Abstract：
BACKGROUND/AIMS:Recent in vivo studies using proton magnetic resonance (1H-MR) spectroscopy showed low levels of myo-inositol in the brain in hepatic encephalopathy; the pathogenetic relevance of this observation is unclear. METHODS:Myo-inositol and glutamine levels in the brain were studied in vivo by 1H-MR spectroscopy in patients with hypo-osmolarity and hepatic encephalopathy. RESULTS:A patient with severe plasma hypo-osmolarity (222 mOsm/L) had almost undetectable signals for myo-inositol and glutamine/glutamate in the brain. Both signals reappeared after normalization of plasma osmolarity, suggesting that both myo-inositol and glutamine were released as organic osmolytes from the brain. A decreased cerebral myo-inositol signal is also found in low-grade hepatic encephalopathy but is accompanied by an increased glutamine signal. Cirrhotics without hepatic encephalopathy have near-normal inositol signals, and patients with acquired immunodeficiency syndrome encephalopathy have increased inositol signals. CONCLUSIONS:The 1H-MR spectroscopic myo-inositol signal in the human brain predominantly reflects an osmosensitive inositol pool. It is hypothesized that its depletion in latent hepatic encephalopathy points to a disturbance of cell volume homeostasis in the brain as an early pathogenetic event. This may partly be caused by a hyperammonemia-induced glutamine accumulation in the brain.
journal_name
Gastroenterologyjournal_title
Gastroenterologyauthors
Häussinger D,Laubenberger J,vom Dahl S,Ernst T,Bayer S,Langer M,Gerok W,Hennig Jdoi
10.1016/0016-5085(94)90552-5subject
Has Abstractpub_date
1994-11-01 00:00:00pages
1475-80issue
5eissn
0016-5085issn
1528-0012pii
S0016508594003410journal_volume
107pub_type
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