title: Does Helicobacter pylori infection protect against esophageal diseases in Asia?
abstract: The speculations on the protective role of Helicobacter pylori against gastroesophageal reflux disease (GERD) originated from epidemiological observations. These studies have shown that the rising trend of GERD is coincident with declining prevalence of H. pylori and peptic ulcer disease in Asia. Furthermore, most case-control and population-based studies suggest a negative association between H. pylori infection and GERD. It is generally believed that the preponderance of cagA+ and vacA+ virulent strains and proinflammatory interleukin-1 beta polymorphism increase the risk of hypochlohydria and protects against the development of GERD in Asian population. Recovery of gastric acid secretion and emergence of reflux esophagitis has been reported after H. pylori eradication in patients with corpus gastritis and atrophic gastritis. Recent studies have also reported that H. pylori eradication leads to recovery of ghrelin secreting cells in the gastric corpus and a rise in plasma ghrelin levels, which may contribute to obesity through its appetite-stimulating action and predispose to GERD. The prevalence of H. pylori infection is generally lower in younger Asians who enjoy improved socioeconomic status and sanitation compared with their older counterparts. The Asian population is probably facing a rising generation with high gastric acid and ghrelin secretion rates. These physiological changes may contribute to increased dietary calorie intake, obesity and increased prevalence of GERD.
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China. justinwu@cuhk.edu.hk
authors.forename: Justin C Y
authors.initials: JC
authors.lastname: Wu
mesh_terms: D001208:Asia / Q000453:epidemiology; D005744:Gastric Acid / Q000378:metabolism*; D005764:Gastroesophageal Reflux / Q000453:epidemiology / Q000382:microbiology / Q000517:prevention & control*; D054439:Ghrelin / Q000097:blood / Q000378:metabolism*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D009765:Obesity / Q000382:microbiology / Q000503:physiopathology; D015995:Prevalence; D014774:Virulence
chemical_list: D054439:Ghrelin