胃内pH值对肝硬化伴幽门螺杆菌感染患者血氨的影响

目的研究胃内pH值对肝硬化伴幽门螺杆菌(Hp)感染患者血氨的影响.方法对37例Hp阳性的肝硬化患者及40例Hp阴性的肝硬化患者,测定基础血氨后,静脉注奥美拉唑针40 mg,同时动态监测胃内pH值的变化,待胃内pH＞6 且持续1 h后,复测血氨.结果Hp阴性与阳性肝硬化患者的基础血氨水平差异无显著性(P＞0.05).胃内pH升高后,发现Hp阴性的肝硬化患者及Hp阳性的肝硬化Child-Pugh A级患者,血氨水平与实验前差异无显著性(P＞0.05).Hp阳性的肝硬化Child-Pugh B、Child-Pugh C级患者血氨水平较前明显升高,分别由 26.33±6.49 μmol/L、35.30±10.25 μmol/L升高至35.80±6.25 μmol/L、52.20±17.01 μmol/L,差异有非常显著性意义(P＜0.01).结论肝功能状况和胃内pH值是影响Hp感染肝硬化患者血氨水平的两个重要因素.     

肝硬化患者幽门螺杆菌感染对血氨的影响

目的探讨幽门螺杆菌(HP)对肝硬化患者高血氨的作用以及根除治疗对血氨的影响。方法100例肝硬化高血氨患者,分为HP阳性组58例,阴性组42例。两组都给予口服乳果糖15mg,3次/日等一般治疗一周,治疗前后分别测空腹静脉血氨。随后将HP阳性组随机分两组,A组30例,以奥美拉唑20mg,2次/日,阿莫西林1.0,2次/日,替硝唑1.0,2次/日,疗程一周;B组28例,奥美拉唑20mg,2次/日×一周,治疗结束及一个月后测空腹静脉血氨(血氨正常值为<75μmol/L)。结果100例高血氨患者中HP阳性58例(58%),肝硬化HP阳性组血氨浓度103.4±9.1μmol/L,高于HP阴性组血氨浓度80.6±16.9μmol/L,P<0.05。经一般治疗后HP阳性组血氨浓度为99.8±18.6μmol/L,与治疗前比较P>0.05,而HP阴性组血氨浓度为41.5±13.7μmol/L,与治疗前比较P<0.01。根除HP治疗后血氨55.6±18.9μmol/L,明显下降(P<0.01),而用洛赛克治疗后血氨轻度升高,但无统计学意义。结论HP感染可使肝功能异常的肝硬化患者血氨升高,根除HP治疗能有效降低血氨。故对肝硬化失代偿期或疑有早期肝性脑病者,应明确是否合并HP感染并及时根除治疗。     

幽门螺杆菌感染对肝硬化患者血氨浓度的影响

探讨肝硬化患者幽门螺杆菌(Hp)感染与血氨的关系,及根除性治疗Hp对血氨的影响。84例肝硬化高血氨患者,分为Hp阳性组51例,阴性组33例。两组都给予支链氨基酸、乳果糖、基础护肝治疗两周,治疗前后分别测空腹静脉血氨。随后将Hp阳性组随机分两组,A组26例,应用三联疗法治疗一周;B组25例,奥美拉唑治疗一周,治疗结束一个月后复查血氨。发现阳性组的血氨与阴性组相比有显著差异(P＜0．01)。阳性组不同肝功能分级组血氨浓度之间有显著差异(P＜0．01);阴性组则否。Hp阴性组治疗前后血氨浓度变化差异有显著性(P＜0．01),阳性组则无显著差异。根除Hp治疗后血氨明显下降(P＜0．01),而用洛赛克治疗后血氨轻度升高,但无统计学意义。说明Hp感染与肝硬化患者血氨升高有密切相关性,根除Hp的治疗能有效降低血氨。     

根除幽门螺杆菌对肝硬化患者血氨和脑电图变化的临床观察

目的 探讨肝硬化患者的幽门螺杆菌(Hp)感染情况并观察根除Hp后肝硬化患者血氨和脑电图的变化.方法 确诊的肝硬化患者52例,经胃镜或14C尿素呼气试验明确Hp感染情况,对Hp阳性者进行Hp根除治疗(一周标准三联疗法),方案为奥美拉唑40 mg/d,克拉霉素1.0 g/d,阿莫西林2.0 g/d,停药4周后复查12C尿素呼气试验,转阴性者判断为Hp根除,记录根除治疗前后血氨和脑电图情况.结果 Hp阳性者血氨水平83.04±20.81 mmol/L及脑电图异常发生率为86.1%,均明显高于Hp阴性者(P＜0.01＜);根除Hp后血氨水平49.10±9.80 mmol/L及脑电图异常发生率3.1%,均明显下降(P＜0.01).结论 Hp感染是引起肝硬化患者高血氨及脑电图异常的重要原因之一.根除Hp有助于治疗和预防肝性脑病.     

幽门螺杆菌感染对鹿城区高氨血症和肝性脑病发病的影响分析

目的探讨幽门螺杆菌(Hp)对鹿城区高氨血症和肝性脑病发病的影响。方法回顾性分析我院2013年6月~2015年6月60例住院肝硬化患者临床资料,并检测患者Hp和血氨水平及肝性脑病症状、数字连接试验结果等。Hp阳性者采用Hp三联根治疗法治疗1周,并于1个月后复查空腹下血氨水平,采用快速尿素酶试验检测其Hp感染情况。结果 60例肝硬化住院患者,其中Hp感染者为37例,占61.7%;肝性脑病者为28例,占46.7%。肝性脑病和亚临床肝性脑病及肝硬化无肝性脑病患者发生Hp感染率分别为75.0%(21/28)、66.7%(10/15)、29.4%(5/17);比较差异有统计学意义(P0.05);肝性脑病和亚临床肝性脑病及肝硬化无肝性脑病患者血氨水平分别为(95.1±51.2)μmol/L、(60.2±19.8)μmol/L、(47.5±14.6)μmol/L,比较差异有统计学意义(P0.05);经Logistic回归分析发现,血氨水平、上消化道出血、Child-Pugh、肝肾综合征及血红蛋白量为肝性脑病发生危险因素。结论根治Hp可有利于临床预防及治疗肝硬化肝性脑病。     

幽门螺杆菌感染对肝硬化患者高氨血症的影响

目的观察肝硬化患者合并幽门螺杆菌(Hp)感染与高氨血症的关系。方法采用尿素酶快速试验(RUT),14C-尿素呼气试验(14C-UBT)和血清抗Hp抗体测定,对64例肝硬化患者行幽门螺杆菌检测和血氨测定。对Hp阳性者给予根除治疗后复查血氨,比较根除治疗前后血氨浓度。结果肝硬化患者Hp感染率为67.2%,在根除Hp治疗后血氨浓度明显下降,与根除前相比差异有显著性(P<0.05);Hp阳性者与Hp阴性者血氨浓度比较差异有显著性(P<0.05)。结论Hp感染可导致肝硬化患者血氨升高,根除Hp后可使血氨水平明显下降。     

急性冠状动脉综合征患者血尿酸水平升高的意义

经冠状动脉造影证实急性冠状动脉综合征(ACS)患者398例和相匹配的378名健康者进入本研究。两组血尿酸均呈正态分布,ACS组血尿酸(322±107)μmol/L明显高于正常对照组(302±77) VanoL/L(P＜0．01)。ACS组中男性高尿酸血症(HUA)患病率为27．0%、女性为25．2%。ACS组空腹血糖、甘油三酯、尿素氮、肌酐、血压均明显高于对照组(均P＜0．01)。调整性别和年龄后多元逐步回归分析显示血胆固醇、尿酸、空腹血糖、平均动脉压为ACS冠状动脉狭窄的危险因素(P＜0．05或P＜0．01),HUA在ACS发病中起一定的作用。     

应用终末期肝病模型评分系统预测血浆置换治疗后重型肝炎患者的预后

目的应用终末期肝病模型(MELD)评分系统预测血浆置换(PE)治疗后重型肝炎患者的预后。方法160例重型肝炎患者随机分为PE组与对照组,应用MELD评分系统对每个患者进行评分,比较两组患者病死率和治疗前后的临床生化指标,探讨与MELD评分的关系。结果MELD分值在30～39的患者PE后总胆红素(TBIL)、凝血酶原时间国际标准化比值(INR)、MELD评分分别为(379．4±40．4)μmol/L、(2．5±0．2)和(30．8±3．8);明显低于治疗前的(509．7±64．6)μmol/L、(3．5±0．3)和(37．3±3．5),差异有统计学意义(P＜0．05)。PE组患者的病死率为50．0%,明显低于对照组的86．7%,差异有统计学意义(P＜0．01)。MELD分值≥40的患者PE后的TBIL、INR及MELD评分分别为(595．6±61．5)μmol/L、(3．8±0．4)、(39．8±3．50),明显低于治疗前的(650．4±66．3)μmol/L、(4．4±0．60)、(45．2±4．2),差异有统计学意义(P＜0．05)。PE组患者病死率为91．2%,与对照组的100%相比,差异无统计学意义(P＞0．05)。结论PE通过降低重型肝炎患者的TBIL、INR、MELD评分,改善肝脏功能。血浆置换可降低MELD分值在30～39之间的重型肝炎患者的病死率,但不能降低MELD分值≥40的患者的病死率。     

慢性乙型肝炎重叠戊型肝炎病毒感染的研究

目的了解慢性乙型肝炎重叠戊型肝炎病毒(HEV)感染的临床特点、乙型肝炎病毒(HBV)复制指标、肝功能损伤程度及预后。方法收集慢性乙型肝炎患者和慢性乙型肝炎重叠HEV感染(重叠感染组)各115例,两组病情(轻、中、重度)和HBV DNA定量相同,对两组患者进行临床分析,慢性乙型肝炎组中74例和重叠感染组中的51例患者,在B超引导下做肝活组织检查；应用酶联免疫吸附试验和聚合酶链反应分别检测两组患者HBV标志物,HBV DNA及抗HEV lgM。结果重叠感染组重型肝炎57例,发生率49．6%,死亡29例,病死率25．2%；慢性乙型肝炎组重型肝炎5例,发生率4．4%,死亡2例,病死率1．7%,两组比较,x~2值分别为58．80和27．01,P值均＜0．01,差异有统计学意义。血清HBV DNA≥10~4患者：重叠感染组占83．7%(36/43),单纯慢性乙型肝炎组占97．1%(67/69),x~2=4．73,P＜0．05；重叠感染组总胆红素平均(495．0±217．0)μmol/L、丙氨酸氨基转移酶平均(967．0±395．0) U/L,单纯慢性乙型肝炎组总胆红素平均(216．0±195．0)μmol/L和丙氨酸氨基转移酶平均(373．0±212．0)U/L,两组比较,t值分别为10．20和14．52,P值均＜0．01,差异有统计学意义；肝组织炎症G3和G4重叠感染组33例,占64．7%,单纯慢性乙型肝炎组25例,占33．8%,x~2=12．46,P＜0．01,差异有统计学意义。结论重叠感染组肝功能损害严重,肝组织炎症程度高,HBV DNA水平低,病死率高,预后差。     

MARS人工肝治疗急慢性肝功能衰竭的临床研究

目的　评价应用分子吸附再循环系统治疗各类原因所致肝功能衰竭的治疗效果。方法　回顾并随访分析5 0例次MARS人工肝治疗的疗效。结果　单次 6～ 8小时MARS人工肝治疗显著降低患者血清总胆红素 ( 5 19.3 7±15 2 .70 μmol/L降至 3 61.0 6± 177.98μmol/L ,p <0 .0 5 )和血氨 ( 167.44± 80 .73 μmol/L降至 86.82± 15 .5 2 μmol/L ,P <0 .0 5 )水平 ;升高凝血酶原活动度 ( 3 6.5 5 %± 15 .2 9%到 74.13 %± 2 5 .40 %,P <0 .0 5 )。而电解质、血常规和血气分析等指标无显著变化 (P >0 .0 5 )。 2 5例患者中治愈和好转 15例 ,10例死亡 ,存活率 60 %。结论　MARS人工肝是治疗肝功能衰竭患者安全、有效的辅助方法     

Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients

AIM： To investigate the relationship between H pylori infection, blood ammonia concentration and hepatic encephalopathy （HE）, and the effect of Hpylori eradication in cirrhotic patients. METHODS： From July 2003 to January 2005, 457 cirrhotic patients in five regions of Zhejiang Province were enrolled. Patients were evaluated for demographics, number connection test, Hpylori infection, liver impairment, blood ammonia concentration and HE. Patients with Hpylori infection were given I wk therapy with omeprazole plus clarithromycin and tinidazole. ^14C urea breath test was performed and mental symptoms and blood ammonia level were reassessed after RESULTS： Overall H pylori infection rate was 60.6%, and HE occurred in 47.5% of cirrhotic patients. Subclinical HE （SHE） was detected in 55 of 117 cirrhotic patients. Blood ammonia concentration in H pylori negative （n = 180） and positive （n = 277） cirrhotic patients was 53.8 ± 51.4 and 78.4 ± 63.6 μmol/L, respectively （P 〈 0.01）, which was significantly reduced to 53.5 ± 37.7 μmol/L after bacterium eradication （n = 126） （P 〈 0.01）. Blood ammonia was 97.5 ± 81.0 μmol/L in H pylori-positive cirrhotic patients, and this did not significantly change in those with persistent infection after Hpylori eradication （n = 11）. HE was more frequently observed in patients with H pylori infection than in those without （58.5% vs 30.6%, P 〈 0.01）. HE rate significantly dropped to 34.1% after H pylori eradiation （P 〈 0.01）. H pylori prevalence significantly differed among cirrhotic patients with HE （74.4%）, SHE （69.1%）, and those without HE （53.2%） （P 〈 0.05）. Blood ammonia level was significantly different among cirrhotic patients with HE （94.5 ± 75.6 μmol/L）, SHE （59.9 ± 49.2 μmol/L）, and without HE （47.3 ± 33.5 μmol/L） （P 〈 0.05）. Logistic regression analysis showed that blood ammonia concentration, Child-Pugh stage, upper gastrointestinal bleeding, electrolyte disturbance, and urea nit     

Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients

AIM: To investigate the relationship between H pylori infection, blood ammonia concentration and hepatic encephalopathy (HE), and the effect of H pylori eradication in cirrhotic patients.METHODS: From July 2003 to January 2005, 457 cirrhotic patients in five regions of Zhejiang Province were enrolled. Patients were evaluated for demographics, number connection test, H pylori infection, liver impairment, blood ammonia concentration and HE. Patients with H pylori infection were given 1 wk therapy with omeprazole plus clarithromycin and tinidazole. 14C urea breath test was performed and mental symptoms and blood ammonia level were reassessed after bacterium eradication.RESULTS: Overall H pylori infection rate was 60.6%, and HE occurred in 47.5% of cirrhotic patients. Subclinical HE (SHE) was detected in 55 of 117 cirrhotic patients. Blood ammonia concentration in H pylori negative (n = 180) and positive (n = 277) cirrhotic patients was 53.8 ± 51.4 and 78.4 ± 63.6 nmol/L, respectively (P < 0.01), which was significantly reduced to 53.5 ± 37.7 nmol/L after bacterium eradication (n = 126) (P < 0.01). Blood ammonia was 97.5 ± 81.0 nmol/L in H py/ori-positive cirrhotic patients, and this did not significantly change in those with persistent infection after H pylori eradication (n = 11). HE was more frequently observed in patients with H pylori infection than in those without (58.5% vs 30.6%, P < 0.01). HE rate significantly dropped to 34.1% after H pylori eradiation (P < 0.01). H pylori prevalence significantly differed among cirrhotic patients with HE (74.4%), SHE (69.1%), and those without HE (53.2%) (P < 0.05). Blood ammonia level was significantly different among cirrhotic patients with HE (94.5 ± 75.6 nmol/L), SHE (59.9 ± 49.2 nmol/L), and without HE (47.3 ± 33.5 nmol/L) (P < 0.05). Logistic regression analysis showed that blood ammonia concentration, Child-Pugh stage, upper gastrointestinal bleeding, electrolyte disturbance, and urea nitrogen were risk factors for HE.CONCLUSION: H pylori infection is an important factor for inducing high blood ammonia concentration and HE in cirrhotic patients. H pylori eradication may be helpful for treatment and prevention of HE.     

Role of Helicobacter pylori infection and its eradication in patients with subclinical hepatic encephalopathy

AIMS: Helicobacter pylori infection in cirrhotic patients has been associated with episodes of hepatic encephalopathy (HE), although conclusive data are still lacking. This prospective study has evaluated the prevalence of H. pylori infection in 37 patients with advanced cirrhosis of the liver and subclinical hepatic encephalopathy (SHE), diagnosed by changes in psychometric tests and/or electrophysiological tests, as well as the repercussion of H. pylori eradication on ammonaemia and the evolution of this disorder. RESULTS: A positive result for H. pylori infection was obtained in 22/37 (59%) patients. Initial fasting blood levels of ammonia were high in both groups. Infected and non-infected patients showed similar levels (62.05 mmol/l v. 62.5 mmol/l), which were lowered by the standard diet, although statistical significance was only reached in the infected patient group (53.05 +/- 26 mmol/l; P < 0.05). Infection was eradicated in 19 patients, but no reduction of blood levels of ammonia was observed after H. pylori eradication among infected patients (52.37 +/- 29 mmol/l). No change has been found in either group after the administration of diet or antimicrobials with regard to psychometric and/or electrophysiological tests. CONCLUSIONS: H. pylori infection does not contribute significantly to high blood levels of ammonia in patients with advanced cirrhosis and SHE. Likewise, H. pylori eradication does not induce any improvement in the psychometric and/or electrophysiological tests used to define SHE.     

Amino acid challenge in patients with cirrhosis: a model for the assessment of treatments for hepatic encephalopathy.

BACKGROUND/AIMS: To mimic episodic hepatic encephalopathy after gastrointestinal bleeding under controlled conditions, cirrhotic patients were challenged with an amino acid mixture of comparable composition to haemoglobin. METHODS: Basal EEG, psychometric score (HE test), reaction times and venous blood ammonia were recorded. Following a 54 or 108 gm oral amino acid challenge, blood ammonia levels and EEG were recorded at 30-min intervals, and psychometric testing was repeated at 180 min. Ten controls (57 +/- 2) and 31 cirrhotics (52 +/- 2) of which 21 were Child's grade A or B and 10 grade C underwent the challenge. Nine had a transjugular intrahepatic porta-systemic shunt in situ. RESULTS: Seventeen patients had abnormal baseline HE scores. Basal blood ammonia and reaction time A were significantly greater in patients (52 +/- 5 micromol/l and 478 +/- 20 ms, respectively) than controls (19 +/- 2 micromol/l and 372 +/- 14 ms) (P < 0.001). Following the challenge, in patients with advanced liver disease (Child's grade B and C) the slowing of reaction time A (+85 +/- 38 and +71 +/- 31 ms, respectively; P < 0.03) and EEG (ratio of slow to fast wave activity +0.31 +/- 0.12 and +0.58 +/- 0.19; P < 0.02) were significantly greater than in controls (-3.3 +/- 8 ms and 0.00 +/- 0.03, respectively). Patients with an abnormal basal HE score had the most pronounced changes (reaction time A +110 +/- 39 ms, P < 0.01, EEG +0.52 +/- 13, P < 0.01, respectively). The change in EEG ratio correlated with the dose of amino acid administered (r = 0.96; P < 0.008). CONCLUSION: The amino acid challenge constitutes a reproducible human model of episodic, Type C hepatic encephalopathy unaffected by the complications usually encountered in clinical practice.     

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.     

Hepatic encephalopathy and Helicobacter pylori: a critical reappraisal

Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis, and plasma ammonia plays a pivotal role in its pathogenesis. Ammonia disposal in cirrhotics depend on intricately balanced enzyme and transport systems, involving liver, large and small bowel, muscle, and kidney. Recently, it has been suggested that Helicobacter pylori could contribute to hyperammonemia in cirrhotics, but conflicting data are available in the literature. This is a systematic review of experimental (animals and humans), epidemiological, case-control, and prospective studies, to evaluate the arguments in favor and against the role of H. pylori in HE pathogenesis. Although H. pylori produces ammonia in the stomach, several studies have shown that both basal ammonia levels and HE prevalence did not significantly differ between cirrhotics with and without infection. Moreover, some prospective studies have documented that both blood ammonia levels and mental status in HE cirrhotics are not significantly affected by H. pylori eradication. Even if a small sub-group of cirrhotics with both a high bacterial density and more severe hepatic impairment seems to benefit by bacterial eradication, data indicate that ammonia production in the stomach by H. pylori urease appears to be inadequate to clinically affect ammonia disposal in the majority of cirrhotic patients. Further studies are warranted in this field.     

Cerebral herniation in patients with acute liver failure is correlated with arterial ammonia concentration

Cerebral edema leading to cerebral herniation (CH) is a common cause of death in acute liver failure (ALF). Animal studies have related ammonia with this complication. During liver failure, hepatic ammonia removal can be expected to determine the arterial ammonia level. In patients with ALF, we examined the hypotheses that high arterial ammonia is related to later death by CH, and that impaired removal in the hepatic circulation is related to high arterial ammonia. Twenty-two patients with ALF were studied retrospectively. In addition, prospective studies with liver vein catheterization were performed after development of hepatic encephalopathy (HE) in 22 patients with ALF and 9 with acute on chronic liver disease (AOCLD). Cerebral arterial-venous ammonia difference was studied in 13 patients with ALF. In all patients with ALF (n = 44), those who developed CH (n = 14) had higher arterial plasma ammonia than the non-CH (n = 30) patients (230 +/- 58 vs. 118 +/- 48 micromol/L; P <. 001). In contrast, galactose elimination capacity, bilirubin, creatinine, and prothrombin time were not different (NS). Cerebral arterial-venous differences increased with increasing arterial ammonia (P <.001). Arterial plasma ammonia was lower than hepatic venous in ALF (148 +/- 73 vs. 203 +/- 108 micromol/L; P <.001). In contrast, arterial plasma ammonia was higher than hepatic venous in patients with AOCLD (91 +/- 26 vs. 66 +/- 18 micromol/L; P <.05). Net ammonia release from the hepatic-splanchnic region was 6.5 +/- 6. 4 mmol/h in ALF, and arterial ammonia increased with increasing release. In contrast, there was a net hepatic-splanchnic removal of ammonia (2.8 +/- 3.3 mmol/h) in patients with AOCLD. We interpret these data that in ALF in humans, vast amounts of ammonia escape hepatic metabolism, leading to high arterial ammonia concentrations, which in turn is associated with increased cerebral ammonia uptake and CH.     

Effect of sodium benzoate on blood ammonia response to oral glutamine challenge in cirrhotic patients: a note of caution

OBJECTIVE: The administration of sodium benzoate provides an alternative pathway for the disposal of waste nitrogen and this substance has been used to treat patients with urea cycle defects and more recently cirrhotics with hepatic encephalopathy. The aim of the study was to assess the ammonia-lowering effect of benzoate in cirrhotic patients without overt hepatic encephalopathy. METHODS: Glutamine challenge, a method to induce an increase of blood ammonia, was performed in six cirrhotics before and after 5 days of benzoate treatment (10 microg/day). Number Connection Test and Posner's Attention Test were also performed before and after benzoate treatment. RESULTS: Blood ammonia increased after the glutamine load both before (from 66 +/- 12 microg/dl to 123 +/- 34 microg/dl and 179 +/- 53 microg/dl after 30 and 60 min, respectively; ANOVA p = 0.0004) and after benzoate treatment (from 102 +/- 27 microg/dl to 185 +/- 49 microg/dl and 250 +/- 39 microg/dl after 30 and 60 min, respectively; ANOVA p = 0.00001). However, after benzoate treatment, the basal values (102 +/- 27 vs 66 +/- 12 microg/dl; p = 0.01) and peak increments of ammonia (166 +/- 56 microg/dl vs 102 +/- 40 microg/dl; p = 0.04) were significantly higher than before. The Number Connection test and the Posner's test were not altered by benzoate treatment. CONCLUSIONS: Benzoate increased both the basal and post-glutamine ammonia levels. These results confirm what has already been observed in experimental animals and suggest a note of caution in the use of sodium benzoate in cirrhotic patients.     

Altered response to oral glutamine challenge as prognostic factor for overt episodes in patients with minimal hepatic encephalopathy

BACKGROUND/AIMS: We assessed the usefulness of oral glutamine challenge (OGC) and minimal hepatic encephalopathy in evaluating risk of overt hepatic encephalopathy in cirrhotic patients.METHODS: Minimal hepatic encephalopathy (MHE) was inferred using neuro-psychological tests. Venous ammonia concentrations were measured pre- and post-60 min (NH(3)-60m) of a 10 g oral glutamine load. Receiver-operating-characteristic curve analysis indicated a pathological glutamine tolerance cut-off value of NH(3)-60m >128 microg/dl. RESULTS: In healthy control subjects (n=10) ammonia concentrations remained unchanged but increased significantly in cirrhotic patients (from 70.41+/-45.2 to 127.43+/-78.6; P<0.001). In multiple logistic regression analysis, altered OGC was related to Child-Pugh (odds ratio, OR=7.69; 95% confidence interval, CI=1.72-33.3; P<0.01) and MHE (OR=5.45; 95% CI=1.17-25.4; P<0.05). In the follow-up 11 patients (15%) developed overt hepatic encephalopathy (HE). In multivariate analysis OGC (OR=14.5; 95% CI=1.26-126.3) and MHE (OR=1.56; 95% CI=1.02-21.9) were independently related with HE in the follow-up. Patients with MHE and altered OGC showed significantly higher risk of overt HE in the follow-up (60%) than patients without MHE and normal OGC (2.8%) (Log rank test=21.60; P<0.0001). CONCLUSIONS: A pathological OGC in patients with MHE appears to be a prognostic factor for the development of overt hepatic encephalopathy, whereas a normal OGC in patients without MHE could exclude risk of overt HE.     

Auditory P300 event-related potentials and number connection test for evaluation of subclinical hepatic encephalopathy in patients with cirrhosis of the liver: a follow-up study

BACKGROUND AND AIMS: The P300 event-related potentials (P3ERP) have been recently advocated for detection of cognitive disturbances in early encephalopathy. However, no systematic follow-up study has been conducted to understand the clinical significance of subclinical hepatic encephalopathy (SHE) detected by this or other methods. The present study was therefore undertaken to examine the diagnostic usefulness of auditory P3ERP in the detection of SHE, to compare it with that of the number connection test (NCT), and to investigate the clinical outcome of patients with SHE in terms of progression to overt encephalopathy. METHODS: P300 event-related potential latencies were measured and the NCT time was recorded in 81 non-encephalopathic cirrhotic patients (Aged 43.8 +/- 11 years, 23 alcoholic and 58 non-alcoholics) attending the outpatient department at our tertiary care hospital (All India Institute of Medical Sciences Hospital). Cut-off values for abnormality in the tests were developed from age-, sex- and education-matched controls. Patients were followed up at regular intervals for the development of overt encephalopathy, and the identifiable precipitating factors were noted. The P3ERP latencies (363 +/- 34 msec vs 349 +/- 23 msec), as well as NCT time (54.6 +/- 30.6 s vs 39.5 +/- 15.8 s) were significantly prolonged (P< 0.01) in patients with liver cirrhosis when compared with the non-cirrhotic controls. RESULTS: The P3ERP defects were seen in 24.6% of cirrhotic patients, while NCT time was prolonged in 19.7% of the patients. Nearly 43% of the patients with SHE progressed to overt encephalopathy within a mean duration of 5 months, while only 3.9% of the non-SHE patients did so. Of the patients who developed overt encephalopathy, 64.2% had P3ERP latency prolongations while 35.7% had abnormal NCT. CONCLUSIONS: The results of the present study suggest that P3ERP and NCT are valid tools for the screening of SHE in cirrhotic patients as there is a greater likelihood of overt encephalopathy development in patients with an abnormality detected by these tests than in patients with no such abnormality.