganglia and circumventricular organs.Patients with cirrhosis have characteristic patterns of brain glycometabolic impairment. F-fluorodeoxyglucose PET/computed tomography may serve as a preclinical biomarker for brain damage in cirrhosis.