Gastric exocrine and endocrine cell morphology under prolonged acid inhibition therapy: results of a 5‐year follow‐up in the LOTUS trial

Sustained acid inhibition with PPI stimulates gastrin secretion, exerting a proliferative drive on enterochromaffin‐like cells (ECL cells) of the oxyntic mucosa. It may also accelerate development of gastric gland atrophy in Helicobacter pylori‐infected individuals.

[1]  C. Ell,et al.  Laparoscopic antireflux surgery vs esomeprazole treatment for chronic GERD: the LOTUS randomized clinical trial. , 2011, JAMA.

[2]  H. El‐Serag,et al.  Gastric histology in children treated with proton pump inhibitors long term, with emphasis on enterochromaffin cell‐like hyperplasia , 2011, Alimentary pharmacology & therapeutics.

[3]  H. Sugihara,et al.  Long-term proton pump inhibitor administration worsens atrophic corpus gastritis and promotes adenocarcinoma development in Mongolian gerbils infected with Helicobacter pylori , 2010, Gut.

[4]  David C. Metz,et al.  Safety of proton pump inhibitor exposure. , 2010, Gastroenterology.

[5]  M. Zoli,et al.  Adverse effects of proton pump inhibitors. , 2010, Best practice & research. Clinical gastroenterology.

[6]  R. Wong,et al.  Chronic Proton Pump Inhibitor Therapy Associated with Increased Development of Fundic Gland Polyps , 2009, Digestive Diseases and Sciences.

[7]  C. Ell,et al.  Comparing laparoscopic antireflux surgery with esomeprazole in the management of patients with chronic gastro-oesophageal reflux disease: a 3-year interim analysis of the LOTUS trial , 2008, Gut.

[8]  C. Ell,et al.  Standardization of Surgical Technique in Antireflux Surgery: The LOTUS Trial Experience , 2008, World Journal of Surgery.

[9]  T Rokkas,et al.  Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report , 2006, Gut.

[10]  H. Boezen,et al.  Increased risk of fundic gland polyps during long‐term proton pump inhibitor therapy , 2006, Alimentary pharmacology & therapeutics.

[11]  L. Lundell,et al.  Changes of gastric mucosal architecture during long‐term omeprazole therapy: results of a randomized clinical trial , 2006, Alimentary pharmacology & therapeutics.

[12]  M. Rugge,et al.  Gastric mucosal atrophy: interobserver consistency using new criteria for classification and grading , 2002, Alimentary pharmacology & therapeutics.

[13]  D. Jonkers,et al.  Serum chromogranin A as a screening test for gastric enterochromaffin‐like cell hyperplasia during acid‐suppressive therapy , 2001, European journal of clinical investigation.

[14]  B. Hirschowitz,et al.  Helicobacter pylori effects on gastritis, gastrin and enterochromaffin‐like cells in Zollinger–Ellison syndrome and non‐Zollinger–Ellison syndrome acid hypersecretors treated long‐term with lansoprazole , 2001, Alimentary pharmacology & therapeutics.

[15]  E. Kuipers,et al.  Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment. , 2000, Human pathology.

[16]  Walsh,et al.  Review article: potential gastrointestinal effects of long‐term acid suppression with proton pump inhibitors , 2000, Alimentary pharmacology & therapeutics.

[17]  J. Dent,et al.  Long-term omeprazole treatment in resistant gastroesophageal reflux disease: efficacy, safety, and influence on gastric mucosa. , 2000, Gastroenterology.

[18]  C. Larkin.  Distribution of Atrophy in Helicobacter pylori-Infected Subjects Taking Proton Pump Inhibitors , 2000, Scandinavian Journal of Gastroenterology.

[19]  Brenna,et al.  Personal review: is profound acid inhibition safe? , 2000, Alimentary pharmacology & therapeutics.

[20]  L. Lundell,et al.  Lack of effect of acid suppression therapy on gastric atrophy. Nordic Gerd Study Group. , 1999, Gastroenterology.

[21]  Stolte,et al.  Changes in Helicobacter pylori‐induced gastritis in the antrum and corpus during 12 months of treatment with omeprazole and lansoprazole in patients with gastro‐oesophageal reflux disease , 1998, Alimentary pharmacology & therapeutics.

[22]  J. Rehfeld,et al.  Basal chromogranin A and gastrin concentrations in circulation correlate to endocrine cell proliferation in type-A gastritis. , 1997, Scandinavian journal of gastroenterology.

[23]  B. Simon,et al.  Gastric mucosa during treatment with lansoprazole: Helicobacter pylori is a risk factor for argyrophil cell hyperplasia. , 1997, Gastroenterology.

[24]  E. Kuipers,et al.  Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. , 1996, The New England journal of medicine.

[25]  E. Kuipers,et al.  Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: implications for long-term safety. , 1995, The American journal of gastroenterology.

[26]  C. Pusey,et al.  Long-term sequelae of Helicobacter pylori gastritis , 1995, The Lancet.

[27]  J. Elder,et al.  Effects of acid suppression on microbial flora of upper gut , 1995, Digestive Diseases and Sciences.

[28]  J. H. Baron,et al.  Changes in the intragastric distribution of Helicobacter pylori during treatment with omeprazole. , 1995, Gut.

[29]  N. Muñoz,et al.  Intestinal metaplasia types and the risk of gastric cancer: A cohort study in Slovenia , 1994, International journal of cancer.

[30]  R. Fiocca,et al.  Cytotoxicity of Helicobacter pylori on human gastric epithelial cells in vitro: role of cytotoxin(s) and ammonia , 1993 .

[31]  P. Hui,et al.  Modes of Helicobacter colonization and gastric epithelial damage , 1992, Histopathology.

[32]  M. Suzuki,et al.  Helicobacter pylori-associated ammonia production enhances neutrophil-dependent gastric mucosal cell injury. , 1992, The American journal of physiology.

[33]  G. Dockray,et al.  Functional control of chromogranin A and B concentrations in the body of the rat stomach , 1992, Regulatory Peptides.

[34]  H. Fusamoto,et al.  Mechanism of gastric mucosal damage induced by ammonia. , 1992, Gastroenterology.

[35]  A. Price.  The Sydney System: Histological division , 1991, Journal of gastroenterology and hepatology.

[36]  N. Havu,et al.  Partial gastric corpectomy results in hypergastrinemia and development of gastric enterochromaffinlike-cell carcinoids in the rat. , 1991, Gastroenterology.

[37]  F. Sundler,et al.  Mechanisms for the Development of Gastric Carcinoids: International Symposium, Mlndal, Sweden, February 1985: Proceedings , 1986 .

[38]  S. Broitman,et al.  Gastric acid barrier to ingested microorganisms in man: studies in vivo and in vitro , 1972, Gut.

[39]  P. Correa,et al.  Carcinoma and intestinal metaplasia of the stomach in Colombian migrants. , 1970, Journal of the National Cancer Institute.

[40]  M. Shiner,et al.  Influence of gastric pH on gastric and jejunal flora. , 1967, Gut.

[41]  Georg Schilffarth.  Duodenalkolonfistel bei Krebs des Colon ascendens , 1925 .

[42]  R. Jensen,et al.  Consequences of long-term proton pump blockade: insights from studies of patients with gastrinomas. , 2006, Basic & clinical pharmacology & toxicology.

[43]  E. Kuipers,et al.  EVect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy , 2000 .

[44]  M. Stolte,et al.  Lack of effect of acid suppression therapy on gastric atrophy. , 2000, Gastroenterology.

[45]  R. Stockbrügger,et al.  Bacteria in the aetio-pathogenesis of gastric cancer: a review. , 1995, Scandinavian journal of gastroenterology. Supplement.

[46]  C. Spirig,et al.  Bactericidal factors in gastric juice , 1992 .

[47]  E. Solcia,et al.  Qualitative studies of gastric endocrine cells in patients treated long-term with omeprazole. , 1989, Scandinavian journal of gastroenterology. Supplement.

[48]  W. Creutzfeldt.  The achlorhydria-carcinoid sequence: role of gastrin. , 1988, Digestion.

[49]  R. Stockbruegger.  Bacterial overgrowth as a consequence of reduced gastric acidity. , 1985, Scandinavian journal of gastroenterology. Supplement.

[50]  C. Bordi,et al.  Pathology of endocrine cells in gastric mucosa. , 1983, Annales de pathologie.

[51]  B. Drasar,et al.  Studies on the intestinal flora. I. The bacterial flora of the gastrointestinal tract in healthy and achlorhydric persons. , 1969, Gastroenterology.