门冬氨酸鸟氨酸注射液抗肝性脑病的疗效观察

目的观察门冬氨酸鸟氨酸治疗肝性脑病的疗效。方法将60例肝性脑病患者随机分为治疗组30例和对照组30例，治疗组在常规综合治疗的基础上将门冬氨酸鸟氨酸10g～20g加入5％葡萄糖注射液250ml中静脉滴注1次／d，治疗7d。观察治疗前后患者的肝功能、静脉血氨浓度和数字连接试验的改善情况。结果门冬氨酸鸟氨酸治疗肝性脑病临床疗效显著优于对照组，治疗后静脉血氨浓度和数字连接试验的改善均有非常显著性差异（P〈0．05），并无明显毒副作用。结论门冬氨酸鸟氨酸治疗肝性脑病疗效确切，安全性好。     

乳果糖治疗亚临床肝性脑病的疗效观察

在临床上，部分慢性肝病患者虽无肝性脑病的症状和体征，但其神经系统电生理检查和心理(智力)测试结果存在异常，这种现象越来越引起人们的重视，从而提出了亚临床肝性脑病(subclinical hepatic encephalopathy，SHE)的概念。本研究通过测定肝硬化患者的静脉血氨浓度、数字连接试验和脑电诱发电位来观察SHE的临床表现，并评价乳果糖治疗SHE的疗效，以提高临床医师对SHE的诊治水平。     

清开冲剂治疗亚临床肝性脑病20例对比观察

目的:探讨清开冲剂对亚临床肝性脑病的治疗作用。方法:以苏威乳果糖为对照用药,观察清开冲剂治疗肝炎后肝硬变亚临床肝性脑病的疗效。结果:1疗程后治疗组(20例)与对照组(19例)患者临床症状均有所好转,两组比较无显著性差异(P>0.05);治疗组ALT、AST下降明显(P<0.05),而对照组下降不明显(P>0.05);两组患者血氨均有所下降,差异不显著(P>0.05)。数字联接试验时间、划线试验时间、划线试验错误次数两组比较无显著性差异(P>0.05)。结论:清开冲剂对肝硬变亚临床肝性脑病有较好的治疗作用,在智力测验方面疗效与乳果糖相当,在改善肝功能方面优于乳果糖。     

地黄饮子治疗轻微型肝性脑病的临床疗效分析

目的:探讨地黄饮子对轻微型肝性脑病患者的临床疗效。方法:选取2017年2月至2018年2月在北京佑安医院就诊的肝硬化并发轻微肝性脑病患者65例,随机分为两组,其中治疗组33例,对照组32例。在基础治疗一致基础上,对照组患者口服乳果糖;治疗组患者采用乳果糖联合地黄饮子治疗。结果:治疗组患者在治疗前后数字连接试验(NCT)、血氨、总体疗效优于对照组,差异显著(P0.05),两组患者治疗前后肝肾功能无显著性差异(P0.05)。结论:地黄饮子治疗轻微型肝性脑病有一定的临床疗效,安全性较好,具有临床使用和推广价值。     

乳果糖联合高压氧治疗亚临床肝性脑病临床研究

亚临床肝性脑病（SHE）是指某些肝硬化患者临床表现、常规精神和神经功能检查正常．但心理学测验或诱发电位检查异常，作为肝性脑病（HE）的特殊类型，在慢性肝病尤其是肝硬化中有较高的发病率，由于无HE的症状和体征而忽视治疗，从而使部分患者发展成HE，危及生命。我们通过测定肝硬化患者的静脉血氨、丙氨酸转氨酶（ALT）、数字连接试验（NCT）、脑干听觉诱发电位（BAEP）异常率及24周随访观察HE的累积发病率，来评估乳果糖联合高压氧治疗SHE的疗效。     

乳果糖对亚临床肝性脑病肝硬化患者的疗效

在无脑病史的肝硬化患者中,亚临床肝性脑病(SHE)的患病率为30％～84％。乳果糖在有明显脑病患者的治疗中有一定的作用。此研究的目的是评价乳果糖治疗SHE患者的疗效。 病人和方法:此研究包括40例肝硬化患者,男性33例,女性7例。SHE的诊断应作定量的精神定量试验,包括数字连接试验(NCT)图像连接试验(FCT)以及Wechsler成人智力量表中的图片完成试验和方块设计试验。其中     

乳果糖与白醋保留灌肠治疗肝性脑病的临床观察

目的 探讨灌肠液在治疗肝性脑病时对血氨浓度及神志的影响.方法 选择肝性脑病Ⅲ～Ⅳ期的患者,每日晨用67%的乳果糖150ml保留灌肠,每晚用30%的白醋200ml保留灌肠.并与单纯的静脉给药不配合灌肠的对照组比较.结果 观察组治疗后血氨浓度间差异有非常显著性意义（P＜0.01）.观察组24h神志清醒12人,占60%,对照组仅2人清醒,占10%,两组比较差异有非常显著性意义（P＜0.01）.结论 乳果糖与白醋保留灌肠能有效降低血氨浓度,从而有效地治疗肝性脑病.     

小肠细菌过度生长相关性轻微肝性脑病患者的血氨变化

目的 观察肝硬化患者小肠细菌过度生长相关性轻微肝性脑病(MHE)患者的血氨水平.探讨血氨与轻微肝性脑病的关系.方法 对90例肝硬化患者及20例健康志愿者进行血氨、葡萄粮氢呼气试验、数宁连接试验和数字符号试验检测.观察小肠细菌过度生长相关性轻微肝性脑病患者的血氨水平差异.结果 肝硬化组小肠细菌过度生长(36.7%,33/90)明显高于健康对照组(5%,1/20).20名健康志愿者未检出 MHE;90例肝硬化患者轻微肝性脑病37例(41.1%),其中伴小肠细菌过度生长肝硬化患者轻微肝性脑病发生率高于不伴小肠细菌过度生长患者.血氨水平均正常,但肝硬化组血氨水平高于健康对照组;肝硬化小肠细菌过度生长组血氨水平(47.9 μmol/L±7.8 μmol/L)高于无小肠细菌过度生长组(34.2μmol/L±6.8 μoL/L,P<0.05);轻微肝性脑病组血氨水平(46.2μmol/L±5.9μmoL/L)高于无轻微肝性脑病组(33.9μmol/L±7.6μmol/L,P<0.05).应用抗生素抑制小肠细菌过度生长及乳果糖治疗1周后葡萄糖氧呼气试验(GHBT)、血氨水平、数字连接试验(NCT-A、NCT-BC)及数字符号试验(DST)检查结果改善.结论 血氨对伴小肠细菌过度生长的轻微肝性脑病的发生及进展可能有一定的关系.     

乳果糖预防消化道出血后诱发肝性脑病的疗效观察

目的探讨乳果糖预防肝硬化患者上消化道出血后诱发肝性脑病的疗效。方法收集我科因乙肝肝硬化、丙肝肝硬化及其他原因导致的肝硬化出现消化道出血患者42例,随机分为观察组(n=22)和对照组(n=20)。观察组在无活动性出血后在常规治疗基础上加用乳果糖口服,对照组除不用乳果糖外,其他治疗与观察组相同。1周后观察临床症状,数字连接试验(NCT),血氨等变化以判断疗效。结果观察组2例发生肝性脑病,发生率为9.1%;对照组8例发生肝性脑病,发生率为40%(χ2=3.9450,P0.05)。两组治疗前血氨含量、NCT检测结果相似,治疗后对照组血氨含量上升、NCT延长的程度明显大于观察组。结论乳果糖是预防肝硬化患者上消化道出血诱发肝性脑病的有效方法。     

双歧三联活菌治疗亚临床肝性脑病的临床研究

目的探讨双歧三联活菌治疗亚临床肝性脑病(SHE)的疗效。方法经智力测验(数字连接试验)诊断SHE64例,随机分为对照组和治疗组各32例。对照组服复合维生素B,治疗组服双歧三联活菌片,25周为1疗程。治疗前后测定血氨、丙氨酸转氨酶、数字连接试验,统计治疗期间肝性脑病(HE)的发病率。结果治疗组治疗后血氨、ALT、NCT较治疗前显著改善,且明显优于对照组(P0.05或P0.01),治疗组HE发病率显著低于对照组(P0.01)。结论双歧三联活菌维持治疗SHE能够降低血氨,改善智力测验结果,降低HE的发病率。     

乳果糖治疗亚临床肝性脑病的临床研究

目的 前瞻性对比乳果糖长、短程治疗对亚临床肝性脑病(SHE)的效果及其对SHE病程的影响。方法 经智力测验(数字连接试验和数字符号试验之一异常)诊断的SHE 64例随机分入对照组(21例)、短程组(21例)和长程组(22例),后2组分别服乳果糖达8周和24周。治疗前以及治疗后每间隔8周行血氨、智力测验和体感诱发电位(SEP)等检查,共随访24周。结果 每组各有20例完成追踪。与对照组和治疗前相比,长程组血氨和智力测验显著改善(P＜0．05—0．01)且SEP的N50波潜伏期稳定不变,短程组治疗到第8周也有改善(P＜0．05),但停药后又逐渐恶化。对照组的血氨、智力测验和N50波潜伏期逐渐恶化,在16周时后2项与治疗前差异有显著性(P＜0．05—0．01);而长程组血氨持续降低,其肝性脑病(HE)患病率(5％)显著低于短程组(30％)和对照组(40％)(P＜0．05)。结论 乳果糖维持治疗能够降低血氨、改善智力测验结果并可能防止SEP的恶化,最终降低HE的患病率。     

Role of Helicobacter pylori infection in hyperammonemia and subclinical hepatic encephalopathy in cirrhosis of liver.

INTRODUCTION: Gastric Helicobacter pylori infection is believed to be associated with a higher risk of hepatic encephalopathy among patients with cirrhosis of liver. However, the role of this infection in causation of subclinical hepatic encephalopathy has not been studied in detail. METHODS: Patients with cirrhosis of liver but no hepatic encephalopathy underwent venous blood ammonia measurement, psychometric tests (number connection tests [NCT] and figure connection tests [FCT]), and gastric biopsies for presence of H. pylori infection. The results of blood ammonia and psychometric tests in the H. pylori-positive and -negative study subjects were compared. RESULTS: Of 58 patients with liver cirrhosis studied, 31 had evidence of gastric H. pylori infection. Venous blood ammonia levels were comparable in patients with (median 29 mmol/L; range 18-47) and without (34 [15-48] mmol/L; p=ns) H. pylori infection. The time taken to complete NCT trail A (median 37 s [range 25-69] versus 36.5 [26-62]), NCT trail B (64 s [48-91] versus 63.5 [42-88]), FCT trail A (59 s [31-115] versus 58 [38-590]) and FCT trail B (76 s [55-187] versus 82 [36-125]) were similar in those with and those without H. pylori infection. For each of the four tests, the proportion of subjects with abnormal test results was similar among H. pylori-positive and -negative subjects. CONCLUSION: Presence of H. pylori infection among patients with cirrhosis of liver but no overt hepatic encephalopathy is not associated with increase in blood ammonia concentration or deterioration in psychomotor function.     

The diagnosis and prevalence of subclinical hepatic encephalopathy in apparently healthy, ambulant, non-shunted patients with cirrhosis

Thirty-seven patients, all with histologic evidence of cirrhosis and with a normal neurological examination and normal mental status were evaluated by psychometric testing for subclinical hepatic encephalopathy. They were all regarded as having well compensated cirrhosis, not requiring any treatment or dietary restrictions and they were working, and many of them driving. A group of 19 patients with a history of alcoholism, or medical disorders, but without clinical or biochemical evidence of cirrhosis, served as controls. They were matched by age, sex, education, and alcohol consumption. Investigations performed were an EEG, fasting arterial ammonia, liver biochemical tests and a series of verbal and performance psychometric tests. The EEG was abnormal in 3 (8.3%) of patients, the ammonia elevated in 17 (45.9%) of patients and 26 patients (70.3%) failed 2 or more psychometric tests, as compared to 2 (10.5%) of the control group. It is concluded that 2 out of 3 patients with stable, well compensated cirrhosis were suffering from subclinical hepatic encephalopathy and that impairment of performance rather than verbal skills occurred. The digital symbol test, trail test (number connection test) and block design tests readily identified the patients with subclinical hepatic encephalopathy. The implication of these observations in patients with cirrhosis, especially those working in mechanical or skilled occupations, needs consideration.     

幽门螺杆菌感染与肝性脑病的相关性

目的探讨肝硬化患者幽门螺杆菌（H．pylori）感染和肝性脑病（HE）发病的相关性。方法收集110例符合诊断标准的肝硬化患者,详细记录H．pylori检测结果、血氨水平、数字连接试验（NCT）结果、HE临床症状。其中71例H．pylori阳性者随机分为观察组和对照组,观察组予泮托拉唑钠肠溶胶囊＋克拉霉素缓释片＋奥硝唑胶囊进行根除治疗,1周后复查血氨。结果H．pylori阳性肝硬化患者的血氨水平及HE的发生率明显高于Hpylori阴性的肝硬化患者,两者差异有统计学意义（P〈0．05）;tt．pylori阳性者中观察组行H．pylori根除治疗,血氨下降明显优于对照组（P〈0．05）。结论H．pylori感染可使肝硬化患者血氨水平升高,根除H．pylori治疗对降低肝性脑病的发生有重要的临床意义。     

Subclinical hepatic encephalopathy predicts the development of overt hepatic encephalopathy

OBJECTIVES: In patients with compensated liver cirrhosis the clinical repercussions of detecting subclinical hepatic encephalopathy (SHE) are unclear. We present a long-term follow-up study in cirrhotic patients to examine the relationship between SHE and subsequent episodes of overt hepatic encephalopathy. METHODS: A total of 63 cirrhotic patients were studied by Number Connection Test and auditory evoked potentials. We determined glutamine, ammonia, zinc, glutamate, urea, and ratio of branched chain amino acids to aromatic amino acids, and Child-Pugh classification. RESULTS: Of 63 patients, 34 (53%) exhibited SHE. Nineteen out of 63 (30%) developed overt hepatic encephalopathy during follow-up. Hepatic encephalopathy in follow-up was related to alcoholic etiology, ammonia, glutamine, zinc, ratio of branched chain amino acids to aromatic amino acids, liver function, presence of esophageal varices, and detection of SHE (84% of patients who exhibited hepatic encephalopathy in follow-up showed SHE). In Cox-regression, glutamine levels, SHE, esophageal varices, and Child-Pugh class were the independent variables related to hepatic encephalopathy in follow-up. CONCLUSIONS: SHE (defined on the basis of number connection test or auditory evoked potentials alteration) could predict a subsequent episode of overt hepatic encephalopathy. Lower glutamine levels, presence of esophageal varices, and liver dysfunction were also related to the development of overt hepatic encephalopathy.     

The diagnostics and therapy of hepatic encephalopathy. Recommendations of of the working group on portal hypertension in the Czech Hepatology Society and the J. E. Purkinje Czech Medical Society

Hepatic encephalopathy (HE) is a set of reversible neuropsychic features which occur in connection with hepatic cirrhosis or acute hepatic failure. We distinguish manifest HE (with clinical symptoms) and minimal FE (normal clinical finding, abnormal psychometric or neurophysiologic exam). The diagnosis is clinical or laboratory one. From the auxiliary examinations in common practice the number connection test is sufficient. Therapy: Presence of hepatic encephalopathy should lead to the consideration of the possibility to solve basic disease by hepatic transplantation. Conservative therapy lies in 1. Basic disease elimination, 2. Measures lowering the ammonia level in blood--optimalization of protein intake, administration of indigestible disaccharides (lactulose, lactitol) and fill sterilisation by antibiotics (Rifaxin, Metronidazol), ornitine-aspartate administration, 3. Influencing the changes in amino acid metabolism (administration of branched chain amino acids--BCAA). Prognosis depends on the advancement of the disease, after hepatic transplantation the clinical symptoms of HE are mostly fully reversible.     

Helicobacter pylori, hyperammonemia and subclinical portosystemic encephalopathy: effects of eradication

BACKGROUND/AIMS: An involvement of Helicobacter pylori in the development of hepatic encephalopathy in cirrhotic patients has been proposed, but data confirming such an association are lacking. This prospective study aimed to assess whether ammonia levels and indicators of subclinical portosystemic encephalopathy were influenced by H. pylori status in a series of 62 cirrhotic patients. The effects of H. pylori eradication on such parameters were also investigated. METHODS: Fasting blood ammonia levels, mental state, number connection test, flapping tremor, and EEG tracings were recorded at baseline, and in H. pylori-positive patients (as diagnosed by rapid urease test and 14C-urea breath test) these parameters were reassessed 2 months following eradication therapy. RESULTS: In this series of non-advanced cirrhotic patients, the prevalence of H. pylori infection was 52%. No significant differences were observed between H. pylori+ and H. pylori- cases with respect to fasting venous blood ammonia concentration (47+/-24 vs. 43+/-22 micromol/l) or to the remaining parameters assessing portosystemic encephalopathy. In addition, H. pylori eradication failed to induce any significant variation in either fasting blood ammonia levels (from 45+/-23 to 48+/-26 micromol/l) or neurologic disturbances. CONCLUSION: These results indicate that H. pylori infection is not a major contributing factor to either fasting blood ammonia levels or parameters assessing subclinical portosystemic encephalopathy in patients with non-advanced liver cirrhosis.     

Sodium benzoate in the treatment of acute hepatic encephalopathy: a double-blind randomized trial.

A prospective randomized double-blind study was conducted to evaluate the efficacy of sodium benzoate in the treatment of acute portal-systemic encephalopathy. Seventy-four consecutive patients with cirrhosis or surgical portasystemic anastomosis and hepatic encephalopathy of less than 7 days duration were randomized to receive lactulose (dose adjusted for 2 or 3 semiformed stools/day) or sodium benzoate (5 gm twice daily). Assessment of response included mental status, asterixis, arterial ammonia level, electroencephalogram and number-connection test. Each was given a score between 0 and 4+. A portal-systemic encephalopathy index was calculated with these scores. Visual, auditory and somatosensory evoked potentials and a battery of psychometric tests for intelligence and memory were also performed to assess improvement. Thirty-eight patients received sodium benzoate; 36 took lactulose. Thirty patients (80%) receiving sodium benzoate and 29 (81%) receiving lactulose recovered; the remaining patients died. Improvement in portal-systemic encephalopathy parameters occurred in both treatment groups and was similar (p greater than 0.1). Electroencephalogram and evoked potentials were not as helpful as mental status in assessing of recovery. Psychometric test scores remained abnormal after recovery of mental status (21 to 42 days) and were probably too sensitive for monitoring of these patients. The incidence of side effects was similar in the two treatment groups. The cost of lactulose for one course of therapy was 30 times that of sodium benzoate. We conclude that sodium benzoate is a safe and effective alternative to lactulose in the treatment of acute portasystemic encephalopathy.     

A randomized controlled trial of acarbose in hepatic encephalopathy.

BACKGROUND & AIMS: Hepatic encephalopathy in cirrhosis is contributed to by toxic products deriving from the proteolytic bacterial flora-related degradation of dietary nitrogen substances. Acarbose is a novel hypoglycemic agent acting through the inhibition of glucose absorption in the gut and the promotion of intestinal saccharolytic bacterial flora at the expense of proteolytic flora. We assessed whether acarbose exerts a beneficial effect on hepatic encephalopathy and on postprandial hyperglycemia in cirrhotic patients with low-grade hepatic encephalopathy and type 2 diabetes mellitus. METHODS: One hundred seven cirrhotic patients with grade 1-2 hepatic encephalopathy and type 2 diabetes mellitus were randomized to acarbose 100 mg 3 times daily or placebo for 8 weeks; after a 2-week washout period, treatments were switched, and patients were followed for 8 more weeks. Ammonia blood levels, Reitan's number connection test, intellectual function, fasting and postprandial glucose levels, glycated hemoglobin values, and C peptide values were determined 2 weeks before and 4, 8, 11, 14, and 18 weeks after treatment. RESULTS: (1) Acarbose significantly decreased ammonia blood levels and improved Reitan's test score and intellectual function score compared with placebo (P < .01). (2) Acarbose caused a 33% decrease in fasting glucose level and an approximately 50% decrease in postprandial glucose level compared with placebo (P < .01). (3) Acarbose significantly lowered glycated hemoglobin values and postprandial C peptide compared with baseline values, whereas placebo did not. (4) No change in biochemical parameters of liver function was observed after acarbose treatment. CONCLUSIONS: Acarbose is a safe and effective drug in cirrhotic patients with low-grade hepatic encephalopathy and type 2 diabetes mellitus.     

Propranolol does not alter cerebral blood flow and functions in cirrhotic patients without previous hepatic encephalopathy

Since it has been suggested that propranolol could lead to hepatic encephalopathy, we undertook a study to assess the effects of propranolol on cerebral blood flow and cerebral functions. Sixteen patients with alcoholic cirrhosis and large esophageal varices and without major hepatic dysfunction (Child-Pugh score less than 14) or previous hepatic encephalopathy were randomized to receive either propranolol or placebo. The following measurements were performed before and 15 min after single intravenous administration of 15 mg propranolol or placebo and again 1 week after chronic oral administration of propranolol 160 mg per day or placebo: cerebral blood flow by the xenon-133 inhalation technique, quantitative electroencephalogram, psychometric test (number connection test), arterial ammonia, pH and pCO2, resting and exercise heart rates (after single administration, electroencephalogram, number connection test and biochemical measurements were not performed). Cerebral blood flow was not significantly modified by treatment (propranolol group: 80 +/- 23 vs. 76 +/- 11 and 83 +/- 9; placebo group: 73 +/- 10 vs. 75 +/- 11 and 81 +/- 18 ml per 100 gm per min, respectively, before and after single and repeated administration). Likewise, neither of the two treatments significantly altered number connection test, quantitative electroencephalogram index, arterial ammonia, pH and pCO2. We conclude that, in this population of cirrhotic patients, propranolol did not alter cerebral blood flow or neuropsychological functions. As a consequence, hemodynamic alterations cannot be considered as causes of possible cerebral side effects of propranolol in cirrhotic patients without severe hepatic dysfunction and previous hepatic encephalopathy.