Helicobacter Pylori Infection / Hepatic Encephalopathy InterRelationship before and after its Eradication

Abstract

Background and study aim: Helicobacter pylori (H. pylori) bacteria convert urea to ammonia, which has been implicated in causation of hepatic encephalopathy(HE) in patients with liver cirrhosis.The aim of this work was to assess the effect of helicobacter pylori infection and its eradication on hepatic encephalopathy. Patients and methods: From March 2010 to November 2011, in Tropical Medicine Department, Zagazig university Hospitals, 90 patients with grade 0-II hepatic encephalopathy were enrolled in the study. The patients diagnosed for hepatic encephalopathy using psychometric tests [number connection test (NCT), and circle connection test( CCT)] and Grading of the symptoms of hepatic encephalopathy was performed, they were evaluated for H. pylori infection (through detection of H. pylori stool Ag) , liver impairment, and blood ammonia concentration. A group of the H. pylori +ve patients were given eradication therapy (triple therapy: 1 wk therapy with omeprazole plus clarithromycin and tinidazole), then patients were revaluated after 2 months using psychometric tests and blood ammonia concentration and compared with untreated group. Results: In our study, the mean level of blood ammonia concentration was significantly higher in H. pylori-positive patients (group II and III: 78.1±9.36 and 82.73±12.22 mmol/L) in comparison to H. pylori-negative patients (group I: 65±17.47 mmol/L ) where P<0.001. Also the time needed to perform NCT and CCT show the lowest mean in H. pylori - negative patients (64.73±13.08 and 35.67±6.66 sec. respectively) in comparison to H. pylori- positive patients with statistically significant difference (P<0.001 for both tests). CCT was significantly reduced in treated and eradicated patients after therapy (30.46±4.9 sec) and shows statistically significant difference (P<0.001) in comparison to untreated or failed to eradicate groups. The blood ammonia concentration in patients with H pylori was significantly reduced after bacterium eradication compared with the concentration after conventional treatment to HE in H. pylori infected controls (49.04± 13.67 vs 61.17±9.81). However, blood ammonia level was reduced in those who received treatment and failed to eradicate in a significant difference from those who didn’t receive eradication therapy (infected controls) (61.17±9.81 vs 75±14.9). Also there was statistically significant difference as regard to hepatic encephalopathy grade pre- and post treatment in infected treated and eradicated group (P=0.04) while there was no statistically significant difference in infected controls or failed to eradicate groups. Conclusion: H pylori infection is an important factor for inducing high blood ammonia concentration in HE patients. Anti-H. pylori therapy results in reduction in blood ammonia levels and may be helpful for treatment and prevention of HE.