Abstract
Background and study aim: Ammonia plays a major role in hepatic encephalopathy pathogenesis. Most of ammonia is known to be produced by the action of colonic bacteria which possess a urease enzyme activity. H. pylori which infects the stomach possesses a stronger urease activity which produce a large amount of ammonia that may precipitate hepatic encephalopathy (HE). The aim of the present study is to determine the correlation between Helicobacter pylori infection and HE in patients with liver cirrhosis. Patients and Methods: One hundred patients (50 patients of liver cirrhosis with hepatic encephalopathy and 50 patients of liver cirrhosis without hepatic encephalo-pathy) were evaluated for presence of H. pylori by stool antigen test (ELISA method) and for blood ammonia level estimation. Results: Pevalence of H. pylori infection in the study groups (patients of liver cirrhosis with and without hepatic encephalopathy) was 70% (liver cirrhosis with hepatic encephalopathy group (A) 80%, and liver cirrhosis without hepatic encephalopathy group (B) 60%). Mean blood ammonia levels were: 82.14± 47.9 mmol/l for group A (liver cirrhosis with hepatic encephalopathy) and 36.44± 17.9 mmol/l for group B (liver cirrhosis without hepatic encephalopathy). Prevalence of H. pylori and blood ammonia level were found significantly increasing with the severity and the degree of hepatic encephalopathy. Conclusion: There is a significant association between H. pylori and hepatic encephalopathy in patients with liver cirrhosis. There may be a role of anti-H. pylori therapy in patients of hepatic encephalopathy and should be investigated further.
Highlights
Hepatic encephalopathy (HE) is a dangerous complication affecting patients with liver cirrhosis.The reversible nature of this neuropsychiatric syndrome with its widespread cerebral changes suggests a metabolic mechanism.The brain is exposed to several neuroactive toxins, in particular ammonia, due to failed hepatic clearance or the abnormal peripheral mechanisms of the cirrhotic [1]
All grades of hepatic encephalopathy were represented in hepatic encephalopathy group (A)
As regarding symptoms halitosis and heart burn were significantly higher in hepatic encephalopathy group (A) than non-hepatic encephalopathy group (B)
Summary
Hepatic encephalopathy (HE) is a dangerous complication affecting patients with liver cirrhosis.The reversible nature of this neuropsychiatric syndrome with its widespread cerebral changes suggests a metabolic mechanism.The brain is exposed to several neuroactive toxins, in particular ammonia, due to failed hepatic clearance or the abnormal peripheral mechanisms of the cirrhotic [1]. Bacterial urease enzyme contributes significantly to absorbed ammonia as a result of daily hydrolysis of 15-30% of total body urea [4]. This activity is usually attributed to faecal bacteria, the stomach, which possesses strong activity when infected with Helicobacter pylori, is considered as an alternative site. Most of ammonia is known to be produced by the action of colonic bacteria which possess a urease enzyme activity. H. pylori which infects the stomach possesses a stronger urease activity which produce a large amount of ammonia that may precipitate hepatic encephalopathy (HE). Prevalence of H. pylori and blood ammonia level were found significantly increasing with the severity and the degree of hepatic encephalopathy. There may be a role of anti-H. pylori therapy in patients of hepatic encephalopathy and should be investigated further
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