摘要
To study whether liver cirrhosis associated with Helicobacter pylori ( H pylori ) infection will induce increased serum ammonia and whether the peripheral serum ammonia reflects the level of portal vein serum ammonia Methods Blood was taken from the portal vein and the cubital vein in cirrhotic patients with and without H pylori infection and non cirrhotic patients (splenic rupture) with and without H pylori infection, and the serum ammonia was measured Results The mean levels of serum ammonia in the group of cirrhotic patients with H pylori infection were 167 82±8 97?μmol/L (portal vein) and 142 2±13 35?μmol/L (cubital vein) They were increased significantly as compared with cirrhotic patients without H pylori infection (47 68±12 03?μmol/L portal vein and 37 23±7 04?μmol/L cubital vein), and also compared with the groups of splenic rupture patients with and without H pylori infection ( P <0 01) There was no significant difference between the serum ammonia level of the cubital vein and portal vein ( P >0 05) Conclusions H pylori infection can induce an increase in serum ammonia in patients with liver dysfunction, and the peripheral serum ammonia measurement may replace the portal vein serum ammonia as a monitoring method Eradication of H pylori in cirrhotic patients may prevent hepatic encephalopathy (HE)
To study whether liver cirrhosis associated with Helicobacter pylori ( H pylori ) infection will induce increased serum ammonia and whether the peripheral serum ammonia reflects the level of portal vein serum ammonia Methods Blood was taken from the portal vein and the cubital vein in cirrhotic patients with and without H pylori infection and non cirrhotic patients (splenic rupture) with and without H pylori infection, and the serum ammonia was measured Results The mean levels of serum ammonia in the group of cirrhotic patients with H pylori infection were 167 82±8 97?μmol/L (portal vein) and 142 2±13 35?μmol/L (cubital vein) They were increased significantly as compared with cirrhotic patients without H pylori infection (47 68±12 03?μmol/L portal vein and 37 23±7 04?μmol/L cubital vein), and also compared with the groups of splenic rupture patients with and without H pylori infection ( P <0 01) There was no significant difference between the serum ammonia level of the cubital vein and portal vein ( P >0 05) Conclusions H pylori infection can induce an increase in serum ammonia in patients with liver dysfunction, and the peripheral serum ammonia measurement may replace the portal vein serum ammonia as a monitoring method Eradication of H pylori in cirrhotic patients may prevent hepatic encephalopathy (HE)
