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Helicobacter pylori infection induces hyperammonaemia in Mongolian gerbils with liver cirrhosis
  1. H Sutoa,
  2. T Azumaa,
  3. S Itoa,
  4. M Ohtania,
  5. M Dojoa,
  6. Y Itoa,
  7. Y Kohlib,
  8. M Kuriyamaa
  1. aSecond Department of Internal Medicine, Faculty of Medicine, Fukui Medical University, Fukui, Japan, bDepartment of Internal Medicine, Aiseikai Yamashina Hospital, Kyoto, Japan
  1. Dr T Azuma, Second Department of Internal Medicine, Faculty of Medicine, Fukui Medical University, 23-3 Shimoaizuki, Matsuoka-cho, Yoshida-gun, Fukui 910-1193, Japan. azuma{at}fmsrsa.fukui-med.ac.jp

Abstract

BACKGROUND AND AIMS We previously reported the effect of Helicobacter pylori eradication on hyperammonaemia in patients with liver cirrhosis. However, the role of H pylori as a cause of hyperammonaemia is controversial. We developed an animal model with liver cirrhosis and investigated the effect ofH pylori infection on hyperammonaemia.

MATERIALS AND METHODS Five week old male Mongolian gerbils were inoculated orally with broth culture of H pylori. Forty eight gerbils were divided into four groups. Gerbils not inoculated with H pylori were fed a commercial rodent diet (group A) or a choline deficient diet (group C). Gerbils inoculated with H pyloriwere fed the commercial rodent diet (group B) or the choline deficient diet (group D). Blood ammonia levels of the femoral vein and portal vein were measured 30 weeks later.

RESULTS All gerbils fed the choline deficient diet developed liver cirrhosis with fatty metamorphosis. The survival rate of group D was significantly lower than that of the other groups. Systemic and portal blood ammonia levels in group D were significantly higher than those in the other groups.

CONCLUSIONS H pylori infection induces hyperammonaemia in gerbils with liver cirrhosis.

  • Helicobacter pylori
  • hyperammonaemia
  • liver cirrhosis
  • Mongolian gerbil
  • hepatic encephalopathy
  • choline deficient diet

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