Long-term omeprazole therapy in peptic ulcer disease: Gastrin, endocrine cell growth, and gastritis

Lamberts, R.; Creutzfeldt, W.; Strüber, Hans G.; Brunner, G.; Solcia, Enrico

doi:10.1016/0016-5085(93)90344-c

Cited by 304 publications

(223 citation statements)

References 54 publications

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“…While there was a positive correlation between the degree of atrophy, inflammation, and CgA level, no correlation was found between neutrophil activity, intestinal metaplasia of the corpus mucosa, and CgA level. It has been reported that there is a correlation between ECL cell hyperplasia and gastritis grade (24); however, these studies do not include the updated Sydney system for their evaluation methods of gastritis. It is possible to make a supposition that atrophy, activity, and inflammation of the corpus mucosa increase the serum CgA levels via the increase in serum gastrin levels and ECL cell hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

Factors associated with elevated serum chromogranin A levels in patients with autoimmune gastritis

Kalkan¹,

Karakaya²,

Soykan³

2016

Turk J Gastroenterol

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Section: Discussionmentioning

confidence: 99%

Factors associated with elevated serum chromogranin A levels in patients with autoimmune gastritis

Kalkan¹,

Karakaya²,

Soykan³

2016

Turk J Gastroenterol

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“…Moreover, Lamberts et al [32] and Klinkenberg-Knol et al [33] indicated that the profound reduction in gastric acid secretion induced by PPIs leads to increased secretion of gastrin, and most PPI users have moderate hypergastrinemia; Havu [34], Gillen and McColl [35], and Kuipers [36] indicated that hypergastrinemia has been associated with an increased risk of gastric cancer.…”

Section: Frequencies Of Duodenal Ulcer and Gastric Cancermentioning

confidence: 99%

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

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“…Gastrin has trophic effects on the gastrointestinal mucosa, and hypergastrinaemia has been associated with an increased risk of gastric carcinoids, and gastric and colonic carcinomas (Havu, 1986;Laine et al, 2000;Gillen and McColl, 2001;Waldum et al, 2005;Kuipers, 2006), although recent results for PPI use and colorectal cancer risk are reassuring (Robertson et al, 2007;Yang et al, 2007;van Soest et al, 2008). Hyperplasia of enterochromaffin-like cells has been seen in long-term PPI users (Lamberts et al, 1993;Eissele et al, 1997;Klinkenberg-Knol et al, 2000); and in patients with Helicobacter pylori (H. Pylori) infection, long-term PPI use has been associated with an increased incidence of atrophic gastritis (Kuipers et al, 1996), a precursor of gastric adenocarcinoma (Uemura et al, 2001;Ye and Nyren, 2003).…”

mentioning

confidence: 99%

Proton pump inhibitors and risk of gastric cancer: a population-based cohort study

et al. 2009

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Proton pump inhibitor (PPI) use leads to hypergastrinaemia, which has been associated with gastrointestinal neoplasia. We evaluated the association between PPI use and risk of gastric cancer using population-based health-care registers in North Jutland, Denmark, during 1990Denmark, during -2003. We compared incidence rates among new users of PPI (n ¼ 18 790) or histamine-2-antagonists (H2RAs) (n ¼ 17 478) and non-users of either drug. Poisson regression analysis was used to estimate incidence rate ratios (IRRs) adjusted for multiple confounders. We incorporated a 1-year lag time to address potential reverse causation. We identified 109 gastric cancer cases among PPI users and 52 cases among H2RA users. After incorporating the 1-year lag time, we observed IRRs for gastric cancer of 1.2 (95% CI: 0.8 -2.0) among PPI users and 1.2 (95% CI: 0.8 -1.8) among H2RA users compared with non-users. These estimates are in contrast to significant overall IRRs of 9.0 and 2.8, respectively, without the lag time. In lag time analyses, increased IRRs were observed among PPI users with the largest number of prescriptions or the longest follow-up compared with H2RA users or nonusers. Although our results point to a major influence of reverse causation and confounding by indication on the association between PPI use and gastric cancer incidence, the finding of increased incidence among PPI users with most prescriptions and longest follow-up warrants further investigation.

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Long-term omeprazole therapy in peptic ulcer disease: Gastrin, endocrine cell growth, and gastritis

Cited by 304 publications

References 54 publications

Factors associated with elevated serum chromogranin A levels in patients with autoimmune gastritis

Factors associated with elevated serum chromogranin A levels in patients with autoimmune gastritis

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

Proton pump inhibitors and risk of gastric cancer: a population-based cohort study

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