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目的探讨幽门螺杆菌感染在肝硬化患者高氨血症发生过程中的作用及其临床意义。方法采用聚合酶链反应法检测８３例肝硬变患者胃液幽门螺杆菌（ＨＰ），同时测定患者静脉血氨，８３例肝硬变患者中ＨＰ阳性５４例，该５４例患者均口服新霉素０．５ｇ，每天３次，共服７天，其中３２例同时口服羟氨苄青霉素０．５ｇ，每天２次，甲硝唑０．４ｇ，每天２次，连服两周，疗程结束后复查静脉血氨。结果合并肝性脑病和无肝性脑病者ＨＰ感染率分别为８０．６％和 ５３．２％（Ｐ＜０．０１），肝功能先代偿期 ＨＰ阳性和 ＨＰ阴性者静脉血氢分别为 １３１．５３±１７．１４ｕｇ／ｄｌ和９２．３１±１９．２７ｕｇ／ｄｌ（Ｐ＜０．０１），根除ＨＰ后血氨浓度（８８．０５±１９．４１ｕｇ／ｄｌ）较治疗前（１３３．８４±１１．３９ｕｇ／ｄｌ）明显降低，肝功能Ｂ级和Ｃ级患者血氨降低幅度更大。结论胃内ＨＰ尿素酶分解产生的氨是肝硬化患者体氨的来源之一，根除ＨＰ有预防和治疗肝性脑病的作用。
Objective To investigate the role of Helicobacter pylori infection in the pathogenesis of hyperammonemia in cirrhotic patients and its clinical significance. Methods Polymerase chain reaction was used to detect Helicobacter pylori (HP) in gastric juice of 83 patients with liver cirrhosis. Meanwhile, 54 patients with positive HP in the patients with venous blood ammonia and 83 patients with cirrhosis were enrolled. All 54 patients were given neomycin 0.5g, 3 times a day for a total of 7 days, of which 32 cases of oral amoxicillin 0.5g, 2 times a day, metronidazole 0.4g, 2 times a day, and even for two weeks after the end of the course of review veins Blood ammonia. Results The HP infection rates in patients with and without hepatic encephalopathy were 80.6% and 53.2%, respectively (P <0.01). The venous blood hydrogen in compensated HP positive and HP negative patients with hepatic function were 131.53 ± 17.14ug / dl and 92.31 ± 19.27ug / dl respectively (P <0.01). The concentration of ammonia after eradication was 88.05 ± 19.41ug / dl, 84 ± 11.39ug / dl) was significantly lower, liver function in patients with B and C levels of blood ammonia greater decline. Conclusions Ammonia produced by the decomposition of HP urease in the stomach is one of the sources of ammonia in patients with cirrhosis. Eradication of HP can prevent and treat hepatic encephalopathy.