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R Arnold - One of the best experts on this subject based on the ideXlab platform.
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gastric mucosa during treatment with lansoprazole helicobacter pylori is a risk factor for argyrophil Cell hyperplasia
Gastroenterology, 1997Co-Authors: R Eissele, G Brunner, Babette Simon, E Solcia, R ArnoldAbstract:Abstract BACKGROUND & AIMS: The mechanisms causing progression of fundic gastritis and changes in argyrophil Cell morphology in patients undergoing long-term treatment with proton pump inhibitors are unknown. The hypothesis of this study was that Helicobacter pylori is a risk factor for both gastritis and argyrophil Cell hyperplasia. METHODS: Forty-two patients with peptic disorders resistant to H2-blockers were treated with 30-90 mg lansoprazole daily for up to 5 years. Serum Gastrin levels, antral Gastrin Cells, fundic argyrophil Cells, parameters of gastritis, and H. pylori infection were evaluated regularly. RESULTS: In nonantrectomized patients, serum Gastrin levels increased from a median of 76 pg/mL to 163 pg/mL within 3 months. Antral Gastrin Cell density increased from 175 to 267 Cells/mm2 (P CONCLUSIONS: H. pylori represents an important factor for the progression of fundic gastritis and the development of argyrophil Cell hyperplasia during long-term treatment with lansoprazole. (Gastroenterology 1997 Mar;112(3):707-17)
Gunter Kloppel - One of the best experts on this subject based on the ideXlab platform.
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precursor lesions in patients with multiple endocrine neoplasia type 1 associated duodenal Gastrinomas
Gastroenterology, 2005Co-Authors: Martin Anlauf, Philipp U Heitz, Aurel Perren, Cora Lu Meyer, Sonja Schmid, Parvin Saremaslani, Marie L Kruse, Eberhard Weihe, Paul Komminoth, Gunter KloppelAbstract:Background & Aims: The identification of precursor lesions has a great impact on the understanding of tumorigenesis. Precursor lesions of endocrine tumors are known to occur in the setting of the MEN1 syndrome. The aim of this study was to test the hypothesis that MEN1-associated duodenal Gastrinomas originate from diffuse preneoplastic Gastrin Cell changes. Precursor lesions may precede the development of duodenal Gastrinomas because, in contrast to sporadic Gastrinomas, these tumors are usually multiple. Methods: The distribution of endocrine Cells in the nontumorous duodenal tissue was analyzed qualitatively and quantitatively for 25 patients operated on for a duodenal Gastrinoma. MEN1 status was assessed clinically and by polymerase chain reaction-based mutational analysis. Results: Fourteen of 25 patients with Gastrinoma had proliferative, hyperplastic lesions consisting of Gastrin Cells in the nontumorous duodenal mucosa, similar to the gastric enterochromaffin-like Cell lesions observed in chronic atrophic gastritis. All patients with Zollinger-Ellison syndrome with proven MEN1 had such proliferative Gastrin Cell lesions, and all patients with Zollinger-Ellison syndrome without precursor lesions were MEN1 negative. Conclusions: Duodenal Gastrinomas in MEN1, but not sporadic duodenal Gastrinomas, are associated with proliferative Gastrin Cell changes within the nontumorous mucosa. It is likely that these lesions precede the development of MEN1-associated duodenal Gastrinomas.
Hansrudolf Berthoud - One of the best experts on this subject based on the ideXlab platform.
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morphological analysis of vagal input to Gastrin releasing peptide and vasoactive intestinal peptide containing neurons in the rat glandular stomach
The Journal of Comparative Neurology, 1996Co-Authors: Hansrudolf BerthoudAbstract:Vagal preganglionic efferents to the rat stomach were labeled anterogradely by injecting the fluorescent carbocyanine dye DiA into the dorsal motor nucleus in vivo. Enteric neurons were labeled in toto by intraperitioneal administration of Fluorogold, and neurochemically characterized by simultaneous single- and double-label immunocytochemistry. Single peptide immunocytochemistry revealed that in all three major areas of the stomach, about one-third of all Gastrin-releasing peptide immunoreactive (GRP-IR) neurons in the myenteric plexus, received vagal contacts. Because the proportion of GRP-IR neurons was 32% in the fundus, 23% in the corpus, and only 8% in the antrum, the absolute number of vagally contacted GRP-IR neurons per cm2 was also different. Double-label immunocytochemistry revealed colocalization of vasoactive intestinal peptide immunoreactivity (VIP-IR) in 45%, and of enkephalin immunoreactivity (ENK-IR) in about 30%, of the GRP-IR myenteric neurons. A subpopulation of myenteric neurons colocalized GRP-IR and VIP-IR and projects almost exclusively to the Gastrin Cell-rich basal mucosa of the antrum and the oxyntic mucosa of the corpus. Another subpopulation containing GRP-IR, but not VIP-IR, projects mainly to the myenteric plexus itself and the external muscle layers, particularly the longitudinal muscle. A third group of neurons containing VIP-IR but not GRP-IR projects heavily to the circular muscle layer, the muscularis mucosae, and to other myenteric neurons. Vagal input to these three subpopulations seems not to be selective, in that an equal proportion of about 20 to 30% of each group was vagally contacted. Vagal inputs to these neurochemically and topographically distinct enteric neurons provide the basis for the physiological vagal control of Gastrin release, gastric acid secretion, and gastric motility.
Lodewijk A A Brosens - One of the best experts on this subject based on the ideXlab platform.
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a parathyroid gut axis hypercalcemia and the pathogenesis of Gastrinoma in multiple endocrine neoplasia 1
Molecular Cancer Research, 2021Co-Authors: Wenzel M Hackeng, Koen M A Dreijerink, Johan G A Offerhaus, Lodewijk A A BrosensAbstract:Patients with multiple endocrine neoplasia 1 (MEN1) syndrome have a germline mutation in the MEN1 gene. Loss of the wild-type allele can initiate endocrine tumorigenesis. Microscopic and macroscopic pituitary, parathyroid, and pancreatic tumors (referred to as the 3 P's) show loss of the wild-type MEN1 allele up to 100%. In contrast, the duodenal Gastrinoma pathogenesis in MEN1 syndrome follows a hyperplasia-to-neoplasia sequence. Gastrinomas have loss of heterozygosity of the MEN1 locus in <50%, and invariably coincide with linear, diffuse, or micronodular Gastrin-Cell hyperplasia. The factor initiating the Gastrin-Cell hyperplasia-to-neoplasia sequence is unknown. In this perspective, we argue that hypercalcemia may promote the Gastrin-Cell hyperplasia-to-neoplasia sequence through the calcium sensing receptor. Hypercalcemia is present in almost all patients with MEN1 syndrome due to parathyroid adenomas. We propose a parathyroid-gut axis, which could well explain why patients with MEN1 syndrome are regularly cured of duodenal Gastrinoma after parathyroid surgery, and might cause MEN1 syndrome phenocopies in MEN1-mutation negative individuals with parathyroid adenomas. This perspective on the pathogenesis of the Gastrin-Cell hyperplasia and neoplasia sequence sheds new light on tumorigenic mechanisms in neuroendocrine tumors and might open up novel areas of Gastrinoma research. It may also shift focus in the treatment of MEN1 syndrome-related Gastrinoma to biochemical prevention.
R Eissele - One of the best experts on this subject based on the ideXlab platform.
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gastric mucosa during treatment with lansoprazole helicobacter pylori is a risk factor for argyrophil Cell hyperplasia
Gastroenterology, 1997Co-Authors: R Eissele, G Brunner, Babette Simon, E Solcia, R ArnoldAbstract:Abstract BACKGROUND & AIMS: The mechanisms causing progression of fundic gastritis and changes in argyrophil Cell morphology in patients undergoing long-term treatment with proton pump inhibitors are unknown. The hypothesis of this study was that Helicobacter pylori is a risk factor for both gastritis and argyrophil Cell hyperplasia. METHODS: Forty-two patients with peptic disorders resistant to H2-blockers were treated with 30-90 mg lansoprazole daily for up to 5 years. Serum Gastrin levels, antral Gastrin Cells, fundic argyrophil Cells, parameters of gastritis, and H. pylori infection were evaluated regularly. RESULTS: In nonantrectomized patients, serum Gastrin levels increased from a median of 76 pg/mL to 163 pg/mL within 3 months. Antral Gastrin Cell density increased from 175 to 267 Cells/mm2 (P CONCLUSIONS: H. pylori represents an important factor for the progression of fundic gastritis and the development of argyrophil Cell hyperplasia during long-term treatment with lansoprazole. (Gastroenterology 1997 Mar;112(3):707-17)
