One study showed a significant improvement in reflux disease-related quality of life scores one year after H. pylori eradication therapy [10]. In another study from the United States, 1611 cases of an African–American population with esophagitis and/or gastritis and confirmed H. pylori GS1101 status were included between 2004 and 2007 and compared with controls [11]. The prevalence of H. pylori in gastritis patients was 40%, in esophagitis patients 4%, and in normal controls 34%. After adjusting for age and gender, the odds ratio of H. pylori infection in the esophagitis group versus the normal group was 0.06 (95% CI 0.01−0.59; p = .01). They concluded that H. pylori has

a significant negative association with esophagitis in African–Americans, which may point to a protective role of H. pylori in the pathogenesis of esophagitis. In addition, another study on 2442 patients referred for upper gastrointestinal endoscopy observed H. pylori infection in 82% of GERD patients. A statistically significant relationship was found between H. pylori positivity and the grade of GERD [12]. In line with these observations, the updated Maastricht consensus on management of H. pylori infection concluded that H. pylori status has no effect on symptom severity, symptom recurrence, and treatment efficacy in GERD [7]. H. pylori eradication does not exacerbate pre-existing GERD nor

affect treatment efficacy. Therefore, the presence medchemexpress HKI-272 supplier of GERD should not dissuade to prescribe an H. pylori eradication treatment when otherwise indicated. Furthermore, long-term efficacy of PPI maintenance treatment for GERD is not influenced by H. pylori status [13]. Functional dyspepsia (FD) is currently

defined as symptoms of epigastric pain, epigastric burning, postprandial fullness, or early satiation, in the absence of any organic, systemic, or metabolic disease that is more likely to explain the symptoms [14]. This chronic, relapsing and remitting disorder is commonly seen in individuals from all around the world. Data from a large population-based study demonstrated no effect on life expectancy and no differences in the numbers of gastrointestinal related deaths between subjects with or without dyspepsia [15]. The exact role of H. pylori in FD is still under debate. Some investigators have argued that if H. pylori gastritis is considered an organic disease, H. pylori-associated FD should not be considered as a functional disorder [16, 17]. Possible mechanisms by which H. pylori may elicit dyspeptic symptoms include alterations of gastric motility, as well as endocrine and acid-secretory abnormalities [18]. Hunger sensations, acid secretion and gastrointestinal motility are regulated by ghrelin, particularly produced by the gastric enteroendocrine cell compartment [18]. Gastric infection with H. pylori is associated with decreased ghrelin secretion [19].