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Serum leptin and body mass index in children with H pylori infection
  1. T Shimzu,
  2. Y Satoh,
  3. Y Yamashiro
  1. Department of Paediatrics, Juntendo University School of Medicine, Tokyo, Japan
  1. Correspondence to:
    T Shimzu;

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Leptin, a protein product of the obese gene expressed primarily by adipocytes, is known to regulate food intake, energy expenditure, and body weight homeostasis. Leptin has recently been detected in rat gastric mucosa,1 and elevated leptin levels have been found in the gastric mucosa of patients with Helicobacter pylori associated gastritis.2 In a study on the effect of H pylori infection on gastric leptin expression, Azuma et al (Gut 2001;49:324–9) demonstrated that gastric leptin may play a role in weight gain after eradication of H pylori infection. I read their article with great interest and would like to add a comment concerning serum leptin and body mass index (BMI). The authors showed a significant increase in gastric leptin expression in patients with H pylori infection, and a significant reduction in gastric leptin expression with a concomitant increase in BMI after successful eradication therapy. On the other hand, serum leptin levels did not change significantly after eradication of H pylori infection. We have also examined the effect of H pylori eradication on serum leptin levels and BMI in 15 children with H pylori infection.

The subjects were 15 children who presented at our hospital with anaemia and gastrointestinal symptoms such as abdominal pain and nausea, and were diagnosed with H pylori infection from a positive 13C urea breath test and histological and culture examinations of the gastric mucosa. There were seven boys and eight girls, ranging in age from 6.2 to 14.2 years (mean 10.6). H pylori eradication therapy was achieved with amoxicillin, clarithromycin, and lansoprazole twice daily for seven days. Two months after therapy, successful eradication of H pylori was confirmed by a negative 13C urea breath test and histological and culture examinations. Serum leptin levels and BMI were evaluated before and six months after eradication therapy. There were no significant differences in serum leptin levels or BMI before (6.10 (2.69) ng/ml and 17.9 (2.66) kg/m2, respectively) and after (6.92 (3.41) ng/ml and 18.6 (2.10) kg/m2, respectively) eradication of H pylori. However, serum leptin levels increased in 7/9 patients who showed an increase in BMI, and decreased in 5/6 patients who showed a decrease in BMI. There was a significant (p<0.01, r=0.796) positive correlation between serum leptin levels and BMI in patients after eradication of H pylori infection.

Given the concomitant change in serum leptin levels with change in BMI and the positive correlation between serum leptin and BMI in patients after successful eradication of H pylori infection, our results corroborate those of Azuma et al by clearly ruling out the effects of serum leptin on anorexia. However, in contrast with their results in adults, we did not observe an increase in BMI after eradication. While we did not examine gastric leptin expression, some differences in gastric leptin expression or the response to leptin between adults and children may help explain why BMI did not increase in children after successful eradication. Azuma et al suggest that gastric inflammation induced by H pylori infection raises the level of gastric leptin expression. On the other hand, the immunopathogenesis of H pylori associated gastritis in children is considered to be different from that in adults.3 This may account for the difference in gastric leptin expression between adults and children.


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