Helicobacter pylori in Ulcerogenesis

References

• Langenberg M L, Tytgat G NJ, Schipper M E, Rietra P JG, Zanen C. Campylobacter-like organisms in the stomach of patients and healthy individuals. Lancet 1984; 1: 1348–9
   PubMedGoogle Scholar
• Wyatt J I, Rathbone B J, Dixon M F, Heatley R V. Campylobacter pyloridis and acid-induced gastric metaplasia in the pathogenesis of duodenitis. J Clin Pathol 1987; 40: 841–8
   PubMed Web of Science ®Google Scholar
• Caselli M, Bovolenta M R, Aleotti E. Epithelial morphology of duodenal bulb and Campylobacter-like organisms. J Submicrosc Cytol, Pathol 1988; 20: 237–42
   PubMedGoogle Scholar
• Talley N J, Cameron A J, Shorter R G, Zinsmeister A R, Phillips S F. Campylobacter pylori and Barrett's esophagus. Mayo Clin Proc 1988; 63: 1176–80
   PubMed Web of Science ®Google Scholar
• DeCothi G A, Newbold K M, O'Connor H J. Campylobacter-like organisms and heterotopic gastric mucosa in Meckel's diverticula. J Clin Pathol 1989; 42: 132–4
   PubMed Web of Science ®Google Scholar
• Pambianco D J, Dye K R, Marshall B J, Frierson H F, MacMillan R H, Franquemont D, et al. Gastritis in the rectum: Campylobacter-like organisms in heterotopic inflamed gastric mucosa. Gastroenterology 1988; 94: A340
   Web of Science ®Google Scholar
• Wyatt J I, Rathbone B J, Heatley R V. Local immune response to gastric Campylobacter in non-ulcer dyspepsia. J Clin Pathol 1986; 38: 863–70
   Google Scholar
• Lam S K, Hasan M, Sircus W. Comparison of maximal acid output and gastrin response to meals in Chinese and Scottish normal and duodenal ulcer subjects. Gut 1981; 21: 324–8
   Web of Science ®Google Scholar
• Baron J H. The clinical application of gastric secretion measurements. Clin Gastroenterol 1973; 2: 293–341
   Google Scholar
• Card W I, Marks I N. The relationship between the acid output of the stomach following 'maximal' histamine stimulation and the parietal cell mass. Clin Sci 1960; 19: 47–63
   Web of Science ®Google Scholar
• Grossman M I, Kirsner J B, Gillespie I E. Basal and histalog-stimulated gastric secretion in control subjects and in patients with peptic ulcer or gastric cancer. Gastroenterology 1963; 45: 14–26
   PubMed Web of Science ®Google Scholar
• Isenberg J I, Grossman M I, Maxwell V, Walsh J H. Increased sensitivity to stimulation of acid secretion by pentagastrin in duodenal ulcer. J Clin Invest 1975; 55: 330–7
   PubMed Web of Science ®Google Scholar
• Lam S K, Isenberg J I, Grossman M I, Lane W H, Walsh J H. Gastric acid secretion is abnormally sensitive to endogenous gastrin released after peptone test meals in duodenal ulcer patients. J Clin Invest 1980; 65: 555–62
   PubMed Web of Science ®Google Scholar
• Blair A J, III, Feldman M, Barnett C, Walsh J H, Richardson C T. Detailed comparison of basal and food-stimulated gastric acid secretion rates and serum gastrin concentrations in duodenal ulcer patients and normal subjects. J Clin Invest 1987; 79: 582–7
   PubMed Web of Science ®Google Scholar
• Creutzfeldt W, Arnold R, Creutzfeldt C, Track N S. Mucosal gastrin concentration, molecular forms of gastrin, number and ultrastructure of G-cells in patients with duodenal ulcer. Gut 1976; 17: 745–54
   PubMed Web of Science ®Google Scholar
• Graham D Y, Opekun A, Lew G M, Evans D J, Jr, Klein P D, Evans D G. Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection. Am J Gastroenterol 1990; 95: 394–8
   Google Scholar
• McColl K EL, Fullarton G M, Chittajallu R. Plasma gastrin, daytime intragastric pH, and nocturnal acid output before and at 1 and 7 months after eradication of Helicobacter pylori in duodenal ulcer subjects. Scand J Gastroenterol 1991; 26: 339–46
   PubMed Web of Science ®Google Scholar
• Prewett E J, Smith J TL, Nwokolo C U. Eradication of Helicobacter pylori abolishes 24-hour hypergastrinaemia: a prospective study in healthy subjects. Aliment Pharmacol Ther 1991; 5: 283–90
   PubMed Web of Science ®Google Scholar
• Sievert W, Allwell L, Lambert J, Hansky J, Soveny C, Korman M. Gastrin release and acid secretion are a critical function of H. pylori infection. Gastroenterology 1994; 106: A180
   Web of Science ®Google Scholar
• Queiroz D MM, Mendes E N, Rocha G A. Effect of Helicobacter pylori eradication on antral gastrin- and somatostatin-immunoreactive cell density and gastrin and somatostatin concentrations. Scand J Gastroenterol 1993; 28: 858–64
   PubMed Web of Science ®Google Scholar
• Le A, Finlay M, Lambert J R, Savino R, Soveny C, Midolo P. Antral gastrin and somatostatin cells in Helicobacter pylori subjects: restitution of D cell number with eradication. Gastroenterology 1993; 104: A1046
   Web of Science ®Google Scholar
• Moss S F, Legon S, Bishop A E, Polak J M, Calam J. Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease. Lancet 1992; 340: 930–2
   PubMed Web of Science ®Google Scholar
• Golodner E H, Territo M C, Walsh J H, Soll A H. Stimulation of gastrin release from cultured canine G cells by Helicobacter pylori and mononuclear cells. Gastroenterology 1992; 102: A630
   Google Scholar
• Le A, Shulkes A, Lambert J R, Lin S K, Tipping P. Effect of tumour necrosis factor-alpha and bombesin on antral mucosal gastrin and somatostatin: influence of H. pylori infection. Gastroenterology 1993; 104: A1047
   Web of Science ®Google Scholar
• El-Omar E, Penman I, Ardill J ES, McColl K EL. The GRP test—a new clinical test of acid secretion—reproducibility data. Gut 1993; 34(Suppl 1)G13
   Google Scholar
• Peterson W L, Barnett C C, Evans D J, Jr, Feldman M, Crmody T, Richardson C, et al. Acid secretion and serum gastrin in normal subjects and patients with duodenal ulcer: the role of Helicobacter pylori. Am J Gastroenterol 1993; 88: 2038–43
   PubMed Web of Science ®Google Scholar
• Levi S, Beardshall K, Desa L A, Calam J. Campylobacter pylori, gastrin, acid secretion and duodenal ulcer. Lancet 1989; 2: 613
   PubMed Web of Science ®Google Scholar
• Montbriand J R, Appelman H D, Cotner E K, Nostrant T T, Elta G H. Treatment of Campylobacter pylori does not alter gastric acid secretion. Am J Gastroenterol 1989; 84: 1513–6
   PubMed Web of Science ®Google Scholar
• El-Omar E, Penman I, Dorrian C A, Ardill J ES, McColl K EL. Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer. Gut 1993; 34: 1060–5
   PubMed Web of Science ®Google Scholar
• McColl K E, El-Omar E. Effect of H. pylori infection on gastrin and gastric acid secretion. Helicobacter pylori: basic mechanisms to clinical cure, R H Hunt, G N Tytgat, 1994; 245–56
   Google Scholar
• Sonnenberg A, Townsend W F. Testing for Helicobacter pylori in the diagnosis of Zollinger-Ellison syndrome. Am J Gastroenterol 1991; 86: 606–8
   PubMed Web of Science ®Google Scholar
• Marshall B J, McGechie D B, Rogers P A, Clancy R J. Pyloric Campylobacter infection and gastroduodenal disease. Med J Aust 1985; 142: 439–44
   PubMed Web of Science ®Google Scholar
• Rauws E A, Langenberg W, Houthoff H J, Zanen H C, Tytgat G N. Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. Gastroenterology 1988; 94: 33–40
   PubMed Web of Science ®Google Scholar
• Jiang S J, Liu W Z, Zhang D Z, Shi Y, Xiao S D, Zhang Z H, et al. Campylobacter-like organisms in chronic gastritis, peptic ulcer, and gastric carcinoma. Scand J Gastroenterol 1987; 22: 553–8
   PubMed Web of Science ®Google Scholar
• Fiocca R, Villani L, Turpini R, Salcia E. High incidence of Campylobacter-like organisms in endoscopic biopsies from patients with gastritis with or without peptic ulcer. Digestion 1987; 38: 234–44
   PubMed Web of Science ®Google Scholar
• Carrick J, Daskalopoulos G, Hazell S. The role of Campylobacter pylori and gastric metaplasia in duodenal ulceration. Aust NZ J Med 1988; 18(Suppl 1)191
   Google Scholar
• Wyatt J I, Rathbone B J, Sobala G M, Shallcross T, Heatley R V, Axon A T, et al. Gastric epithelium in the duodenum: its association with Helicobacter pylori and inflammation. J Clin Pathol 1990; 43: 981–6
   PubMed Web of Science ®Google Scholar
• McConnell R B. Peptic ulcer: early genetic evidence—families, twins and markers. The genetics and heterogeneity of common gastrointestinal disorders, J I Rotter, I M Samloff, D L Rimoin. Academic Press, New York 1980; 31–41
   Google Scholar
• Roberts D F, Jackson R H, Cowan W K. Genetic of duodenal ulcer and gastric ulcer. Clin Gastroenterol 1973; 2: 539–46
   Google Scholar
• Rotter J I, Sones J Q, Samloff I M. Duodenal ulcer disease associated with elevated serum pepsinogen I: an inherited autosomal dominant disorder. N Engl J Med 1979; 300: 63–6
   PubMed Web of Science ®Google Scholar
• Malaty H M, Engstrand L, Pedersen N L, Graham D Y. Helicobacter pylori infection: genetic and environmental influences—a study of twins. Ann Intern Med 1994; 120: 982–6
   PubMed Web of Science ®Google Scholar
• Nomura A, Stemmermann G N, Chyou P H, Perez-Perez G I, Blaser M J. Helicobacter pylori infection and the risk for duodenal ulcer and gastric ulceration. Ann Intern Med 1994; 120: 977–81
   PubMed Web of Science ®Google Scholar
• Sipponen P, Vans K, Fraki O, Korri U M, Seppala K, Siurala M. Cumulative 10-year risk of symptomatic duodenal and gastric ulcer in patients with or without chronic gastritis. A clinical follow-up study of 454 outpatients. Scan J Gastroenterol 1990; 25: 966–73
   PubMed Web of Science ®Google Scholar
• Tytgat G NJ, Noach L A, Rauws E AJ. Helicobacter pylori infection and duodenal ulcer disease. Gastroenterol Clin North Am 1993; 22: 127–39
   PubMed Web of Science ®Google Scholar
• Martin D F, Montgomery E, Bobek A S, Patrissi G A, Peura D A. Campylobacter pylori NSAIDs and smoking risk factors for peptic ulcer disease. Am J Gastroenterol 1989; 84: 1268–72
   PubMed Web of Science ®Google Scholar
• Heresbach D, Raoul J L, Donnio P Y, Siproudhis L, Minet J. Helicobacter pylori: a risk and severity factor in NSAIDs induced gastropathy. Gastroenterology 1991; 100: A82
   PubMed Web of Science ®Google Scholar
• Katz B, Lambert J R, Nicholson L, Lin S K, Schembri M, Morand E, et al. Helicobacter pylori infection, upper gastrointestinal (UGI) symptoms and blood loss in patients with rheumatoid arthritis on NSAID. Gastroenterology 1991; 100: A96
   Google Scholar
• Louw J A, Falck V, van Rensburg C, Zak J, Adams G, Marks I N. Distribution of Helicobacter pylori colonisation and associated gastric inflammatory changes: differences between patients with duodenal and gastric ulcer. J Clin Pathol 1993; 46: 754–6
   PubMed Web of Science ®Google Scholar
• Cover T L, Dooley C P, Blaser M J. Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity. Infect Immun 1990; 58: 603–10
   PubMed Web of Science ®Google Scholar
• Murakami A, Yanai Tadam H. Effect of Helicobacter pylori on gastric mucosal blood flow. Proceedings of World Congresses of Gastroenterology. Sydney 1990
   Google Scholar
• Hazell S L, Lee A, Brady L, Hennessy W. Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium. J Infect Dis 1986; 153: 658–63
   PubMed Web of Science ®Google Scholar
• Bode G, Malfertheiner P, Ditschuneit H. Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease. Scand J Gastroenterol 1988, Suppl 142: 25–39
   Google Scholar
• Barer M R, Elliott T SJ, Berkeley D, Thomas J E, Eastham E J. Cytopathic effects of Campylobacter pylori urease. J Clin Pathol 1988; 41: 597
   PubMed Web of Science ®Google Scholar
• Hazell S L, Lee A. Campylobacter pyloridis, urease, hydrogenion back diffusion, and gastric ulcers. Lancet 1986; 2: 15–7
   PubMed Web of Science ®Google Scholar
• Levi S, Beardshall K, Haddad G, Playford R, Ghosh P, Calam J. Campylobacter pylori and duodenal ulcers: the gastrin link. Lancet 1989; 1: 1167–8
   PubMed Web of Science ®Google Scholar
• Chittajallu R S, Neithercut W D, Macdonald A MI, McColl K EL. Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. Gut 1991; 32: 21–4
   PubMed Web of Science ®Google Scholar
• Nujumi A ME, Dorrian C A, Chittajallu R S, Neithercut W D, McColl K EL. Effect of inhibition of H. pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. Gut 1991; 32: 866–71
   PubMed Web of Science ®Google Scholar
• Thomson L, Tasman-Yones L, Morris A, Wiggins P, Lee S, Forlong C. Ammonia produced by Campylobacter pylori neutralizes H+ moving through gastric mucus. Scand J Gastroenterol 1989; 24: 761–8
   PubMed Web of Science ®Google Scholar
• Thomson L, Tasman-Jones C, Morris A. Na+/H+ Ion-exchange property of postmortem luman gastric mucus. The effects of Campylobacter pylori infection and sucralfate. Scand J Gastroenterol 1989; 24: 781–6
   PubMed Web of Science ®Google Scholar
• Murakami M, Yoo J K, Inada M, Miyake T. Effect of ammonia on the gastric mucosa in rates: pathophysiological importance of urease in gastric ulcer disease. Jpn J Pharmacol 1988; 47: 330–2
   PubMedGoogle Scholar
• Hazell S L, Borody T J, Gal A, Lee A. Campylobacter pyloridis gastritis I: Detection of urease as a marker of bacterial colonization and gastritis. Am J Gastroenterol 1987; 82: 292–6
   PubMed Web of Science ®Google Scholar
• Parsons C L, Stauffer C, Mulholland S G, Griffith D P. Effect of ammonium on bacteria adherence to bladder transitional epithelium. J Urol 1984; 132: 365–6
   PubMed Web of Science ®Google Scholar
• Mai U E, Perez-Perez G I, Allen J B, Wahl S M, Blaser M J, Smith P D. Surface proteins from Helicobacter pylori exhibit chemotactic activity for human leukocytes and are present in gastric mucosa. J Exp Med 1992; 175: 517–25
   PubMed Web of Science ®Google Scholar
• Tee W, Lambert J R, Pegorer M, Dwyer B. Cytotoxin production by H. pylori more common in peptic ulcer disease. Gastroenterology 1993; 104: A789
   PubMedGoogle Scholar
• Figura N, Guglielmetti P, Rossolini A, Barberi A, Cusi G, Musmanno R A. Cytotoxin production by Campylobacter pylori strains isolated from patients with peptic ulcers and from patients with chronic gastritis only. J Clin microbiol 1989; 27: 225–6
   PubMed Web of Science ®Google Scholar
• Tummuru M KR, Cover T L, Blaser M J. Cloning and expression of a Hihg-Molecular-Mass major antigen of Helicobacter pylori: evidence of linkage to cytotoxin production. Infect Immun 1993; 61: 1799–809
   PubMed Web of Science ®Google Scholar
• Covacci A, Cenini S, Bugnoli M, Petracca R. Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci USA 1993; 90: 5791–5
   PubMed Web of Science ®Google Scholar
• Macchia G, Mssone A, Burroni D, Covacci A, Censini S, Rappuoli R. The Hsp60 protein of Helicobacter pylori: structure and immune response in patients with gastroduodenal diseases. Mol Microbiol 1993; 9: 645–52
   PubMed Web of Science ®Google Scholar
• Rautelin H, Blomberg B, Fredlund H, Jarnerot G, Danielsson D. Incidence of Helicobacter pylori strains activating neutrophils in patients with peptic ulcer disease. Gut 1993; 34: 599–603
   PubMed Web of Science ®Google Scholar
• Suzuki M, Miura S, Suematsu M, Fukumura D, Kurose I, Suzuki H, et al. Helicobacter pylori associated ammonia production enhances neutrophil-dependent gastric mucosal cell injury. Am J Physiol 1992; 263: G719–25
   PubMed Web of Science ®Google Scholar
• Yoshimura H H, Evans D G, Graham D Y. DNA-DNA hybridization demonstrates apparent genetic differences between Helicobacter pylori from patients with duodenal ulcer and asymptomatic gastritis. Dig Dis Sci 1993; 38: 1128–31
   PubMed Web of Science ®Google Scholar
• NIH Consensus Development Panel for Helicobacter pylori in peptic ulcer disease. Helicobacter pylori in peptic ulcer disease—NIH consensus conference. JAMA 1994; 272: 65–9
   PubMed Web of Science ®Google Scholar