Abstract
Brain edema and increased intracranial pressure, well recognised major complications of fulminant hepatic failure,1 have recently been documented in patients with end-stage cirrhosis.2 Neuroradiological evidence of cerebral edema in patients with chronic liver disease is associated with a poor prognosis. Medical treatments for brain edema in patients with cirrhosis have limited efficacy and, in general, liver transplantation is the only intervention which may prevent a fatal outcome.2 During the last 10 years several in vivo studies using magnetic resonance spectroscopy (MRS) have contributed to progress in understanding the neurochemical mechanisms responsible for hepatic encephalopathy (HE) and brain edema in cirrhotic patients.3–11 Proton (1H-) and carbon (13C-) MRS studies of the brain of cirrhotic patients with overt and minimal HE have typically shown an increase in glutamine,3,5–8,12 a decrease in glutamate,6,8–10 and a decrease in the cerebral osmolyte myoinositol.4–7 An increase in brain glutamine, the result of ammonia detoxification in astrocytes, has been implicated as the key metabolic change determining cell swelling and increased brain water in patients with HE.13,14 Studies on rats have shown that inhibition of glutamine synthesis with methionine-sulfoximine prevents the development of ammonia-induced brain edema,15 decreases ammonia-induced astrocyte swelling,16 and reduces brain edema after portacaval anastomosis and ammonia infusion.17 The impaired cell volume homeostasis and brain edema in patients with HE may be the result of intracellular accumulation of osmotically active glutamine associated with a progressive depletion of myo-inositol and other osmolytes.
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Lodi, R. et al. (2003). Brain diffusion weighted MRI in cirrhosis. In: Jones, E.A., Meijer, A.J., Chamuleau, R.A.F.M. (eds) Encephalopathy and Nitrogen Metabolism in Liver Failure. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0159-5_26
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DOI: https://doi.org/10.1007/978-94-010-0159-5_26
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