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World J Gastroenterol. Mar 28, 2008; 14(12): 1914-1918
Published online Mar 28, 2008. doi: 10.3748/wjg.14.1914
Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients
Shu-Jie Chen, Liang-Jing Wang, Qin Zhu, Jian-Ting Cai, Tao Chen, Jian-Min Si
Shu-Jie Chen, Qin Zhu, Jian-Min Si, Department of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, Zhejiang Province, China
Liang-Jing Wang, Jian-Ting Cai, Tao Chen, Department of Gastroenterology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
Author contributions: Chen SJ and Wang LJ contributed equally to this work.
Correspondence to: Liang-Jing Wang, Department of Gastro-enterology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China. wanglj2001@tom.com
Telephone: +86-571-86006788
Fax: +86-571-86006788
Received: October 24, 2007
Revised: December 30, 2007
Published online: March 28, 2008

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 &mgr;mol/L, respectively (P < 0.01), which was significantly reduced to 53.5 ± 37.7 &mgr;mol/L after bacterium eradication (n = 126) (P < 0.01). Blood ammonia was 97.5 ± 81.0 &mgr;mol/L in H pylori-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 &mgr;mol/L), SHE (59.9 ± 49.2 &mgr;mol/L), and without HE (47.3 ± 33.5 &mgr;mol/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.

Keywords: Cirrhosis, Helicobacter Pylori, Hepatic encephalopathy, Hyperammonemia