Published online Jan 21, 2018. doi: 10.3748/wjg.v24.i3.397
Peer-review started: November 4, 2017
First decision: November 14, 2017
Revised: November 30, 2017
Accepted: December 4, 2017
Article in press: December 4, 2017
Published online: January 21, 2018
The stomach participates in the production of ghrelin and leptin, two important neuroendocrine hormones in food intake modulation. Helicobacter pylori (H. pylori) infection has been associated with several pathologies affecting the gastroduodenal mucosa, for which reason it would be important to find out whether it could alter circulating levels of these hormones and ultimately, the body mass index (BMI).
Although the influence of H. pylori infection on the hormonal regulation of food intake has been addressed lately, the results are controversial.
The present study aimed to evaluate the relationship between H. pylori infection, cagA genotype, type of gastric pathology, serum ghrelin and leptin concentrations and nutritional status in patients with gastrointestinal symptoms.
This cross-sectional study included fasted dyspeptic adults (18-70 y) referred for an upper digestive endoscopy. We conducted a survey for sociodemographic variables evaluation and a 24 h dietary recall for food intake estimation. H. pylori status was determined by three methods: histological analysis, PCR amplification of the vacA constitutive H. pylori gene and 13C -Urea Breath Test. Total ghrelin and leptin serum concentrations were measured by enzyme-linked immunosorbent assay and enzyme amplified sensitivity immunoassay respectively. During an upper gastrointestinal endoscopy, four gastric biopsies were obtained. One sample of each gastric site was used for histological assessment and the others for PCR amplification of H. pylori vacA and cagA genes. Statistical analysis was performed using χ2, Mann-Whitney U, Kruskal-Wallis tests, Spearman’s correlation and linear regression.
Prevalence of persistent H. pylori infection was 53.4% (95%CI: 45.7%-65.8%) in our population of 163 adults. Mean age was 40.8 ± 14.0 years, and 98 (60.1%) were female. Nutrient intake did not differ significantly between H. pylori positive and negative patients, neither did BMI. We observed significantly lower serum ghrelin levels in infected patients [median 311.0 pg/mL (IQR 230.0-385.5)] than in uninfected ones [median 355.0 pg/mL (IQR 253.8-547.8)] (P = 0.025), even after adjusting for BMI and gender (P = 0.03). A tendency towards lower ghrelin levels could be detected from antrum and corpus cagA positive patients; however, differences with cagA negative patients did not reach statistical significance (P = 0.50 and P = 0.49, respectively). Lower serum ghrelin concentration was associated with the type and severity of gastric pathology in the corpus (P = 0.04), independently of H. pylori status. Serum leptin levels did not differ significantly between H. pylori positive and negative patients [median 1.84 ng/mL (0.80-4.85) vs 1.84 ng/mL (0.50 - 5.09), (P = 0.51)].
Our study demonstrated that H. pylori infection and the severity of gastric pathology of the corpus are associated with lower ghrelin serum concentrations. We also observed lower, but not significantly different ghrelin levels in patients carrying cagA positive strains, an observation that should be evaluated further in future studies.
Our conclusions highlight the importance of investigating the effect of H. pylori eradication on ghrelin circulating levels regarding the genotype of infecting strains.