<i>Helicobacter pylori</i>and Peptic Ulcer Disease

Hulst, R. W. M. Van Der; Tytgat, G. N. J.

doi:10.3109/00365529609094744

Cited by 43 publications

(20 citation statements)

References 79 publications

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“…Recent studies have reported that, although gastric acid secretion was low in H pylori positive patients with gastritis of the corpus, clearance of H pylori organisms rapidly improved the decreased acid secretion 17-1920 21 the acid secretion, which was subnormal before eradication, increased when the gastric inflammation subsided after eradication in patients with GU. The mechanism by which body gastritis inhibits gastric acid secretion is not clear, but inflammatory cytokines such as interleukin-1 or proteins produced by H pylori may be responsible for reversible inhibition of acid secretion 22-24…”

Section: Discussionmentioning

confidence: 99%

Changes in gastric acid secretion assayed by endoscopic gastrin test before and after Helicobacter pylori eradication

Iijima

Ohara²,

Sekine³

et al. 2000

Gut

114

112

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Background-It remains controversial whether or not Helicobacter pylori infection causes altered gastric acid secretion. A novel test for evaluating gastric acid secretion (endoscopic gastrin test; EGT) has recently been developed. Aim-To investigate by EGT the eVects of H pylori eradication on the state of gastric acid secretion in patients with peptic ulcer. Methods-Twenty six patients with duodenal ulcer and 33 with gastric ulcer, for all of whom H pylori infection had been documented, were studied by EGT, histological examination of gastric mucosa, and measurement of plasma gastrin levels before and one and seven months after H pylori eradication. Results-In patients with duodenal ulcer, the mean EGT value before H pylori eradication was higher than that in H pylori negative controls, but it had decreased significantly seven months after the treatment. In contrast, the mean EGT value of patients with gastric ulcer before H pylori eradication was lower than that in H pylori negative controls, but it had increased one month after the treatment; this was followed by a slight decrease at seven months. In both groups, mean EGT values seven months after the treatment were not significantly diVerent from the mean control value. Conclusions-The reduced acid secretion in gastric ulcer patients and gastric acid hypersecretion in duodenal ulcer patients were both normalised after the clearance of H pylori.

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Section: Discussionmentioning

confidence: 99%

Changes in gastric acid secretion assayed by endoscopic gastrin test before and after Helicobacter pylori eradication

Iijima

Ohara²,

Sekine³

et al. 2000

Gut

114

112

View full text Add to dashboard Cite

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“…Thus, gastric acid has been believed to be an important etiologic factor for peptic ulcers in ZES. 3 On the other hand, it is well established that the vast majority of patients with chronic peptic ulcer disease are infected with H. pylori, 4 and that the infection plays a pivotal role in the development of peptic ulcer disease. 5 Recent studies have shown that H. pylori infection modulates gastric acid secretion in various ways.…”

Section: Introductionmentioning

confidence: 99%

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Watanabe

Matsushima

Nakase

et al. 2000

Journal of Gastroenterology

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Both Zollinger-Ellison syndrome (ZES) and Helicobacter pylori infection are major etiologic factors for peptic ulcer. The aim of this study was to investigate the effect of H. pylori infection on ZES with special reference to acid secretion. Sixteen patients with ZES were selected (median age, 59 years; range, 39-66 years; M/F, 9/7), and H. pylori status, ulcer location, gastric acid secretion, serum pepsinogen (PG) I and II concentrations, and PG I/II ratio were determined. The seroprevalence of H. pylori infection was 50%, whereas active H. pylori infection was seen in only 25% of the patients. Thirteen patients had duodenal ulcer (DU), 1 had gastric ulcer (GU), and 2 had both GU and DU. DU was seen in both H. pylori-positive and H. pylori-negative patients, whereas GU was found only in H. pylori-positive patients. Both basal and maximal acid outputs were significantly lower in H. pylori-positive patients than in H. pylori-negative patients (P< 0.05). Moreover, both serum PG I and the PG I/II ratio were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. These results indicate that ZES is an independent risk factor for DU, but H. pylori infection may play some role in the development of GU in ZES. In patients with ZES, H. pylori infection may reduce both hypersecretion from parietal cells and PG I secretion from chief cells, and hyperacidity of the stomach in ZES may have eradicated H. pylori in some patients.

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“…It is now very well known that Helicobacter pylori (H. pylori) infection plays an important role in the pathogenesis of peptic ulcer disease, chronic gastritis, maltoma and adenocarcinoma of the stomach (1), and the eradication of this bacteria significantly reduces the relapse of peptic ulcers (2)(3)(4)(5). Recently, it has been shown that H. pylori eradication may alleviate dyspeptic symptoms in 20-35% of patients who have functional dyspepsia (6).…”

Section: Introductionmentioning

confidence: 99%

A multicenter, randomized, prospective study of 14-day ranitidine bismuth citrate- vs. lansoprazolebased triple therapy for the eradication of Helicobacter pylori in dyspeptic patients

Avşar

Tıftıkcı²,

Poturoğlu³

et al. 2013

Turk J Gastroenterol

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Background/aims: Proton-pump inhibitor-and ranitidine bismuth citrate-based triple regimens are the two recommended firstline treatments for the eradication of 74,6% and 69,2% of cases, respectively (p>0,05). Intention-to-treat analysis (n=279) revealed that eradication rates were 65,1% and 63,6% in ranitidine bismuth citrateand in lansoprazole-based regimens, respectively (p>0,05). Both regimes were well-tolerated, and no serious adverse event was observed during the study. Conclusion: Ranitidine bismuth citrate-based regimen is at least as effective and tolerable as the classical proton-pump inhibitor-based regimen, but none of the therapies could achieve the recommendable eradication rate.

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Helicobacter pyloriand Peptic Ulcer Disease

Cited by 43 publications

References 79 publications

Changes in gastric acid secretion assayed by endoscopic gastrin test before and after Helicobacter pylori eradication

Changes in gastric acid secretion assayed by endoscopic gastrin test before and after Helicobacter pylori eradication

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

A multicenter, randomized, prospective study of 14-day ranitidine bismuth citrate- vs. lansoprazolebased triple therapy for the eradication of Helicobacter pylori in dyspeptic patients

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