Häussinger D, Laubenberger J, vom Dahl S, Ernst T, Bayer S, Langer M, Gerok W, Hennig J
Medizinische und Radiologische Universitätsklinik Freiburg, Germany.
Gastroenterology. 1994 Nov;107(5):1475-80. doi: 10.1016/0016-5085(94)90552-5.
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.
Myo-inositol and glutamine levels in the brain were studied in vivo by 1H-MR spectroscopy in patients with hypo-osmolarity and hepatic encephalopathy.
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.
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.
背景/目的：近期利用质子磁共振（1H-MR）波谱进行的体内研究显示，肝性脑病患者脑内的肌醇水平较低；这一观察结果的发病机制相关性尚不清楚。
通过1H-MR波谱对低渗性肝性脑病患者脑内的肌醇和谷氨酰胺水平进行体内研究。
一名严重血浆低渗（222 mOsm/L）患者脑内的肌醇以及谷氨酰胺/谷氨酸信号几乎无法检测到。血浆渗透压恢复正常后，这两种信号均重新出现，表明肌醇和谷氨酰胺均作为有机渗透溶质从脑内释放。在轻度肝性脑病患者中也发现脑内肌醇信号降低，但同时谷氨酰胺信号增加。无肝性脑病的肝硬化患者肌醇信号接近正常，而获得性免疫缺陷综合征脑病患者的肌醇信号增加。
人脑1H-MR波谱中的肌醇信号主要反映对渗透压敏感的肌醇池。据推测，其在潜在肝性脑病中的消耗表明脑内细胞体积稳态紊乱是早期发病机制事件。这可能部分是由高氨血症诱导的脑内谷氨酰胺蓄积所致。
