Induced hyperammonemia may compromise the ability to generate restful sleep in patients with cirrhosis
Induced hyperammonemia may compromise the ability to generate restful sleep in patients with cirrhosis
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DOI：
10.1002/hep.24741
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发表时间：
2012-03-01
期刊：
影响因子：
13.5
通讯作者：
Montagnese, Sara
中科院分区：
文献类型：
--
作者：
Bersagliere, Alessia;Raduazzo, Iolanda D.;Montagnese, Sara
在肝硬化患者中，高氨血症和肝性脑病在胃肠道出血后很常见，可通过氨基酸激发（AAC）或给药模拟血红蛋白组成的氨基酸混合物来模拟。本研究的目的是探讨临床、心理测量和清醒/睡眠脑电图（EEG）与诱导高氨血症的相关性。10名肝硬化患者和10名匹配的健康志愿者进行了：(1)8天的睡眠质量/时间监测；(2) AAC基线/术后神经精神评估；(3) AAC后8小时每小时氨/主观嗜睡评价；(4)基线/ AAC后的睡眠EEG记录（午睡时间：17:00-19:00）。神经精神病学表现根据年龄/教育调整后的意大利标准进行评分。睡眠阶段以20秒为周期进行视觉评分；计算连续20秒时段的功率密度谱，并确定最小共同长度非快速眼动（non-REM）睡眠巩固发作的平均谱。AAC导致：(i)患者和健康志愿者的氨浓度/主观嗜睡增加；（ii）两名（20%）患者的神经精神表现恶化（醒脑电图减慢），而没有健康志愿者；（iii）健康志愿者的非快速眼动睡眠时间增加[49.3（26.6）分钟对30.4（15.6）分钟]；P = 0.08]；（iv）健康志愿者睡眠脑电图β波功率（快速活动）下降；(v)患者睡眠脑电图δ波功率下降。结论：AAC导致肝硬化患者白天主观嗜睡显著增加，随后睡眠发作的脑电图结构发生变化，表明恢复性睡眠能力降低。(肝脏病学2012)
In patients with cirrhosis, hyperammonemia and hepatic encephalopathy are common after gastrointestinal bleeding and can be simulated by an amino acid challenge (AAC), or the administration of a mixture of amino acids mimicking the composition of hemoglobin. The aim of this study was to investigate the clinical, psychometric, and wake-/sleep-electroencephalogram (EEG) correlates of induced hyperammonemia. Ten patients with cirrhosis and 10 matched healthy volunteers underwent: (1) 8-day sleep quality/timing monitoring; (2) neuropsychiatric assessment at baseline/after AAC; (3) hourly ammonia/subjective sleepiness assessment for 8 hours after AAC; (4) sleep EEG recordings (nap opportunity: 17:00-19:00) at baseline/after AAC. Neuropsychiatric performance was scored according to age-/education-adjusted Italian norms. Sleep stages were scored visually for 20-second epochs; power density spectra were calculated for consecutive 20-second epochs and average spectra determined for consolidated episodes of non-rapid eye movement (non-REM) sleep of minimal common length. The AAC resulted in: (i) an increase in ammonia concentrations/subjective sleepiness in both patients and healthy volunteers; (ii) a worsening of neuropsychiatric performance (wake EEG slowing) in two (20%) patients and none of the healthy volunteers; (iii) an increase in the length of non-REM sleep in healthy volunteers [49.3 (26.6) versus 30.4 (15.6) min; P = 0.08]; (iv) a decrease in the sleep EEG beta power (fast activity) in the healthy volunteers; (v) a decrease in the sleep EEG delta power in patients. Conclusion: AAC led to a significant increase in daytime subjective sleepiness and changes in the EEG architecture of a subsequent sleep episode in patients with cirrhosis, pointing to a reduced ability to produce restorative sleep. (HEPATOLOGY 2012)