Abstract
Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. H pylori was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower in H pylori negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p < 0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmol/l, 19 (7.1-33.1) mmol/l, 44 (25.1-63.1) mmol/l, and 36 (31.6-39.8) mmol/l respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During all predefined time periods, intragastric acidity was significantly higher in patients with H pylori positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between the H pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylori infection have normal gastric acidity.
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Selected References
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- Barthel J. S., Westblom T. U., Havey A. D., Gonzalez F., Everett E. D. Gastritis and Campylobacter pylori in healthy, asymptomatic volunteers. Arch Intern Med. 1988 May;148(5):1149–1151. [PubMed] [Google Scholar]
- Blair A. J., 3rd, 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 Feb;79(2):582–587. doi: 10.1172/JCI112850. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Brady C. E., 3rd, Hadfield T. L., Hyatt J. R., Utts S. J. Acid secretion and serum gastrin levels in individuals with Campylobacter pylori. Gastroenterology. 1988 Apr;94(4):923–927. doi: 10.1016/0016-5085(88)90548-3. [DOI] [PubMed] [Google Scholar]
- Chittajallu R. S., Neithercut W. D., Macdonald A. M., McColl K. E. Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. Gut. 1991 Jan;32(1):21–24. doi: 10.1136/gut.32.1.21. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Feldman M., Richardson C. T., Lam S. K., Samloff I. M. Comparison of gastric acid secretion rates and serum pepsinogen I and II concentrations in Occidental and Oriental duodenal ulcer patients. Gastroenterology. 1988 Sep;95(3):630–635. doi: 10.1016/s0016-5085(88)80008-8. [DOI] [PubMed] [Google Scholar]
- Feldman M., Richardson C. T. Total 24-hour gastric acid secretion in patients with duodenal ulcer. Comparison with normal subjects and effects of cimetidine and parietal cell vagotomy. Gastroenterology. 1986 Mar;90(3):540–544. doi: 10.1016/0016-5085(86)91106-6. [DOI] [PubMed] [Google Scholar]
- Graham D. Y., Alpert L. C., Smith J. L., Yoshimura H. H. Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria. Am J Gastroenterol. 1988 Sep;83(9):974–980. [PubMed] [Google Scholar]
- Graham D. Y., Malaty H. M., Evans D. G., Evans D. J., Jr, Klein P. D., Adam E. Epidemiology of Helicobacter pylori in an asymptomatic population in the United States. Effect of age, race, and socioeconomic status. Gastroenterology. 1991 Jun;100(6):1495–1501. doi: 10.1016/0016-5085(91)90644-z. [DOI] [PubMed] [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 Apr;85(4):394–398. [PubMed] [Google Scholar]
- Hui W. M., Lam S. K., Chau P. Y., Ho J., Lui I., Lai C. L., Lok A. S., Ng M. M. Persistence of Campylobacter pyloridis despite healing of duodenal ulcer and improvement of accompanying duodenitis and gastritis. Dig Dis Sci. 1987 Nov;32(11):1255–1260. doi: 10.1007/BF01296375. [DOI] [PubMed] [Google Scholar]
- Lanzon-Miller S., Pounder R. E., Hamilton M. R., Chronos N. A., Ball S., Mercieca J. E., Olausson M., Cederberg C. Twenty-four-hour intragastric acidity and plasma gastrin concentration in healthy subjects and patients with duodenal or gastric ulcer, or pernicious anaemia. Aliment Pharmacol Ther. 1987 Jun;1(3):225–237. doi: 10.1111/j.1365-2036.1987.tb00622.x. [DOI] [PubMed] [Google Scholar]
- Levi S., Beardshall K., Haddad G., Playford R., Ghosh P., Calam J. Campylobacter pylori and duodenal ulcers: the gastrin link. Lancet. 1989 May 27;1(8648):1167–1168. doi: 10.1016/s0140-6736(89)92752-9. [DOI] [PubMed] [Google Scholar]
- Marshall B. J., Goodwin C. S., Warren J. R., Murray R., Blincow E. D., Blackbourn S. J., Phillips M., Waters T. E., Sanderson C. R. Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacter pylori. Lancet. 1988 Dec 24;2(8626-8627):1437–1442. doi: 10.1016/s0140-6736(88)90929-4. [DOI] [PubMed] [Google Scholar]
- McColl K. E., Fullarton G. M., Chittajalu R., el Nujumi A. M., MacDonald A. M., Dahill S. W., Hilditch T. E. 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 Mar;26(3):339–346. doi: 10.3109/00365529109025052. [DOI] [PubMed] [Google Scholar]
- McColl K. E., Fullarton G. M., el Nujumi A. M., Macdonald A. M., Brown I. L., Hilditch T. E. Lowered gastrin and gastric acidity after eradication of Campylobacter pylori in duodenal ulcer. Lancet. 1989 Aug 26;2(8661):499–500. doi: 10.1016/s0140-6736(89)92105-3. [DOI] [PubMed] [Google Scholar]
- McKinlay A. W., Upadhyay R., Gemmell C. G., Russell R. I. Helicobacter pylori: bridging the credibility gap. Gut. 1990 Aug;31(8):940–945. doi: 10.1136/gut.31.8.940. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Merki H. S., Fimmel C. J., Walt R. P., Harre K., Röhmel J., Witzel L. Pattern of 24 hour intragastric acidity in active duodenal ulcer disease and in healthy controls. Gut. 1988 Nov;29(11):1583–1587. doi: 10.1136/gut.29.11.1583. [DOI] [PMC free article] [PubMed] [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 Dec;84(12):1513–1516. [PubMed] [Google Scholar]
- Morris A., Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol. 1987 Mar;82(3):192–199. [PubMed] [Google Scholar]
- Oderda G., Vaira D., Holton J., Ainley C., Altare F., Ansaldi N. Amoxycillin plus tinidazole for Campylobacter pylori gastritis in children: assessment by serum IgG antibody, pepsinogen I, and gastrin levels. Lancet. 1989 Apr 1;1(8640):690–692. doi: 10.1016/s0140-6736(89)92206-x. [DOI] [PubMed] [Google Scholar]
- Peterson W. L. Helicobacter pylori and peptic ulcer disease. N Engl J Med. 1991 Apr 11;324(15):1043–1048. doi: 10.1056/NEJM199104113241507. [DOI] [PubMed] [Google Scholar]
- Rauws E. A., Tytgat G. N. Cure of duodenal ulcer associated with eradication of Helicobacter pylori. Lancet. 1990 May 26;335(8700):1233–1235. doi: 10.1016/0140-6736(90)91301-p. [DOI] [PubMed] [Google Scholar]
- Savarino V., Mela G. S., Scalabrini P., Sumberaz A., Fera G., Celle G. 24-hour study of intragastric acidity in duodenal ulcer patients and normal subjects using continuous intraluminal pH-metry. Dig Dis Sci. 1988 Sep;33(9):1077–1080. doi: 10.1007/BF01535781. [DOI] [PubMed] [Google Scholar]
- Smith J. T., Pounder R. E., Nwokolo C. U., Lanzon-Miller S., Evans D. G., Graham D. Y., Evans D. J., Jr Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori. Gut. 1990 May;31(5):522–525. doi: 10.1136/gut.31.5.522. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Wagner S., Freise J., Bär W., Fritsch S., Schmidt F. W. Epidemiologie und Therapie der Campylobacter-pylori-Infektion. Dtsch Med Wochenschr. 1989 Mar 17;114(11):407–413. doi: 10.1055/s-2008-1066609. [DOI] [PubMed] [Google Scholar]
- Wagner S., Gebel M., Haruma K., Bär W., Lange P., Freise J., Gladziwa U., Schmidt F. W. Bismuth subsalicylate in the treatment of H2 blocker resistant duodenal ulcers: role of Helicobacter pylori. Gut. 1992 Feb;33(2):179–183. doi: 10.1136/gut.33.2.179. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Wagner S., Gladziwa U., Gebel M., Schüler A., Freise J., Schmidt F. W. Circadian pattern of intragastric acidity in duodenal ulcer patients: a study of variations in relation to ulcer activity. Gut. 1991 Oct;32(10):1104–1109. doi: 10.1136/gut.32.10.1104. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Wagner S., Schüler A., Gebel M., Freise J., Schmidt F. W. Campylobacter pylori and acid secretion. Lancet. 1989 Sep 2;2(8662):562–562. doi: 10.1016/s0140-6736(89)90684-3. [DOI] [PubMed] [Google Scholar]
- Whittingham S., Naselli G., McNeilage L. J., Coppel R. L., Sturgess A. D. Serological diagnosis of primary Sjögren's syndrome by means of human recombinant La (SS-B) as nuclear antigen. Lancet. 1987 Jul 4;2(8549):1–3. [PubMed] [Google Scholar]
- Wolfe M. M., Soll A. H. The physiology of gastric acid secretion. N Engl J Med. 1988 Dec 29;319(26):1707–1715. doi: 10.1056/NEJM198812293192605. [DOI] [PubMed] [Google Scholar]
- el Nujumi A. M., Dorrian C. A., Chittajallu R. S., Neithercut W. D., McColl K. E. Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. Gut. 1991 Aug;32(8):866–870. doi: 10.1136/gut.32.8.866. [DOI] [PMC free article] [PubMed] [Google Scholar]
