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幽门螺杆菌感染对高氨血症和肝性脑病发病的影响
引用本文:Wang LJ,Cai JT,Chen T,Lü B,Si JM.幽门螺杆菌感染对高氨血症和肝性脑病发病的影响[J].中华内科杂志,2006,45(8):654-657.
作者姓名:Wang LJ  Cai JT  Chen T  Lü B  Si JM
作者单位:1. 310009,杭州,浙江大学医学院附属第二医院消化科
2. 浙江中医药大学附属省中医院消化科
3. 浙江大学邵逸夫临床医学研究所胃肠病研究室
基金项目:浙江省卫生研究基金资助项目(2003A071)
摘    要: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。

关 键 词:螺杆菌  幽门    肝性脑病
收稿时间:03 6 2006 12:00AM
修稿时间:2006-03-06

The effects of Helicobacter pylori infection on hyperammonaemia and hepatic encephalopathy in cirrhotic patients
Wang Liang-jing,Cai Jian-ting,Chen Tao,Lü Bin,Si Jian-min.The effects of Helicobacter pylori infection on hyperammonaemia and hepatic encephalopathy in cirrhotic patients[J].Chinese Journal of Internal Medicine,2006,45(8):654-657.
Authors:Wang Liang-jing  Cai Jian-ting  Chen Tao  Lü Bin  Si Jian-min
Institution:Department of Gastroenterology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Abstract:OBJECTIVE: To evaluate the relationship among Helicobacter pylori (Hp)infection, blood ammonia concentrations, and hepatic encephalopathy (HE) status, and to investigate the effect of Hp eradication on blood ammonia levels and hepatic encephalopathy status in cirrhotic patients. METHODS: From July 2003 to Jan 2005, cirrhotic patients in 5 regions of Zhejiang Province were enrolled. Patients were evaluated for the demographic checklists, number connection test, Hp infection, liver impairment level, blood ammonia concentrations and hepatic encephalopathy status. Patients with Hp infection were given one week therapy with omeprazole plus clarithromycin and tinidazole. (14)C urea breath test was performed and the mental symptoms and blood ammonia levels were reassessed after the eradication therapy. RESULTS: (1) 457 cirrhotics were enrolled, the overall Hp infection rate was 60.6%, and HE happened with 47.5%. Subclinical hepatic encephalopathy (SHE) were detected 55 in 47.0% of 117 cirrhotics. (2) Blood ammonia concentration in Hp (-) and Hp (+) cirrhotics was (53.8 +/- 51.4) micromol/L and (78.4 +/- 63.6) micromol/L respectively (P < 0.01), which was significantly reduced to (53.5 +/- 37.7) micromol/L after Hp eradication (P < 0.01). HE was more frequently observed in patients with Hp infection than without it (58.5% vs 30.6%, P < 0.01). HE rate were significantly dropped to 34.1% after Hp eradication (P < 0.01). (3) Hp prevalence significantly differed among cirrhotic with HE (74.4%), those with SHE (69.1%), or without HE (53.2%) (P < 0.05). The level of blood ammonia had significant difference among the cirrhotics with HE (94.5 +/- 75.6) micromol/L, those with SHE (59.9 +/- 49.2) micromol/L, or without HE (47.3 +/- 33.5) micromol/L (P < 0.05). CONCLUSIONS: Hp infection was an important factor of inducing with high blood ammonia concentration and hepatic encephalopathy in cirrhotic patients. Hp eradication may be helpful for treatment and prevention of HE.
Keywords:Helicobacter pylori  Ammonia  Hepatic encephalopathy
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