肝硬化与幽门螺杆菌感染关系的临床研究

背景：在肝硬化患者中，胃幽门螺杆菌（H．pylori）感染可导致产氨增加，使肝性脑病的发病率升高，但H．pylori感染是否为肝硬化血氨水平升高的致病原因仍存在争议。目的：研究肝硬化患者的H．pylori感染状况及其与血氨水平和轻微肝性脑病（MHE）的关系。方法：选取符合诊断标准的肝硬化患者和健康志愿者，胃镜下取胃窦和胃体黏膜行快速尿素酶试验并作病理学检查检测H．pylori，两项均阳性判为H．pylori感染；检查血氨水平；行数字连接试验A（NCT—A）、数码符号试验（DST）和脑电图（EEG）检查，其中任一项异常即可诊断MHE。随机选取H．pylori感染者予奥美拉唑、阿莫西林和克拉霉素～周标准三联根除治疗，停药6—8周后行^13C-尿素呼气试验判断H．pylori根除情况。所有研究对象于停药6～8周后或第一次检查后7-9周复查血氨水平、NCT—A、DST和EEG。结果：106例肝硬化患者和30名健康志愿者进入本研究。肝硬化组的H．pylori感染率（46．2％，491106）高于健康对照组（30．0％，9／30），但差异无统计学显著性（P〉0．05）。各组H.pylori感染者根除治疗前后的血氨水平均无显著差异（P〉0．05），肝硬化MHE组H．pylori根除后NCT—A、DST和EEG检查结果未见改善。结论：肝硬化患者MHE的发生和血氨水平与H．pylori感染无关。     

门冬氨酸鸟氨酸治疗肝硬化伴发肝性脑病68例疗效观察

目的评价门冬氨酸鸟氨酸（瑞甘）在治疗肝硬化伴发肝性脑病中的临床疗效。方法将2004年3月至2012年8月我院消化内科收治的肝硬化并发肝性脑病患者132例,按随机分配的方法分为观察组、对照组。对照组64例给予常规抗肝昏迷治疗,观察组68例在对照组治疗的基础上给予门冬氨酸鸟氨酸（瑞甘）静脉滴注,对比两组患者治疗前及治疗后血清转氨酶、血氨、总胆红素水平及两组的治疗总有效率。结果两组患者血清转氨酶、血氨、总胆红素治疗后与治疗前比较均有明显好转（P〈0．05）,观察组比对照组改善更显著（P〈0．05）;观察组的治疗总有效率明显高于对照组（P〈0．05）。结论门冬氨酸鸟氨酸可显著改善肝硬化伴发肝性脑病患者的生化指标,疗效确切,值得在肝硬化伴发肝性脑病患者的治疗中推广应用。     

门冬氨酸鸟氨酸联合乳果糖治疗肝性脑病的疗效分析

目的探讨门冬氨酸鸟氨酸联合乳果糖治疗肝性脑病患者的临床疗效。方法将80例重型肝炎或肝炎肝硬化并发肝性脑病患者随机分为治疗组（42例）和对照组（38例）。治疗组给予门冬氨酸鸟氨酸静脉滴注,乳果糖溶液灌肠;对照组给予精氨酸静脉滴注,0．9％氯化钠溶液灌肠。两组疗程均为7天,观察患者治疗前后的临床表现（症状和体征的变化）,检测血氨和肝肾功能,判断临床疗效变化。结果治疗组总有效率（81．0％）明显高于对照组（52．6％）（P〈0．01）;治疗后治疗组AST、ALT、TBil、血氨显著降低（P〈0．05,P〈0．01）,对照组血氨降低（P〈0．05）,两组AST、TBil、血氨间的差异有统计学意义（P〈0．05）;两组患者肝性脑病分期均有明显改善（P〈0．05,P〈0．01）,治疗组优于对照组（P〈0．05）。结论门冬氨酸鸟氨酸联合乳果糖对改善肝功能、纠正肝性脑病有较好的治疗效果。     

肝性脑病74例临床分析

[目的]分析肝性脑病（HE）的发生及与预后的关系，以提高HE的防治水平。[方法]回顾性地对比分析74例肝炎肝硬化并发HE的患者的临床资料及主要肝功能、血氨检测指标。[结果]HE占同期住院肝硬化病例的29．36％；男女比例4：1；Child-PughC级占61％；抢救成功率为64．86％；血清清蛋白、凝血酶原活动度值较对照组明显降低（P〈0．05）；血氨明显高于（82．00％）对照组（P〈0．01），但预后与血氨的增高程度无关（P〉0．05）；HE组上消化道出血、电解质紊乱及肝肾综合征的发生率明显高于对照组（P〈0．01）。[结论]HE是失代偿期肝硬化的常见并发症，严重影响预后。其发生与肝功能严重障碍、血氨增高及并发症出现有关，需采取综合性防治措施。     

幽门螺杆菌感染对高氨血症和肝性脑病发病的影响

目的了解幽门螺杆菌(Hp)感染和血氨水平、肝性脑病(HE)发病的关系,并探讨根除Hp对血氨水平和HE发生的影响。方法2003年7月-2005年1月在浙江省5个地区收集肝硬化住院患者,记录患者的一般资料、数字连接试验结果、Hp感染情况、肝功能Child-Pugh分级、血氨水平和HE情况。Hp(+)患者予“奥美拉唑+克拉霉素+替硝唑”1周根除治疗,1个月后查~(14)C尿素呼气试验,并记录患者的神经精神症状和血氨水平。结果(1)共收集肝硬化住院患者457例,Hp感染率60．6%,HE发生率47．5%。检出亚临床肝性脑病(SHE)患者55例,SHE占未发生HE肝硬化患者的47．0%(55/117)。(2)Hp(+)和Hp(-)肝硬化患者血氨浓度分别为(78．4±63．6)μmoL/L和(53．8±51．4)μmol/L(P＜0．01);根除Hp后血氨显著下降至(53．5±37．7)μmol/L(P＜0．01)。Hp(+)和Hp(-)肝硬化患者HE发生率差异有统计学意义(58．5%比30．6%,P＜0．01);根除Hp后HE发生率下降至34．1%(P＜0．01)。(3)HE、SHE和肝硬化患者的Hp感染率分别为74．4%、69．1%和53．2%(P＜0．05)。三组患者的血氨水平分别为(94．5±75．6)μmol/L、(59．9±49．2)μmol/L和(47．3±33．5)μmol/L(P＜0．05)。结论Hp感染是引起肝硬化高氨血症和并发HE的重要因素,根除Hp有利于治疗和预防HE的发生。     

血浆置换、大黄灌肠及门冬氨酸鸟氨酸联合治疗重型肝炎合并肝性脑病临床观察

目的评价血浆置换、大黄灌肠及门冬氨酸鸟氨酸联合治疗重型肝炎合并肝性脑病（HE）的疗效。方法将106例重型肝炎合并HE患者随机分为治疗组和对照组,两组均接受内科综合治疗加血浆置换术,治疗组联合大黄煎剂灌肠及门冬氨酸鸟氨酸治疗,观察两组的疗效及治疗前后肝功能、凝血酶原活动度和血氨的变化。结果治疗组总有效率显著高于对照组（P〈0．05）;治疗组肝功能、凝血酶原活动度和血氨下降幅度均优于对照组（P〈0．05）。结论血浆置换、大黄灌肠及门冬氨酸鸟氨酸联合能有效治疗重型肝炎合并肝性脑病。     

幽门螺杆菌感染及其根除治疗对轻微肝性脑病患者的临床价值

目的探讨幽门螺杆菌(H.pylori)感染与轻微肝性脑病(mild hepatic encephalopathy, MHE)的关系,分析根除H.pylori对MHE的临床价值。方法选取我院2018年11月至2020年8月诊断为MHE的患者56例,同期健康体检者40名,将~(13)C呼气检测H.pylori阳性的42例患者随机分为观察组和对照组,各21例。检测两组患者ALT、AST、总胆红素(TBIL)、直接胆红素(DBIL)、间接胆红素(IBIL)、血氨水平及NCT、DST评分,同时对观察组患者行H.pylori根除治疗,比较两组治疗前后上述指标水平的变化情况。结果与健康体检者相比,MHE患者更易合并H.pylori感染,差异有统计学意义(χ~2=4.61,P0.05);观察组与对照组H.pylori根除治疗前ALT、AST、TBIL、DBIL、IBIL、血氨水平变化及NCT、DST评分方面差异均无统计学意义(P0.05),根除治疗后较治疗前DST评分值升高,余指标均下降,且对照组明显优于观察组,差异有统计学意义(P0.05)。结论 H.pylori感染与MHE密切相关,H.pylori根除治疗后能够改善患者肝功能,降低血氨水平,缓解患者的临床症状,对治疗MHE具有一定的指导意义。     

根除幽门螺杆菌与胃食管反流病的关系研究

目的探讨根除幽门螺杆菌（H．pylori）与胃食管反流病（GERD）的关系。方法本研究采用食管内24hpH监测的方法，定量观察H．pylori阳性GERD患者根除H．pylori和单用兰索拉唑治疗3月后食管酸暴露的变化，以及H．pylori阳性慢性浅表性胃炎（CSG）根除H．pylori和姑息治疗3月后食管酸暴露的变化。RE组：反流性食管炎（RE）表现患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组采用丽珠唯三联＋兰索拉唑方案，对照组单用兰索拉唑。CSG组：慢性浅表性胃炎（CSG）患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组均采用丽珠唯三联方案，对照组不采用药物治疗。以上两组待H．pylori根除后，对比研究H．pylori根除组和对照组3月后食管24hpH监测参数。结果RE组：H．pylori根除和单用兰索拉唑治疗3月后两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。CSG组：H．pylori根除和姑息治疗3月两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。结论GERD患者根除幽门螺杆菌后食管酸暴露无明显改变，CSG患者根除幽门螺杆菌后食管酸暴露无明显改变，H．pylori感染可能与GERD的转归和发生无关。     

连续性血液滤过治疗重型肝炎合并肝性脑病16例临床疗效观察

目的观察连续性血液滤过（CVVH）治疗重型肝炎合并肝性脑病的临床疗效。方法将32例重型肝炎合并肝性脑病患者随机分为两组。治疗组：内科综合疗法＋CVVH。对照组：内科综合疗法。治疗前后分别检测肝肾功能、血氨、TNF和IL-6等。结果治疗组、对照组患者的清醒率分别为75．0％和31．3％。CVVH治疗后血清尿素氮、肌酐、氨、TNF及IL-6比对照组明显下降（P〈0．05）。血清胆红素、TBA下降与对照组比较无显著性差异（P〉0．05）。治疗组肝性脑病Ⅰ-Ⅱ期患者的存活率明显高于Ⅲ-Ⅳ期（P〈0．05）。结论CVVH是辅助治疗重型肝炎合并肝性脑病的有效方法,早期治疗能进一步提高疗效。     

消化性溃疡与ABO血型、Lewis表型分布及幽门螺杆菌感染的相关性研究

目的探讨消化性溃疡（PU）与ABO血型、Lewis表型的分布及幽门螺杆菌（H．pylori）感染的关系。方法70例消化性溃疡患者为研究组,96例健康志愿者为对照组,比较ABO血型、Lewis表型分布和H．pylori感染的差异。结果PU组O型血者占52．9％,明显高于O型血在正常人群中的分布（31．3％,P〈0．05）;在非O型血患者中Lewis表型为Le（a＋b＋）者占51．5％,明显高于Le（a＋b＋）表型在对照组非O型血中的频率（9．1％,P〈0．001）。PU组不同ABO血型者H．pylori感染率比较无统计学差异（P〉0．05）;PU组Le（a-b＋）表型者H．pylori感染率为67．6％,明显高于其他Lewis表型（P〈0．05）。结论ABO血型中O型血者易患消化性溃疡,且非O型血Lewis表型为Le（a＋b＋）者也是消化性溃疡的高危人群。ABO血型间H．pylofi感染比较无显著性差异,Le（a-b＋）表型可能是H．pylori感染的一个危险因素。     

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.     

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     

Helicobacter pylori infection in hepatic encephalopathy: Relationship to plasma endotoxins and blood ammonia

Background/Aim: Hepatic encephalopathy (HE) is frequently observed in patients with advanced liver disease and manifests a wide variety of neuropsychiatric signs and symptoms. Ammonia toxicity and bacterial endotoxins have been suggested as key determinants of HE onset whereas a role for Helicobacter pylori infection has not been established. We investigated the correlation between H. pylori infection and HE severity (evaluated through functional tests) in 60 outpatients with established liver cirrhosis and 20 non-cirrhotic controls. Methods: Fasting arterial blood ammonia, plasma endotoxins, and H. pylori infection status were investigated in all subjects. Results: H. pylori infection was documented in 35/60 (58%) patients and in 6/20 (30%) controls (P = 0.039). Significant differences were observed between patients with and withoutHE for age, presence of ascites, fasting arterial blood ammonia, plasma endotoxin, and H. pylori infection. Further, a significant increase in fasting arterial blood ammonia and plasma endotoxin was associated with H. pylori infection in cirrhotic patients. Last, medical treatment of H. pylori infection led to a significant decrease in HE severity and fasting arterial blood ammonia levels. Conclusion: In conclusion, we submit that H. pylori infection might, in fact, play a role in increasing the circulating levels of ammonia and endotoxins in cirrhotic patients, thus facilitating the onset 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.     

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.     

Helicobacter pylori, gastric juice, and arterial ammonia levels in patients with cirrhosis

Helicobacter pylori urease activity is a potential source of ammonia in the stomach of patients with cirrhosis. However, the possible role of H. pylori in the pathogenesis of hepatic encephalopathy deserves further investigations. The current study evaluates the relationship among H. pylori infection, gastric juice ammonia concentrations, and arterial ammonia levels in patients with cirrhosis. Overall, 14 patients with cirrhosis with overt hepatic encephalopathy, 19 with subclinical hepatic encephalopathy, and 13 without encephalopathy were enrolled. All patients underwent upper endoscopy, and gastric biopsy specimens were taken for H. pylori assessment (rapid urease test, histology, and culture). A gastric juice sample and an arterial blood sample were obtained for ammonia level assessment. Patients with overt encephalopathy had both higher arterial ammonia levels and a more severe hepatic impairment than the remaining patients, whereas gastric juice ammonia concentrations did not differ among the three groups. H. pylori prevalence was similar among groups. Patients with H. pylori infection had significantly higher gastric juice ammonia concentrations than those without infection (2.3 +/- 1.3 vs. 0.9 +/- 0.6 mmol/L, respectively; p = 0.003); however, no difference in arterial ammonia levels emerged between the two groups (37.7 +/- 18.6 vs. 37.6 +/- 18.8 micromol/L, respectively). No significant correlation was found between gastric juice ammonia concentrations and arterial ammonia levels. The data suggest that liver impairment remains crucial in ammonia disposal in patients with cirrhosis, whereas H. pylori infection does not seem to play a major role in the pathogenesis of hyperammonemia in these patients.     

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.     

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.     

Breath and blood ammonia in liver cirrhosis

BACKGROUND/AIMS: Hyperammonemia causes dysfunction of multiple organs in patients with cirrhosis, including hepatic encephalopathy. Blood ammonia concentrations are monitored with respect to disease progression and efficacy of treatment. Fetor hepaticus, the characteristic breath odor in hepatic encephalopathy has called little quantitative attention to breath ammonia. We studied the dynamics of ammonia metabolism in cirrhosis in terms of the relationship between breath and blood ammonia. METHODOLOGY: Breath and blood ammonia levels were measured simultaneously in 20 cirrhotic patients and in 10 healthy volunteers. Breath ammonia was measured using ammonia electrodes in collected expired air. Helicobacter pylori serum antibody titers were also measured, since the organism produces ammonia. RESULTS: Blood ammonia correlated positively with breath ammonia in patients with cirrhosis. Breath ammonia levels were significantly higher in cirrhotic patients (0.745 ppm) than in controls (0.278 ppm), and higher in cirrhotic patients with hyperammonemia (0.997 ppm) than in those without (0.558 ppm). Breath and blood ammonia decreased together with treatment of hyperammonemia. H. pylori seropositivity was 20% in controls, 27.3% in cirrhotic patients with normal blood ammonia, and 66.7% in those with hyperammonemia. CONCLUSIONS: Breath ammonia measurement may be useful in diagnosis, treatment assessment, and follow-up in hepatic encephalopathy.