China
Africa
Explore chapters and articles related to this topic
Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Neuroendocrine tumors (NETs) arise from cells of the nervous and hormonal (i.e., endocrine) systems. They are thought to originate in cells whose normal function is at the neuroendocrine interface (e.g., Kulchitsky or similar enterochromaffin-like cells). Such cells are found not only in endocrine glands themselves, but also in a number of other organs and body tissues that respond to hormones (e.g., GI and pulmonary systems). Many neuroendocrine tumors are benign, but some are malignant and can arise in different areas of the body, although they are most often located in the GI tract (i.e., intestine) or lungs. However, they can also occur in the pancreas, thymus, thyroid, parathyroid, pituitary, adrenomedullary glands, liver, gallbladder, breast, genitourinary tract, and skin (e.g., Merkel cell skin carcinoma).
Gastric cancer
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Jacob S Ecanow, Richard M Gore
Gastric neuroendocrine tumours (‘gNET’) are rare tumours that arise from the mucosal enterochromaffin-like cells (ECL cells) and are described in detail in Chapter 24. They comprise four types, each with a unique aetiology, clinical behaviour, and management approach (155–157). Carcinoid syndrome can occur in patients with gNET tumour metastases, but is rare (155). These lesions are best understood in relation to their aetiology and how they disrupt normal gastric hormone physiology (156) (Table 10.9). Imaging plays an important role in detecting and diagnosing gNET tumours, and the subtype can often be suggested by certain typical imaging features (134,155,158) (Table 10.10, Figures 10.26 and 10.27). MDCT of the abdomen and pelvis are obtained for staging of type I and II gNETs that are larger than 2 cm and for all type III and IV tumours (155,156). Treatment of gNET tumours is determined by the subtype, size of the tumour, histological grade, depth of invasion, Ki-67 expression, and the presence of vascular invasion (155).
The digestive system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Gastrin is a hormone produced by gastric endocrine tissue, specifically, the G cells in the pyloric gland area. It is released into the blood and carried back to the stomach. The major function of gastrin is to enhance acid secretion by directly stimulating both parietal cells (HCl) and chief cells (pepsinogen). Gastrin also stimulates the local release of histamine from enterochromaffin-like cells in the wall of the stomach. Histamine stimulates parietal cells to release HCl.
An unusual case of proton pump inhibitor induced hyperchromograninemia
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Kwabena Oware Adu-Gyamfi, Richmond Gyamfi, Sandeep Patri
Could an actual carcinoid tumor be indeed present in our patient? Enterochromaffin-like cell hyperplasia is noted to be a predisposing factor for carcinoid tumors of the stomach [5]. Some animal studies have shown gastric carcinoid tumors of ECL origin to develop in rats treated with high doses of PPIs [22,23]. The possibility of chronic PPI use as a cause of gastric or intestinal tract neoplasms has been postulated for humans also, but not been conclusively proven and is the subject of ongoing research [24,25]. It is plausible to think that an early precursor stage to actual carcinoid tumor development may have been present in our patient which rapidly regressed upon withdrawal of PPI. The resolution of hyperchromograninemia and all his symptoms after discontinuation of PPI would argue against the presence of an established carcinoid tumor. His level of chromogranin A elevation would typically correlate with a heavy carcinoid tumor disease burden which we do not expect to have been missed on PET/CT scan.
Cardiac remodeling in obesity and after bariatric and metabolic surgery; is there a role for gastro-intestinal hormones?
Published in Expert Review of Cardiovascular Therapy, 2019
Elijah Sanches, Marieke Timmermans, Besir Topal, Alper Celik, Magnus Sundbom, Rui Ribeiro, Chetan Parmar, Surendra Ugale, Monika Proczko, Pieter S. Stepaniak, Juan Pujol Rafols, Kamal Mahawar, Marc P. Buise, Aleksandr Neimark, Rich Severin, Sjaak Pouwels
The G cells in the duodenum and the pyloric antrum of the stomach mainly produce gastrin, after modifying its precursor preprogastrin. Its primary function is stimulating acid secretion by releasing histamine from enterochromaffin-like cells [222]. Historically, it was the first gut hormone to be studied in bariatric surgery in 1975 [223,224]. Earlier studies showed an increase of gastrin after small bowel resection [223,224]. A small number of studies is available studying the effects of gastrin after bariatric surgery of which a few studies reveal an increase in basal and postprandial levels mainly in jejunoileal bypass [225,226], the vast majority of bypass procedures reveal either no significant change or a decrease of both circulating and post-prandial levels [143–145,147,151,223–225,227]. In gastric banding, the study of Shak et al. [167] showed no significant postoperative changes. In VBG surgery an increase was seen in both basal and postprandial levels [151,228]. It is postulated that gastric pouch ulcers might be related to the increase of gastrin seen after VBG [229].
Cannabinoid hyperemesis syndrome: potential mechanisms for the benefit of capsaicin and hot water hydrotherapy in treatment
Published in Clinical Toxicology, 2018
John R. Richards, Jeff M. Lapoint, Guillermo Burillo-Putze
Pituitary adenylate-cyclase activating polypeptide is another peptide hormone released from capsaicin-sensitive receptors. Pituitary adenylate-cyclase activating polypeptide stimulates enterochromaffin-like cells in the gastrointestinal tract [113,114]. It also modulates psychogenic and metabolic stress response by activating catecholamine secretion and biosynthesis in the adrenal medulla [115]. Pituitary adenylate-cyclase activating polypeptide acts as an emergency response peptide and is required for survival by promoting gluconeogenesis to counter life-threatening hypoglycemia [116]. Genetic variations in the pituitary adenylate-cyclase activating polypeptide receptor have been implicated in maladaptive responses to stress, anxiety, and fear, and are believed to be important factors in the development of post-traumatic stress disorder [117–119]. Thus, stimulation of pituitary adenylate-cyclase activating polypeptide may be another benefit of capsaicin treatment, in that fasting and emotional stress has been reported as a common precipitant of acute episodes of cannabinoid hyperemesis syndrome in genetically predisposed individuals [10,11,53].