Post Helicobacter pylori Gastric Diseases
A variety of researches have been focused on Helicobacter pylori (H. pylori) in gastroenterological field, and H. pylori has been recognized as etiologically responsible for gastritis-associated peptic ulcers and the majority of gastric cancers. The incidence rate of H. pylori infection is higher in Asian countries including Japan than in Western countries. However, past natural circumstances in Japan suitable for an inhabiting of H. pylori have been improved in parallel with the sanitary developments. In addition, the eradication therapy has been permitted with national insurance to most patients with H. pylori infection in 2013. As a result, the present infection rate is gradually decreasing. Based on the above surrounding environment, an age-depending decrease in acid secretion due to mucosal atrophy caused by chronic H. pylori infection is recently lacking. Therefore, certain acid secretion is continuously maintained with no age relationship. Accordingly, most Japanese physicians must switch their focus to the acid-related diseases (H. pylori-non-associated diseases) from the H. pylori-associated diseases throughout the entire generations.
As post H. pylori gastric diseases, this part will give the information about (1) H. pylori-negative mucosal injury excluding gastric cancer because it is introduced in the next chapter, (2) functional dyspepsia whose pathophysiology is in part associated with mucosal sensitivity to acid exposure, and (3) association of non-alcoholic fatty liver disease with gastroesophageal diseases.
KeywordsAcid secretion Chemical sensitivity Functional disorders Metabolic syndrome
- 5.International Agency for Research on Cancer, World Health Organization. Schistosomes, liver flukes and Helicobacter pylori. IARC Monogr Eval Carcinog Risks Hum. 1994;61:177–241.Google Scholar
- 6.International Agency for Research on Cancer. Helicobacter pylori. Biologic agents: a review of human carcinogens, vol. 100B. Leon: International Agency for Research on Cancer; 2012. p. 385–435.Google Scholar
- 14.Hawkey CJ, Tulassay Z, Szczepanski L, van Rensburg CJ, Filipowicz-Sosnowska A, Lanas A, et al. Randomised controlled trial of Helicobacter pylori eradication in patients on non-steroidal anti-inflammatory drugs: HELP NSAIDs study. Helicobacter eradication for lesion prevention. Lancet. 1998;352:1016–21.CrossRefGoogle Scholar
- 15.de Leest HT, Steen KS, Lems WF, Bijlsma JW, van de Laar MA, Huisman AM, et al. Eradication of Helicobacter pylori does not reduce the incidence of gastroduodenal ulcers in patients on long-term NSAID treatment: double-blind, randomized, placebo-controlled trial. Helicobacter. 2007;12:477–85.CrossRefGoogle Scholar
- 26.Moayyedi P, Soo S, Deeks J, Delaney B, Innes M, Forman D. Pharmacological interventions for non-ulcer dyspepsia. Cochrane Database Syst Rev. 2006;(5):178–85.Google Scholar
- 30.Sakurai K, Nagahara A, Inoue K, Akiyama J, Mabe K, Suzuki J, et al. Efficacy of omeprazole, famotidine, mosapride and teprenone in patients with upper gastrointestinal symptoms: an omeprazole-controlled randomized study (J-FOCUS). BMC Gastroenterol. 2012;12:42. https://doi.org/10.1186/1471-230X-12-42.CrossRefPubMedPubMedCentralGoogle Scholar
- 36.Fujikawa Y, Tominaga K, Fujii H, Machida H, Okazaki H, Yamagami H, et al. High prevalence of gastroesophageal reflux symptoms in patients with non-alcoholic fatty liver disease associated with serum levels of triglyceride and cholesterol but not simple visceral obesity. Digestion. 2012;86:228–37.CrossRefGoogle Scholar
- 37.Ledeboer M, Mascle AAM, Biemond I, Lamers CBHW. Effect of medium- and long-chain triglycerides onlower esophageal sphincter pressure: role of CCK. Am J Phys. 1998;274:1160–5.Google Scholar