Efect of helicobacter pylori on urea/ammonia ratio in gastric juice and blood ammonia levels in patients with chronie liver diseases

ABSTRACT

Helicobacter pylori HP has high urease activity which enables it to hydrolyze gastric juice urea produciug ammonia. It has been proposed that infection with HP in patient with advanced liver disease may implicate an increased level of blood ammonia which have a non benign effect in the pathogenesis of hepatic encephalopathy. To investigate this hypothesis, the present work measured the blood ammonia and the urease activity of HP using Urea/ Ammonia ratio [U/A] in gastric juice of patients suffering from chronic liver disease associated with HP infection. Gastric juice aspiration, gastric biopsies and blood samples were taken from 27 patients with chronic liver disease and portal hypertension. Their liver affection was classified into Child A[14], Child B[6] and Child C [7]. The HP was identified using 3 kinds of tests, rapid urease, rapid latex and enzyme Immunoassay tests. The intragastric and blood ammonia levels were measured by an ultraviolet method, gastric urea was determined using an enzymatic method. It was found that all patients harboured HP organism, the ammonia levels correlated with the severity of the liver affection [p<0.01]. Comparing the mean ammonia levels of the severest stage of liver disease [Child C] with the mild stage [Child A], it showed a high significant mean value in both the blood and gastric juice [p<0.01], The moderate stage [Child B] had its mean ammonia values higher than Child A, but it was only the blood level which was significantly higher [p<0.05]. U /A ratio in gastric juice were 1.1, 0.6 and 0.4 in Child A, B and C respectively, showing statistical significant decrease between Child B and C when compared with Child A group [p<0.01]. U/A ratio in gastric juice may be a good indicator of HP infection and related to the Child score. It was concluded that due to HP infection there is an increased urease enzyme production leading to increased ammonia intragastrically. This may have a local damaging effect on the gastric mucosa. There is also an increased absorption and accumulation of ammonia in the blood of patients with chronic liver disease, as a result of liver decompensation. Thus eradication of HP infection in these patients may minimize the development of complications and decrease the incidence of encephalopathy