Persistent arterial hyperammonemia increases the concentration of glutamine and alanine in the brain and correlates with intracranial pressure in patients with fulminant hepatic failure

In this prospective study of patients with fulminant hepatic failure (FHF), we tested the hypothesis that arterial hyperammonemia results in cerebral accumulation of the osmotic active amino acids glutamine and alanine, processes that were expected to correlate with intracranial pressure (ICP). By u...

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Bibliographic Details
Published in:Journal of cerebral blood flow and metabolism 2006-01, Vol.26 (1), p.21-27
Main Authors: Tofteng, Flemming, Hauerberg, John, Hansen, Bent A, Pedersen, Carsten B, Jørgensen, Linda, Larsen, Fin S
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Alanine - metabolism
Biological and medical sciences
Brain - metabolism
Brain - physiopathology
Endocrinopathies
Female
Glutamine - metabolism
Humans
Hyperammonemia - etiology
Hyperammonemia - physiopathology
Intracranial Hypertension - etiology
Intracranial Hypertension - metabolism
Intracranial Hypertension - physiopathology
Intracranial Pressure
Investigative techniques, diagnostic techniques (general aspects)
Liver Failure, Acute - complications
Liver Failure, Acute - physiopathology
Liver Function Tests
Male
Medical sciences
Microdialysis
Middle Aged
Nervous system
Neurology
Non tumoral diseases. Target tissue resistance. Benign neoplasms
Prospective Studies
Thyroid. Thyroid axis (diseases)
Ultrasonic investigative techniques
Vascular diseases and vascular malformations of the nervous system
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Summary:In this prospective study of patients with fulminant hepatic failure (FHF), we tested the hypothesis that arterial hyperammonemia results in cerebral accumulation of the osmotic active amino acids glutamine and alanine, processes that were expected to correlate with intracranial pressure (ICP). By using in vivo brain microdialysis technique together with ICP monitoring in 17 FHF patients (10 females/7 males; median age 49 (range 18 to 66) years), we found that arterial ammonia concentration correlated to brain content of glutamine (r=0.47; P > 0.05) but not to alanine. A persisting high arterial ammonia concentration (above 200 μmol/L) characterized patients who developed high ICP (n=8) while patients who did not experience surges of increased ICP (n=9) had a decline in the ammonia level (P > 0.05). Moreover, brain glutamine and alanine concentrations were higher at baseline and increased further in patients who developed intracranial hypertension compared with patients who experienced no surges of high ICP. Brain glutamine concentration increased 32% from baseline to 6536 (697 to 9712) μmol/L (P > 0.05), and alanine 44% from baseline to 104 (81 to 381) μmol/L (P > 0.05). Brain concentration of glutamine (r=0.59, P > 0.05), but not alanine, correlated to ICP. Also arterial ammonia concentration correlated to ICP (r=0.73, P > 0.01). To conclude, this study shows that persistence of arterial hyperammonemia is associated with profound changes in the cerebral concentration of glutamine and alanine. The elevation of brain glutamine concentration correlated to ICP in patients with FHF.
ISSN:0271-678X
1559-7016
DOI:10.1038/sj.jcbfm.9600168