1986
DOI: 10.1016/s0140-6736(86)92193-8
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Effect of Duodenal Ulcer Surgery and Enterogastric Reflux on Gampylobacter Pyloridis

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Cited by 124 publications
(44 citation statements)
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“…We observed that the prevalence decreased with time after surgery, although there was no intentional eradication. Inhibition of H. pylori colonization by bile reflux has been observed [16], and a transition from H. pyloriassociated gastritis to reflux gastritis in the GR after peptic ulcer surgery was suggested [25]. Similar findings were demonstrated in the present study.…”
Section: Discussionsupporting
confidence: 91%
See 1 more Smart Citation
“…We observed that the prevalence decreased with time after surgery, although there was no intentional eradication. Inhibition of H. pylori colonization by bile reflux has been observed [16], and a transition from H. pyloriassociated gastritis to reflux gastritis in the GR after peptic ulcer surgery was suggested [25]. Similar findings were demonstrated in the present study.…”
Section: Discussionsupporting
confidence: 91%
“…Eradication of H. pylori in the post-operative GR after gastrectomy for early-stage primary gastric carcinoma has been recommended [15]. Several studies have investigated the effect of partial gastrectomy on H. pylori infection [16][17][18]. Most of these were, however, studies of peptic ulcer patients, and to date there have been only a few small studies of H. pylori involvement after gastric cancer operation [19,20].…”
Section: Introductionmentioning
confidence: 99%
“…A possible explanation was proposed by O'Connor and colleagues (95,96). They found that C. pylori seemed to be absent in patients with high duodenogastric reflux and suggested that reflux gastritis represents a distinct entity.…”
Section: Nudmentioning
confidence: 97%
“…Ultrastructual studies have demon strated a close relationship between the bac teria and epithelial cell damage [32], C. py lori are rarely found in patients with histo logically normal antral mucosa [28,33,34] and are not present in areas of intestinal metaplasia [35], The organisms do not col onize patients with chronic specific gastritis, such as gastric Crohn's disease or eosino philic gastritis in children [36]. C. pylori tend to be seen uncommonly in patients with type A gastritis [37] and in postgastrectomy patients with duodenogastric-reflux associ ated gastritis [38], The data suggest that the organisms are specifically associated with id iopathic type B gastritis. Moreover, in two separate experiments a healthy volunteer has ingested C. pylori [39,40]; both volunteers developed acute gastritis, and in one case active chronic gastritis has persisted [40].…”
Section: Infection and Chronic Gastritis Campylobacter Pylorimentioning
confidence: 99%
“…In these patients duodenogastric re flux may play an important role [38,55]. Indeed, duodenogastric reflux has been asso ciated with antral but not fundal gastritis in the intact stomach [56], This may not be a cause-and-effect relationship, however, other studies have been unable to correlate duodenogastric reflux with gastritis [57,58], and improvement in histology following bile diversion operations are not well docu mented [55,59], Alternatively, trophic gas trointestinal hormones such as gastrin may be interfered with by antrectomy, and possi bly vagotomy, predisposing to gastritis [60].…”
Section: Duodenogastric Reflux and Postgastrectomy Gastritismentioning
confidence: 99%