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Gut. 1994 March; 35(3): 317–322.
PMCID: PMC1374582

Effect of Helicobacter pylori and its eradication on gastric juice ascorbic acid.

Abstract

The presence of ascorbic acid in gastric juice may protect against gastric carcinoma and peptic ulceration. This study examined the effect of Helicobacter pylori (H pylori) on the secretion of ascorbic acid into gastric juice by measuring fasting plasma and gastric juice ascorbic acid concentrations in patients with and without the infection and also before and after its eradication. Gastric juice ascorbic acid concentrations in 19 H pylori positive patients were significantly lower (median 2.8, range 0-28.8 micrograms/ml) than those in 10 H pylori negative controls (median 17.8, range 5.6-155.4 micrograms/ml) (p < 0.0005) despite similar plasma ascorbic acid concentrations in both groups. The median gastric juice:plasma ascorbic acid ratio in the H pylori positive patients was only 1.16 (range 0.02-6.67), compared with a median ratio of 4.87 (range 0.76-21.33) in H pylori negative controls (p < 0.01). In the patients with H pylori infection there was a significant negative correlation between the severity of the antral polymorphonuclear infiltrate and gastric juice ascorbic acid concentrations (correlation coefficient -0.52, p = 0.02). After eradication of H pylori in 11 patients, gastric juice ascorbic acid concentrations rose from 2.4 (0-12.8 micrograms/ml) to 11.2 (0-50 micrograms/ml) (p = 0.01). The median gastric juice: plasma ascorbic acid ratio also increased from 1.33 (0.05-6.67) to 2.89 (0.01-166) (p = 0.01). In conclusion, the high gastric juice:plasma ascorbic acid ratio in H pylori negative subjects shows active secretion of ascorbic acid into gastric juice. Secondly, H pylori infection causes a reversible lowering of gastric juice ascorbic acid concentrations, which may predispose to gastric carcinoma and peptic ulceration.

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Selected References

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  • Rathbone BJ, Johnson AW, Wyatt JI, Kelleher J, Heatley RV, Losowsky MS. Ascorbic acid: a factor concentrated in human gastric juice. Clin Sci (Lond) 1989 Mar;76(3):237–241. [PubMed]
  • Sobala GM, Schorah CJ, Sanderson M, Dixon MF, Tompkins DS, Godwin P, Axon AT. Ascorbic acid in the human stomach. Gastroenterology. 1989 Aug;97(2):357–363. [PubMed]
  • Sobala GM, Pignatelli B, Schorah CJ, Bartsch H, Sanderson M, Dixon MF, Shires S, King RF, Axon AT. Levels of nitrite, nitrate, N-nitroso compounds, ascorbic acid and total bile acids in gastric juice of patients with and without precancerous conditions of the stomach. Carcinogenesis. 1991 Feb;12(2):193–198. [PubMed]
  • Stähelin HB, Rösel F, Buess E, Brubacher G. Dietary risk factors for cancer in the Basel Study. Bibl Nutr Dieta. 1986;(37):144–153. [PubMed]
  • Jedrychowski W, Wahrendorf J, Popiela T, Rachtan J. A case-control study of dietary factors and stomach cancer risk in Poland. Int J Cancer. 1986 Jun 15;37(6):837–842. [PubMed]
  • Cuello C, Correa P, Haenszel W, Gordillo G, Brown C, Archer M, Tannenbaum S. Gastric cancer in Colombia. I. Cancer risk and suspect environmental agents. J Natl Cancer Inst. 1976 Nov;57(5):1015–1020. [PubMed]
  • Risch HA, Jain M, Choi NW, Fodor JG, Pfeiffer CJ, Howe GR, Harrison LW, Craib KJ, Miller AB. Dietary factors and the incidence of cancer of the stomach. Am J Epidemiol. 1985 Dec;122(6):947–959. [PubMed]
  • Coghlan JG, Gilligan D, Humphries H, McKenna D, Dooley C, Sweeney E, Keane C, O'Morain C. Campylobacter pylori and recurrence of duodenal ulcers--a 12-month follow-up study. Lancet. 1987 Nov 14;2(8568):1109–1111. [PubMed]
  • Rauws EA, Langenberg W, Houthoff HJ, Zanen HC, Tytgat GN. Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. Gastroenterology. 1988 Jan;94(1):33–40. [PubMed]
  • Marshall BJ, McGechie DB, Rogers PA, Glancy RJ. Pyloric Campylobacter infection and gastroduodenal disease. Med J Aust. 1985 Apr 15;142(8):439–444. [PubMed]
  • Parsonnet J, Friedman GD, Vandersteen DP, Chang Y, Vogelman JH, Orentreich N, Sibley RK. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med. 1991 Oct 17;325(16):1127–1131. [PubMed]
  • Nomura A, Stemmermann GN, Chyou PH, Kato I, Perez-Perez GI, Blaser MJ. Helicobacter pylori infection and gastric carcinoma among Japanese Americans in Hawaii. N Engl J Med. 1991 Oct 17;325(16):1132–1136. [PubMed]
  • Forman D, Newell DG, Fullerton F, Yarnell JW, Stacey AR, Wald N, Sitas F. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. BMJ. 1991 Jun 1;302(6788):1302–1305. [PMC free article] [PubMed]
  • Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ, Heatley RV, Axon AT. Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations. Gut. 1991 Nov;32(11):1415–1418. [PMC free article] [PubMed]
  • el Nujumi AM, Rowe PA, Dahill S, Dorrian CA, Neithercut WD, McColl KE. Role of ammonia in the pathogenesis of the gastritis, hypergastrinaemia, and hyperpepsinogenaemia I caused by Helicobacter pylori infection. Gut. 1992 Dec;33(12):1612–1616. [PMC free article] [PubMed]
  • Mooney C, Keenan J, Munster D, Wilson I, Allardyce R, Bagshaw P, Chapman B, Chadwick V. Neutrophil activation by Helicobacter pylori. Gut. 1991 Aug;32(8):853–857. [PMC free article] [PubMed]
  • Lunec J, Blake DR. The determination of dehydroascorbic acid and ascorbic acid in the serum and synovial fluid of patients with rheumatoid arthritis (RA). Free Radic Res Commun. 1985;1(1):31–39. [PubMed]
  • Licht WR, Tannenbaum SR, Deen WM. Use of ascorbic acid to inhibit nitrosation: kinetic and mass transfer considerations for an in vitro system. Carcinogenesis. 1988 Mar;9(3):365–372. [PubMed]
  • Mirvish SS, Wallcave L, Eagen M, Shubik P. Ascorbate-nitrite reaction: possible means of blocking the formation of carcinogenic N-nitroso compounds. Science. 1972 Jul 7;177(4043):65–68. [PubMed]
  • Ohshima H, Bartsch H. Quantitative estimation of endogenous nitrosation in humans by monitoring N-nitrosoproline excreted in the urine. Cancer Res. 1981 Sep;41(9 Pt 1):3658–3662. [PubMed]
  • Reed PI, Johnston BJ, Walters CL, Hill MJ. Effect of ascorbic acid on the intragastric environment in patients at increased risk of developing gastric cancer. IARC Sci Publ. 1991;(105):139–142. [PubMed]
  • Aruoma OI, Halliwell B, Dizdaroglu M. Iron ion-dependent modification of bases in DNA by the superoxide radical-generating system hypoxanthine/xanthine oxidase. J Biol Chem. 1989 Aug 5;264(22):13024–13028. [PubMed]
  • Clemens MR. Free radicals in chemical carcinogenesis. Klin Wochenschr. 1991 Dec 15;69(21-23):1123–1134. [PubMed]
  • Santamaria L, Bianchi-Santamaria A. Free radicals as carcinogens and their quenchers as anticarcinogens. Med Oncol Tumor Pharmacother. 1991;8(3):121–140. [PubMed]
  • Del Maestro R, Thaw HH, Björk J, Planker M, Arfors KE. Free radicals as mediators of tissue injury. Acta Physiol Scand Suppl. 1980;492:43–57. [PubMed]
  • Salim AS. Role of oxygen-derived free radicals in mechanism of acute and chronic duodenal ulceration in the rat. Dig Dis Sci. 1990 Jan;35(1):73–79. [PubMed]
  • Salim AS. Oxygen-derived free radicals and the prevention of duodenal ulcer relapse: a new approach. Am J Med Sci. 1990 Jul;300(1):1–8. [PubMed]
  • Salim AS. A possible new approach to the problem of refractory peptic ulceration. A role for free radical scavengers? Scott Med J. 1991 Feb;36(1):19–20. [PubMed]

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