Hypergastrinemia

Dacha, Sunil; Razvi, Mohammed; Massaad, Julia; Cai, Qiang; Wehbi, Mohammad

doi:10.1093/gastro/gov004

Cited by 84 publications

(72 citation statements)

References 74 publications

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“…A high level of secondary bile acid has been shown to cause toxic, inflammatory, and DNA damaging effects on liver cells and bile duct cells, leading to HCC and cholangiocarcinoma . The generally weaker associations observed for H2RAs could reflect the weaker acid suppression and the less marked effect on gastrin associated with these medications . Alternatively, various features of the observed association do not support a causal interpretation including the lack of dose‐response (the most marked association was seen for less than 6 prescriptions), the possibility of confounding by indication, and the possibility of reverse causation (suggested by the attenuation of associations when prescriptions in the period prior to diagnosis where removed).…”

Section: Discussionmentioning

confidence: 99%

“…Proton pump inhibitors (PPIs) and histamine‐2 receptor antagonists (H2RAs) are widely prescribed medications, used primarily for the treatment of peptic ulcers, dyspepsia, and gastro‐oesophageal reflux disease (GERD). Despite their widespread use, there have been concerns about potential adverse effects of PPIs and H2RAs potentially caused by a range of mechanisms including the reduced absorption of nutrients, hypergastrinemia and the overgrowth of bacteria (due to lower stomach acid levels) . Many studies have investigated the effect of PPIs and H2RAs on the stomach, and particularly on gastric cancer risk .…”

Section: Introductionmentioning

confidence: 99%

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Proton pump inhibitor and histamine‐2 receptor antagonist use and risk of liver cancer in two population‐based studies

Tran

McMenamin

Hicks

et al. 2018

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Proton pump inhibitor and histamine‐2 receptor antagonist use and risk of liver cancer in two population‐based studies

Tran

McMenamin

Hicks

et al. 2018

Aliment Pharmacol Ther

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“…Hypergastrinemia is reported to be caused by other several factors such as Helicobacter pylori , or H. pylori- related atrophic gastritis, autoimmune gastritis, renal failure, gastrin-producing tumor, and so on [1, 12-15]. Japanese serum gastrin levels are thought to be higher because of the high prevalence of H. pylori infection and atrophic gastritis compared to Western people, although the basic gastrin levels decreased with the decline of H. pylori prevalence in recent years, especially in the younger generation [16].…”

Section: Introductionmentioning

confidence: 99%

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Shiotani¹,

Katsumata²,

Gouda³

et al. 2018

Digestion

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Background/Aim: The use of proton pump inhibitors (PPIs) is known to lead to hypergastrinemia; however, the data in patients with atrophic gastritis is still lacking. The aim of this study was to investigate the effects of long-term PPIs use on the gastrin levels in patients with atrophic gastritis and to determine factors affecting hypergastrinemia in long-term users of PPIs. Methods: Serum Helicobacter pylori IgG, gastrin and pepsinogen levels were measured. Atrophic gastritis was assessed by upper gastrointestinal endoscopies based on the Kimura-Takemoto classification and pepsinogen levels. CYP2C19 polymorphisms were assessed using DNA extracted from peripheral blood. Results: A total number of 382 patients (275 men and 107 women) were enrolled. Median serum gastrin levels were higher in PPI users than in non- users (234 vs. 113 pg/mL, p < 0.001) and in women than in men (252 vs. 155 pg/mL, p = 0.006). Gastrin levels were significantly associated with corpus atrophy only in the subgroup of non-users of PPIs. Multivariate analysis revealed that hypergastrinemia (over 150 pg/mL) was significantly associated with PPI use (OR 5.30; 95% CI 3.32–8.47), women (OR 2.22; 95% CI 1.33–3.72) and corpus atrophy (OR 1.82; 95% CI 1.14–2.90). Conclusion: PPI use, women and corpus atrophy were risk factors for hypergastrinemia. Gender, but not corpus atrophy, affected the gastrin levels in long-term users of PPIs.

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“…Patients with atrophic gastritis are known to develop hypergastrinemia. Destruction of parietal cells in atrophic gastritis leads to profound hypochlorhydria which induces G-cell (gastrin-producing) hyperplasia and consequently hypergastrinemia [19, 20]. Hypergastrinemia from underlying atrophic gastritis may be a possible mechanistic link in the association of GAVE with atrophic gastritis.…”

Section: Discussionmentioning

confidence: 99%

Hemorrhage from Extra-Antral Gastric Antral Vascular Ectasia in a Patient with Duodenal Heterotopic Gastric Mucosa

Gubatan

Raines

Khosravi

et al. 2016

Case Reports in Gastrointestinal Medicine

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Gastric antral vascular ectasias (GAVE) have been increasingly recognized as an uncommon cause of chronic gastrointestinal bleeding and anemia, although their underlying pathogenesis is not completely well understood. Heterotopic gastric mucosa (HGM) has been reported to occur at various sites along the gastrointestinal tract and although relatively common, it is often asymptomatic. We report a case of a 60-year-old woman with a prior history of GAVE who developed melena and symptomatic anemia during her hospitalization following cardiac catheterization. Initial EGD demonstrated nonbleeding antral GAVE and a newly discovered duodenal mass. Duodenal mass biopsies were ultimately notable for HGM along with histologic features of extra-antral GAVE. The patient required blood transfusions and consequently had a small bowel endoscopy notable for fresh blood in the proximal small bowel. The patient underwent a small bowel push enteroscopy which demonstrated active bleeding of the duodenal mass and overlying oozing GAVE, which was cauterized with Argon-Plasma Coagulation with adequate hemostasis. We present for the first time a novel association between GAVE and HGM. Our case illustrates that extra-antral GAVE may occur with HGM in the duodenum. We explore potential mechanisms by which HGM may be involved in the pathogenesis of GAVE.

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Hypergastrinemia

Cited by 84 publications

References 74 publications

Proton pump inhibitor and histamine‐2 receptor antagonist use and risk of liver cancer in two population‐based studies

Proton pump inhibitor and histamine‐2 receptor antagonist use and risk of liver cancer in two population‐based studies

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Hemorrhage from Extra-Antral Gastric Antral Vascular Ectasia in a Patient with Duodenal Heterotopic Gastric Mucosa

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