Abstract
Before the importance of H. pylori was realized, gastric acid was thought to be the main cause of duodenal ulcers (DU). This was rational because DU patients secrete more acid than controls and suppression of acid both heals and prevents ulcers. At present we know that H. pylori causes DU, but it is not clear how it does so. Recent work shows that H. pylori causes some of the abnormalities of acid secretion previously described in DU disease. Thus H. pylori might produce ulcers by increasing acid secretion. Research has also revealed abnormalities of gastrin and somatostatin physiology which probably underlie the altered acid secretion. This chapter will first summarize the abnormalities of acid secretion and gastrin in DU disease and then describe the extent to which these are explained by H. pylori infection.
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References
Moss SF, Calam J. itHelicobacter pylori and peptic ulcers: the present position. Gut. 1992;33:289–292.
Soll AH. Duodenal ulcer and drug therapy. In: Sleisenger MH, Fordrtan JS, editors. Gastrointestinal disease, 4th edn. Philadelphia: W.B. Saunders; 1989:814–879.
Aoyogi T, Summerskill WH. Gastric secretion with ulcerogenic islet cell tumour: importance of basal acid output. Arch Intern Med. 1966;117:667–672.
Moss S, Ayesu K, Calam J. Gastrin and gastric acid output 1 year after eradication of Helicobacter pylori in duodenal ulcer patients. Regul Pept. 1991;35:251.
Kekki M, Sipponen P, Siurala M. Progression of antral and body gastritis in active and healed duodenal ulcer and duodenitis. Scand J Gastroenterol. 1984;19:382–388.
Kaneko H, Nakada K, Mitsuma T et al. H. pylori infection induces a decrease in immunoreactive-somatostatin concentrations of the human stomach. Dig Dis Sci. 1992;37:409–416.
Blair AJ, Feldman M, Barnett C et al. 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;79:582–587.
Walsh JH, Richardson CT, Fordtran JS. pH dependence of acid secretion and gastrin release in normal and ulcer subjects. J Clin Invest. 1975;55:462–468.
Taylor IL, Calam J, Rotter J et al. Family studies of hypergastrinaemic, hyperpepsinogenemic I duodenal ulcer disease. Ann Intern Med. 1981;95:421–425.
Hirchowitz BI, Tim LO, Helman CA et al. Bombesin and G-17 dose responses in duodenal ulcer and controls. Dig Dis Sci. 1985;10:1092–1103.
Levi S, Beardshall K, Playford R et al. Campylobacter pylori and duodenal ulcers: the gastrin link. Lancet. 1989;i: 1167–1168.
Beardshall K, Moss S, Gill J et al. Suppression of Helicobacter pylori reduces gastrin releasing peptide stimulated gastrin release in duodenal ulcer patients. Gut. 1992;33:601–603.
Kovaks TOG, Sytnik B, Calam J et al. Helicobacter pylori infection impairs pH inhibition in non-duodenal ulcer subjects. Gastroenterology. 1993;104:A123.
Cave DR, Vargas M. Effect of a Campylobacter pylori protein on acid secretion by parietal cells. Lancet. 1989;ii:187–189.
Hunt RH. Campylobacter pylori and spontaneous hypochlorhydria. In: Rathbone BJ, Heatley RV, editors. Campylobacter pylori and gastroduodenal disease. London: Blackwell Scientific; 1989:176–184.
Negrini R, Lisatolo L, Zanelli I et al. Helicobacter pylori infection induces antibodies cross reacting with human gastric mucosa. Gastroenterology. 1991;101:437–446.
Moss SF, Calam J. Acid secretion and sensitivity to gastrin in duodenal ulcer patients: effect of eradicating the organism. Gut. 1993;34:888–892.
El-Omar E, Penman I, Dorrian CA et al. Eradicating Helicobacter pylori infection lowers gastrin-mediated acid secretion by two-thirds in duodenal ulcer patients. Gut. 1993;34: 1060–1065
Moss S, Ayesu K, Li SK et al. Gastrin, gastric acid and pepsin responses during intragastric titration in duodenal ulcer patients: effect of suppressing Helicobacter pylori. Gut. 1991;32:A1206–1207.
Yamada T, Chiba T. Somatostatin. In: Schultz SG, Makhlouf GM, Rauner BB, editors. Handbook of physiology, section 6, vol. II, Bethesda, Maryland: American Physiological Society; 1989:431–453.
Moss SF, Legon S, Bishop AE et al. Effects of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease. Lancet. 1992;340:930–932.
El Nujumi AM, Dorrian CA, Chitajallu RS et al. Effect of inhibition of H. pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. Gut. 1991;32:866–870.
Beardshall K, Adamson D, Gill J et al. Helicobacter pylori raises the pH of the juxta epithelial region of the mucus layer of the gastric antrum and body. Gut. 1991;32: A569–570.
Golodner EH, Soll AH, Walsh JH et al. Release of gastrin from cultured canine G-cells by interferon-γ and tumour necrosis factor-α. Gastroenterology. 1993;104:A89.
Blaser MJ. Hypothesis on the pathogenesis and natural history of Helicobater pylori induced inflammation. Gastroenterology. 1992;102:720–727.
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Calam, J. (1993). Acid secretion. In: Northfield, T., Mendall, M., Goggin, P.M. (eds) Helicobacter pylori Infection. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-2216-0_6
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DOI: https://doi.org/10.1007/978-94-011-2216-0_6
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