Oppong K N, Al-Mardini H, Thick M, Record C O
Freeman Hospital Newcastle upon Tyne, Department of Medicine, University of Newcastle upon Tyne, UK.
Hepatology. 1997 Oct;26(4):870-6. doi: 10.1002/hep.510260411.
Latent or sub-clinical hepatic encephalopathy is a recognized complication of cirrhosis and is thought to represent one end of the spectrum of neuropsychiatric impairment, which occurrs as a result of portal-systemic shunting. We studied the psychometric, analyzed electroencephalography (EEG), and venous blood ammonia responses to an oral glutamine challenge in 17 patients with cirrhosis and in 4 normal controls. The cirrhotics were attending for liver transplant assessment and had no clinical evidence of hepatic encephalopathy. The oral glutamine challenge was repeated following liver transplantation. Five of sixteen patients (31%) showed impaired performance on at least one of the baseline psychometric tests. There was a correlation between fasting venous ammonia and choice reaction time (r = .7, P < .01). Following glutamine challenge there was a significant increase in blood ammonia from a mean fasting value ranging between 58 micromol/L to 120 micromol/L (P < .01), between significant prolongation of reaction times of 387 ms to 428 ms (P < .01), and an increase in mean EEG amplitude between 68.5 microV to 78.6 microV (P < .001). Four normal controls who were challenged with glutamine and 6 cirrhotic patients who were challenged with water showed no change in any of these parameters. Following orthotopic liver transplantation (OLT) the eight patients studied had normal baseline psychomotor performance with significant improvements in digit symbol, digit span, information processing, number connection tests (P < .05), and reaction time (P < .005). Posttransplantation, there were no significant changes in blood ammonia, analyzed EEG, or choice reaction time in response to oral glutamine challenge (six patients). We conclude that short lived changes in blood ammonia (in cirrhotics) can cause significant impairment of sensitive tests of brain function and that psychometric performance is improved following OLT.
潜在性或亚临床型肝性脑病是肝硬化一种公认的并发症，被认为是神经精神功能损害谱系的一端，其发生是由于门体分流所致。我们研究了17例肝硬化患者和4例正常对照者在口服谷氨酰胺激发试验后的心理测量、脑电图（EEG）分析及静脉血氨反应。这些肝硬化患者正在接受肝移植评估，且无肝性脑病的临床证据。肝移植后重复进行口服谷氨酰胺激发试验。16例患者中有5例（31%）在至少一项基线心理测量测试中表现受损。空腹静脉血氨与选择反应时间之间存在相关性（r = 0.7，P < 0.01）。谷氨酰胺激发试验后，血氨从平均空腹值58微摩尔/升至120微摩尔/升显著升高（P < 0.01），反应时间显著延长387毫秒至428毫秒（P < 0.01），平均EEG波幅从68.5微伏增加至78.6微伏（P < 0.001）。4例接受谷氨酰胺激发试验的正常对照者和6例接受水激发试验的肝硬化患者在这些参数上均无变化。原位肝移植（OLT）后，所研究的8例患者基线精神运动表现正常，数字符号、数字广度、信息处理、数字连接测试（P < 0.05）及反应时间（P < 0.005）均有显著改善。移植后，口服谷氨酰胺激发试验（6例患者）后血氨水平、EEG分析或选择反应时间均无显著变化。我们得出结论，血氨的短期变化（在肝硬化患者中）可导致脑功能敏感测试的显著损害，且OLT后心理测量表现有所改善。
