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Stomach and duodenum
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The secretion of gastric acid and pepsin tends to run in parallel, although the understanding of the mechanisms of gastric acid secretion is considerably greater than that of pepsin. Numerous factors are involved to some degree in the production of gastric acid. These include neurotransmitters, neuropeptides and peptide hormones. This complexity need not detract from the fact that there are basic principles that are relatively easily understood (Figure63.4). Hydrogen ions are produced by the parietal cell by the proton pump. Although numerous factors can act on the parietal cell, the most important of these is histamine, which acts via the H2-receptor. Histamine is produced, in turn, by the ECL cells of the stomach and acts in a paracrine (local) fashion on the parietal cells. These relationships explain why proton pump inhibitors can abolish gastric acid secretion, as they act on the final common pathway - hydrogen ion secretion. H2-receptor antagonists have profound effects on gastric acid secretion, but this is not insurmountable (Figure63.4). The ECL cell produces histamine in response to a number of stimuli that include the vagus nerve and gastrin. Gastrin is released by the G cells in response to the presence of the food in the stomach. The production of gastrin is inhibited by acid, creating a negative feedback loop. Various other peptides, including secretin, inhibit gastric acid secretion.
Neurohormonal Regulation of Gastric Mucosal Growth
Published in Jean Morisset, Travis E. Solomon, Growth of the Gastrointestinal Tract: Gastrointestinal Hormones and Growth Factors, 2017
The extreme sensitivity of ECL cells, which was notably higher than that of the common progenitor cell, to the mitogenic influence of this treatment may explain why ECL carcinoids and no adenocarcinoma are observed after prolonged administration of such potent antisecre-tagogues. An alternative explanation is that ECL cells are not as quickly desquamated in the gastric lumen as the epithelial mucous cells.15 ECL cells survive in the mucosa for a long time and might therefore represent more “stable” targets for potential carcinogens.
Neuroendocrine tumours
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Sairah R Khan, Kathryn L Wallitt, Adil Al-Nahhas, Tara D Barwick
The most common gastric NETs are enterochromomaffin-like (ECL) cell histamine-producing tumours. The other hormone-producing NETs include EC-cell (serotonin-producing) of G-cell gastrin-producing tumours (also known as gastrinomas). The ECL-cell NETs are categorized into three subtypes based on histology of adjacent mucosa, antral G-cell hyperplasia, hypergastrinaemia, and clinical course (106). Type I ECL-cell NETs, the most common subtype, are associated with hypergastrinemia and autoimmune chronic atrophic gastritis. They are typically multiple small lesions (0.5–1.0 cm) predominantly observed in the fundus and body of the stomach. The diagnosis is often made incidentally at endoscopy for dyspepsia. All type-1 ECL-cell NETs are categorized as G1 NETs (107).Type II ECL-cell NETs are rare and occur in patients with MEN 1 or Zollinger–Ellison syndrome: 30% of patients with MEN1 have gastric carcinoids. Tumours arise from the enterochromaffin-like cells, are multicentric, but have an increased tendency to metastasize to regional lymph nodes and liver, although the prognosis is generally good.Type III gastric NETs are sporadic, are not associated with hypergastrinemia, and account for 13% of cases of gastric carcinoid. There is a strong male predominance (80%). The tumour is usually solitary, large, and may ulcerate. Local invasion and metastases are common, and there is only a 20% 5-year survival rate.
Long-term changes in serum gastrin levels during standard dose vonoprazan therapy
Published in Scandinavian Journal of Gastroenterology, 2022
Satoshi Shinozaki, Hiroyuki Osawa, Yoshimasa Miura, Yoshikazu Hayashi, Hirotsugu Sakamoto, Tomonori Yano, Alan Kawarai Lefor, Hironori Yamamoto
Gastrin is the main regulator of enterochromaffin-like (ECL) cell function and proliferation, and long-term hypergastrinemia results in the development of ECL cell hyperplasia of the stomach [16]. In patients with pernicious anemia, an increase in fundal mucosal endocrine cells is associated with elevated serum gastrin levels [17]. In animal models, gastrin induces a dose dependent increase in ECL cell density and its maximal trophic effect is reached with efficient inhibition of acid secretion [18]. Therefore, an increase in gastrin levels due to VPZ is considered to reach concentrations giving near maximal trophic effects [17,18]. Since long-term acid suppression has the potential to cause ECL cell derived tumors, further studies are necessary to clarify the safety of long-term VPZ use.
Clinical consequences of controversies in gastric physiology
Published in Scandinavian Journal of Gastroenterology, 2020
Taking into consideration that gastrin is a peptide hormone that accordingly has to interact with its membrane receptor to exert any effect, it is amazing that the interest on its role in tumorigeneses for a long-time was concentrated on the colon [62]. There is no known physiological gastrin receptor there, and more importantly, gastrin in vivo does not have any proliferative effect on this organ [63]. The sole cell with an undisputed stimulatory gastrin receptor is the ECL cell located in the oxyntic mucosa of the stomach. It is therefore strange that when a group examine the role of gastrin in gastric carcinogenesis, antral carcinomas were investigated [64]. Gastrin has no positive trophic effect on the antrum [63], and if there exists a gastrin receptor there, it would be expected to be a negative one located on the G cell.
Gastric cancer and gastrin: on the interaction of Helicobacter pylori gastritis and acid inhibitory induced hypergastrinemia
Published in Scandinavian Journal of Gastroenterology, 2019
Helge L. Waldum, Jens F. Rehfeld
There are many classifications of gastric carcinomas, but they are all focused on the glandular growth pattern. More than fifty years ago, Laurén classified gastric carcinomas into intestinal and diffuse types with glandular growth in the intestinal and no such growth pattern in the diffuse type [31], that nevertheless was classified as adenocarcinoma due to PAS positivity presumed to reflect mucin. A subgroup of about 15% of the carcinomas had traits of both groups and could not be included in either group [31]. Since 1990 we have examined gastric carcinomas for neuroendocrine differentiation by immunohistochemical methods of high sensitivity [32] as well as in-situ-hybridization [33], and have found such neuroendocrine differentiation mainly in the gastric carcinomas of diffuse type [32,34–40]. Markers compatible with ECL cell origin have also been shown in many of these studies. Finally, we have long stressed that PAS staining is not specific for mucin [39–41] and have not been able to verify an occurrence of mucin in PAS positive gastric carcinoma cells – neither by immunohistochemistry nor by in-situ hybridization [39]. Thus, gastric carcinomas at least of diffuse type may originate from the ECL-cell, which is the main target cell for gastrin.