Previous studies on EE have shown that increased body mass index

Previous studies on EE have shown that increased body mass index (BMI), especially visceral fat, is associated with a higher prevalence of EE [41,42]. A cross-sectional study of 9840 Japanese men found that BMI and PI3K Inhibitor Library chemical structure triglycerides were predictors of an increased prevalence of EE (OR = 1.063 and 1.001; 95% CI = 1.020–1.108 and 1.001–1.002, p = .004 and p < .001 respectively), and H. pylori infection significantly and independently decreased the prevalence of EE (OR = 0.346, 95% CI = 0.299–0.401, p < .001) [43]. Weight gain following H. pylori eradication could possibly

increase the risk of GERD. A randomized controlled trial in the UK compared change in BMI in a group of H. pylori-infected patients randomized to eradication therapy versus placebo [44] and found more participants gained ≥3 kg in the intervention group (138/720, 19%) compared with the placebo group (92/706, 13%) [OR 1.57 (95% CI: 1.17, 2.12)]. Dyspepsia was less frequently reported by the intervention

group participants (168/736, 23%) versus placebo group 209/711, 29%), OR 0.71 (95% CI: 0.55, 0.93). Lane et al. suggested weight gain after H. pylori eradication might be due to Tyrosine Kinase Inhibitor Library resolution of dyspepsia. However, the increase in BMI following eradication therapy may also be due to the negative effects of H. pylori on circulating ghrelin levels, as discussed in a recent paper from Australia [45]. Ghrelin is one of the hormones secreted by the stomach and plays a central role in the neurohormonal regulation of food intake and energy homeostasis. It stimulates appetite and induces

apositive energy balance that can lead to weight gain. There is increasing interest in the relationship between H. pylori infection and gastric mucosal production of ghrelin and its octanoylation into ghrelin o-acyltransferase by the gastric enteroendocrine cells. The authors have declared no conflicts of interest. “
“The best opportunity to reduce gastric cancer (GC)-related mortality remains prevention. Mass eradication of Helicobacter pylori infection in a Taiwanese population >30 years of age reduced GC incidence with an effectiveness of 25% (rate ratio 0.753, 95% CI 0.372–1.524). medchemexpress In the Shandong intervention trial conducted on a Chinese population aged 35–64 years, cancer incidence was reduced by 39% in subjects who received H. pylori treatment compared with the placebo group after 14.7 years of follow-up (absolute risk 3.0 vs 4.6%; odds ratio 0.61, 95% CI 0.38–0.96; p = .03). A high incidence of severe gastric atrophic changes and noninvasive gastric neoplasia has been reported in a Portuguese case-control study on first-degree relatives of patients with early-onset gastric carcinoma (i.e., diagnosed before 45 years), which emphasizes again the importance of GC screening in this population. For patients with advanced GC, new targeted therapies to improve survival are under scrutiny.

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