{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T20:00:12Z","timestamp":1765656012952,"version":"3.48.0"},"reference-count":41,"publisher":"BMJ","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[1994,8]]},"abstract":"<jats:p>Patients with chronic dyspepsia were categorised by macroscopic appearance at oesophagogastroduodenoscopy as having duodenal ulceration (DU), other diagnosed lesions such as reflux oesophagitis, carcinoma of stomach, etc, or no organic lesion (non-ulcer dyspepsia, NUD). Material was collected to identify gastric infection with Helicobacter pylori (H pylori) by CP urease test, culture, and histological examination and to make the microscopic diagnosis of active chronic gastritis. Each patient in the DU and NUD categories was then invited to volunteer for a gastric secretion study in which maximal gastric secretion in response to histamine was measured. Sixty two gastric secretion tests were performed (31 DU, 31 NUD). The presence of H pylori was associated with active chronic gastritis (100%). DU patients secreted more acid than the NUD patients. H pylori positivity was associated with decreased maximal gastric secretion in both groups. There was a positive correlation between smoking and maximal acid output shown only in H pylori negative but not in H pylori positive patients. These findings were clear cut when all corrections of maximal gastric secretion were made for pyloric loss, duodenogastric reflux, and stature. This study failed to show any aetiological link between H pylori and DU by increased maximal gastric secretion.<\/jats:p>","DOI":"10.1136\/gut.35.8.1033","type":"journal-article","created":{"date-parts":[[2007,9,18]],"date-time":"2007-09-18T17:41:31Z","timestamp":1190137291000},"page":"1033-1036","source":"Crossref","is-referenced-by-count":20,"title":["Duodenal ulcer, Helicobacter pylori, and gastric secretion."],"prefix":"10.1136","volume":"35","author":[{"given":"K","family":"Chandrakumaran","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D","family":"Vaira","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Hobsley","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[1994,8,1]]},"reference":[{"key":"ref_1","first-page":"439","article-title":"Pyloric Campylobacter infection and gastroduodenal disease","volume":"142","author":"Marshall, B.J.; McGechie, D.B.; Rogers, P.A.; Glancy, R.J.","year":"1985","unstructured":"Marshall BJ, McGechie DB, Rogers PA, Glancy RJ. 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Campylobacter pylori gastrin, acid secretion and duodenal ulcer [letter]. Lancet 1989; ii: 613.","journal-title":"Lancet"},{"key":"ref_13","doi-asserted-by":"crossref","first-page":"1504","DOI":"10.1136\/bmj.299.6714.1504","article-title":"Antral Helicobacter pylori, hypergastrinaemia and duodenal ulcer: effects of eradicating the organisms","volume":"299","author":"Levi, S.; Davies, K.A.A.; Playford, R.; Ghosh, P.; Price, M.J.; Calam, J.","year":"1989","unstructured":"Levi S, Davies KAA, Playford R, Ghosh P, Price MJ, Calam J, et al. Antral Helicobacter pylori, hypergastrinaemia and duodenal ulcer: effects of eradicating the organisms. 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The likelihood of a disease in relation to the magnitude of a risk factor: the example of duodenal ulcer. Theor Surg 1987; 2: 106-9."},{"key":"ref_17","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1007\/BF01970656","article-title":"A standardised technique for the performance of accurate gastric secretion studies","volume":"9","author":"Whitfield, P.F.; Hobsley, M.","year":"1979","unstructured":"Whitfield PF, Hobsley M. A standardised technique for the performance of accurate gastric secretion studies. Agents Actions 1979; 9: 327-32.","journal-title":"Agents Actions"},{"key":"ref_18","doi-asserted-by":"crossref","first-page":"812","DOI":"10.1136\/jcp.41.7.812","article-title":"Urease tests for Campylobacter pylori (CP): care in interpretation","volume":"41","author":"Vaira, D.; Holton, J.; Cairns, S.; Falzon, M.; Polydorou, A.; Dowsett, J.","year":"1988","unstructured":"Vaira D, Holton J, Cairns S, Falzon M, Polydorou A, Dowsett J, et al. 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The accurate assessment of maximal gastric secretion in control subjects and patients with duodenal ulcer. BrJ_ Surg 1971; 58: 171-9.","journal-title":"BrJ_ Surg"},{"key":"ref_23","first-page":"101","article-title":"Hypersecretion and length of history in duodenal ulceration","volume":"ii:","author":"Hobsley, M.; Whitfield, P.F.; Faber, P.G.; Parkin, J.V.","year":"1975","unstructured":"Hobsley M, Whitfield PF, Faber PG, Parkin JV. Hypersecretion and length of history in duodenal ulceration. Lancet 1975; ii: 101-4.","journal-title":"Lancet"},{"key":"ref_24","doi-asserted-by":"crossref","first-page":"749","DOI":"10.1136\/bmj.302.6779.749","article-title":"Prevalence of endoscopic and histological findings in subjects with and without dyspepsia","volume":"302","author":"Johnsen, R.; Brenersen, B.; Straume, B.; Forde, O.H.; Bostad, L.; Burtol, P.G.","year":"1991","unstructured":"Johnsen R, Brenersen B, Straume B, Forde OH, Bostad L, Burtol PG. 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