Background: Hepatic encephalopathy (HE) is considered to be mainly due to increased ammonia metabolism of the brain. If this hypothesis is true, cerebral glucose utilisation, which is considered to represent brain function, should be closely related to cerebral ammonia metabolism. The aim of the present study was to analyse if cerebral ammonia and glucose metabolism in cirrhotic patients with early grades of HE are as closely related as could be expected from current hypotheses on HE.
Methods: 13N-ammonia- and 18F-fluorodesoxyglucose (FDG) - PET, magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) were performed in 21 cirrhotic patients with grade 0 -1 HE. Quantitative values of cerebral ammonia uptake and retention rate and glucose utilisation were derived for several regions of interest and were correlated to the MRS data of the basal ganglia, the white matter and the frontal cortex.
Results: A significant correlation between plasma ammonia levels and cerebral ammonia metabolism, respectively, and MRS alterations could be shown only for the white matter. In contrast, the MRS alterations in all three regions studied were significantly correlated with the glucose utilisation of several brain regions. Cerebral ammonia and glucose metabolism were not correlated.
Conclusion: Increase of cerebral ammonia metabolism is an important but not the exclusive causal factor for the development of hepatic encephalopathy.
- early hepatic encephalopathy
- liver cirrhosis
- magnetic resonance spectroscopy
- positron emission tomography
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