PROTON MAGNETIC-RESONANCE SPECTROSCOPY STUDIES ON HUMAN BRAIN MYO-INOSITOL IN HYPO-OSMOLARITY AND HEPATIC-ENCEPHALOPATHY

Citation
D. Haussinger et al., PROTON MAGNETIC-RESONANCE SPECTROSCOPY STUDIES ON HUMAN BRAIN MYO-INOSITOL IN HYPO-OSMOLARITY AND HEPATIC-ENCEPHALOPATHY, Gastroenterology, 107(5), 1994, pp. 1475-1480
Citations number
38
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
107
Issue
5
Year of publication
1994
Pages
1475 - 1480
Database
ISI
SICI code
0016-5085(1994)107:5<1475:PMSSOH>2.0.ZU;2-6
Abstract
Background/Aims: Recent in vivo studies using proton magnetic resonanc e (H-1-MR) spectroscopy showed low levels of myo-inositol in the brain in hepatic encephalopathy; the pathogenetic relevance of this observa tion is unclear. Methods: Myo-inositol and glutamine levels in the bra in were studied in vivo by H-1-MR spectroscopy in patients with hypo-o smolarity and hepatic encephalopathy. Results: A patient with severe p lasma hypoosmolarity (222 mOsm/L) had almost undetectable signals for myo-inositol and glutamine/glutamate in the brain. Both signals reappe ared after normalization of plasma osmolarity, suggesting that both my o-inositol and glutamine were released as organic osmolytes from the b rain. A decreased cerebral myo-inositol signal is also found in low-gr ade hepatic encephalopathy but is accompanied by an increased glutamin e signal. Cirrhotics without hepatic encephalopathy have near-normal i nositol signals, and patients with acquired immunodeficiency syndrome encephalopathy have increased inositol signals. Conclusions: The H-1-M R spectroscopic myo-inositol signal in the human brain predominantly r eflects an osmosensitive inositol pool. It is hypothesized that its de pletion in latent hepatic encephalopathy points to a disturbance of ce ll volume homeostasis in the brain as an early pathogenetic event. Thi s may partly be caused by a hyperammonemia-induced glutamine accumulat ion in the brain.