A recent study showed a higher prevalence of the infection in obese patients living in the Istanbul area [73]. Specific IgG were detected in 57.2% of patients and 27.0% of controls matched for age and socioeconomic

status (OR = 2.1). Unpublished data from a member of our group (NF) showed similar ratios of infection in obese patients and in controls (approximately 45%); furthermore, Paclitaxel cell line the ghrelin levels were significantly reduced in infected obese patients with CagA serum antibodies. The role of H. pylori infection in such disorders has not been completely defined. In a large, population-based cohort in the USA, no association was established between H. pylori status and BMI [74]. A recent study demonstrated that gastric and systemic ghrelin concentrations depend on the presence and extension of gastric mucosal atrophy [75]; therefore, our observation that ghrelin levels diminished in cases of infection by strains expressing CagA may simply reflect the likely development of gastric mucosal atrophy in the patients infected by CagA-positive H. pylori. The question becomes

even more complicated considering the results of a recent study performed on middle-aged Polish patients with dyspepsia and without gastric mucosa atrophy, which showed that ghrelin mucosal concentrations selleck kinase inhibitor were increased in H. pylori-infected women, independently of the cagA status. Similar observations were made in male patients, but only for samples taken from the antral mucosa [76]. In conclusion, taking into consideration the fact that many factors may influence the local and systemic levels of ghrelin and consequently the development of obesity, i.e. H. pylori infection, Atazanavir the genotype of the infecting organism, the patient’s gender and age, the presence of gastric mucosa atrophy, and the gastric areas from which the biopsies are taken

– three different major hypothetical scenarios can be delineated: 1, in countries with an intense circulation of CagA-positive H. pylori, such as Asia, Japan, and Central America, the corpus atrophy which occurs frequently and early in life destroys ghrelin-producing cells and contributes to a decrease in appetite: thus, infected people are slim; 2, in Western countries, in the absence of infection and consequent gastric atrophy, GR cells are spared and levels of ghrelin are elevated, which favors the development of obesity; 3, intermediate conditions are characterized by a moderate prevalence of H. pylori infection, such as those observed in Poland and Italy. In these areas, what makes the difference is the degree of circulation of strains harboring cagA (and most likely also the types of the host’s inflammatory cytokines). If the spread of CagA-positive H.