Helicobacter pylori, hyperammonemia and subclinical portosystemic encephalopathy: effects of eradication

Citation
C. Vasconez et al., Helicobacter pylori, hyperammonemia and subclinical portosystemic encephalopathy: effects of eradication, J HEPATOL, 30(2), 1999, pp. 260-264
Citations number
34
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
JOURNAL OF HEPATOLOGY
ISSN journal
01688278 → ACNP
Volume
30
Issue
2
Year of publication
1999
Pages
260 - 264
Database
ISI
SICI code
0168-8278(199902)30:2<260:HPHASP>2.0.ZU;2-4
Abstract
Background/Aims: An involvement of Helicobacter pylori in the development o f 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 cirrho tic 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. py lori-positive patients (as diagnosed by rapid urease test and C-14-urea bre ath test) these parameters were reassessed 2 months following eradication t herapy. Results: In this series of non-advanced cirrhotic patients, the prevalence of H. pylori infection was 52%, No significant differences were observed be tween H. pylori+ and H. pylori- cases with respect to fasting venous blood ammonia concentration (47+/-24 vs 43+/-22 mu mol/l) or to the remaining par ameters assessing portosystemic encephalopathy. In addition, H. pylori erad ication failed to induce any significant variation in either fasting blood ammonia levels (from 45+/-23 to 48+/-26 mu mol/l) or neurologic disturbance s. Conclusion: These results indicate that H. pylori infection is not a major contributing factor to either fasting blood ammonia levels or parameters as sessing subclinical portosystemic encephalopathy in patients with non-advan ced liver cirrhosis.