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Region Hovedstaden - en del af Københavns Universitetshospital
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Gastric cancer and gastrin: on the interaction of Helicobacter pylori gastritis and acid inhibitory induced hypergastrinemia

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  1. Pathophysiological-based treatments of complications of cirrhosis

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  2. True Chromogranin A concentrations in plasma from patients with small intestinal neuroendocrine tumours

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  3. Plasma calprotectin is superior to serum calprotectin as a biomarker of intestinal inflammation in ulcerative Colitis

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  4. The clinical course of common bile duct stone clearance with endoscopic retrograde cholangio-pancreaticography

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  1. Oral D/L-3-Hydroxybutyrate stimulates cholecystokinin and insulin secretion and slows gastric emptying in healthy males

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  2. Bilio-enteric flow and plasma concentrations of bile acids after gastric bypass and sleeve gastrectomy

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  3. Increased oral sodium chloride intake in humans amplifies selectively postprandial GLP-1 but not GIP, CCK, and gastrin in plasma

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  4. Changes in the homeostatic appetite system after weight loss reflect a normalization toward a lower body weight

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Vis graf over relationer

Gastric cancer, a disease with a reduced frequency for decades, now appears to be on the rise again in young Americans. The epidemiology of gastric cancer differs between tumors in the cardia and those of the more distal parts of the stomach. The tumors are divided into the intestinal type showing glandular growth pattern and the diffuse type with a different pattern. The latter often expresses neuroendocrine and more specifically ECL-cell markers suggesting that they originate from the ECL cell, the target cell for the antral hormone, gastrin. Helicobacter pylori gastritis is accepted as the major cause of gastric cancer, but only after having induced oxyntic atrophy which reduces gastric acid secretion and thus induces hypoacidity leading to hypergastrinemia. Long-term hypergastrinemia is known to induce malignant neoplasia in the stomach of animals as well as man. Recently treatment with proton pump inhibitor after Helicobacter pylori eradication in patients with gastroesophageal reflux disease, has been reported to predispose to gastric cancer. Since profound acid inhibition is a well-known cause of gastric neoplasia, it is to be expected that Helicobacter pylori infection and profound acid inhibition has an additive or possibly potentiating effect on the development of gastric cancer.

OriginalsprogEngelsk
TidsskriftScandinavian Journal of Gastroenterology
Vol/bind54
Udgave nummer9
Sider (fra-til)1118-1123
Antal sider6
ISSN0036-5521
DOI
StatusUdgivet - sep. 2019

ID: 58076743