title: Helicobacter pylori and plasma ammonia levels in cirrhotics: role of urease inhibition by acetohydroxamic acid.
abstract: OBJECTIVE
  The role of Helicobacter pylori as a cause of hyperammonaemia in cirrhotics has still not been fully clarified. This study was aimed at evaluating the effect of acute Helicobacter pylori urease inhibition by oral acetohydroxamic acid administration on blood ammonia levels in cirrhotic patients.
  
  
  METHODS
  Twenty-nine cirrhotics (14 males, 15 females; mean age: 63 years; Child-Pugh class: 14 A, 9 B, and 6 C) undergoing upper gastrointestinal endoscopy were enrolled in the study. The presence of Helicobacter pylori infection was assessed by rapid urease test and histology. A semi-quantitative grading of bacterial density was also performed at histology. All patients received oral acetohydroxamic acid 750 mg, and blood samples for assessment of ammonia levels were taken before and at 15, 30, 60 and 90 minutes after administration.
  
  
  RESULTS
  Helicobacter pylori infection was detected in 20 patients, while 9 patients were uninfected. Acetohydroxamic acid administration led to a significant reduction in blood ammonia levels at 15 and 30 minutes (mean +/- SD, 113 +/- 44 vs 101 +/- 43 and 93 +/- 38 micrograms/dl, respectively; p = 0.002) only in patients with Helicobacter pylori infection. Moreover, the reduction was statistically significant only in Child-Pugh B/C class patients and in those with moderate/marked Helicobacter pylori density in gastric mucosa. Basal ammonia levels did not differ between Helicobacter pylori positive and negative patients, nor in patients with mild and moderate/marked Helicobacter pylori density in gastric mucosa, while Child-Pugh class B/C cirrhotics had higher basal ammonia levels than class A cirrhotics, in both Helicobacter pylori positive and negative groups.
  
  
  CONCLUSIONS
  Our data showed that Helicobacter pylori urease inhibition by acetohydroxamic acid administration significantly reduces blood ammonia levels in patients with more advanced liver cirrhosis and in those with a high bacterial density in gastric mucosa.
authors.affiliation: Department of Clinical Medicine, Gastroenterology II, University of Rome La Sapienza, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Zullo
authors.forename: V
authors.initials: V
authors.lastname: Rinaldi
authors.forename: C
authors.initials: C
authors.lastname: Hassan
authors.forename: S
authors.initials: S
authors.lastname: Folino
authors.forename: S
authors.initials: S
authors.lastname: Winn
authors.forename: G
authors.initials: G
authors.lastname: Pinto
authors.forename: A F
authors.initials: AF
authors.lastname: Attili
mesh_terms: D000368:Aged; D000641:Ammonia / Q000097:blood* / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology; D016481:Helicobacter Infections / Q000175:diagnosis; D016480:Helicobacter pylori / Q000378:metabolism*; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology*; D008103:Liver Cirrhosis / Q000097:blood / Q000382:microbiology*; D008297:Male; D008875:Middle Aged; D018709:Statistics, Nonparametric; D014510:Urease / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D006877:Hydroxamic Acids; D000641:Ammonia; D014510:Urease