Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric carcinoid tumor formation has been reported with prolonged achlorhydria in both animals and human beings. The hypothesis in this study was that the ablation of parietal cell function in an animal (mastomys) genetically predisposed to gastric neuroendocrine neoplasia would promote and accelerate tumor formation. Loxtidine, an irreversible H2-receptor blocker, was administered at 1 mg/kg/day in drinking water for 4 months to young mastomys (n = 16). After 4 months of treatment, 14 of 16 animals had gastric carcinoids compared with 0 of 16 young control animals and 4 of 16 older control animals. Ultrastructurally, these tumors were characterized by the presence of neurosecretory granules. Serum gastrin levels were elevated (230 +/- 40 pmol/L) in loxtidine-treated animals compared with control animals (26 +/- 8 pmol/L) (p less than 0.05). In addition, both peptide YY (620 +/- 160 pmol/L) and enteroglucagon (500 +/- 147 pmol/L) were significantly elevated compared with control groups (p less than 0.05). Similarly, in tumor tissue, peptide YY (676 +/- 152 pmol/gm) and enteroglucagon (551 +/- 164 pmol/gm) were found in large quantities, whereas gastrin was undetectable. These observations provide substantial support for the possible pathophysiologic role of gut peptides, particularly gastrin, in the generation of endocrine neoplasia. The advent of endocrine tumors after inhibition of a gut secretory cell (parietal) may be of considerable significance in understanding the genesis of endocrine neoplasia. Whether the drug acts as a neoplastic promoter of enterochromaffin-like cells or the tumor development is related to elevation of peptides such as gastrin cannot be established in this study. Long-term H2-receptor blockade with new potent, irreversible agents as an alternative to surgery may have potential grave implications that require careful consideration.
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PMID:H2-receptor blockade induces peptide YY and enteroglucagon-secreting gastric carcinoids in mastomys. 257 58

A man with long-standing pernicious anaemia developed multiple gastric carcinoid tumours with a background of diffuse enterochromaffin-like cell hyperplasia. There is evidence that enterochromaffin-like cells synthesis and store histamine and that their proliferation is stimulated by high serum gastrin levels. Gastric carcinoid tumours can be difficult to differentiate from the more common adenocarcinomas and may be a more frequent complication of pernicious anaemia than is currently recognised.
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PMID:Diffuse enterochromaffin-like (ECL) cell hyperplasia and multiple gastric carcinoids: a complication of pernicious anaemia. 722 60

Gastric carcinoid tumors were previously believed to be rare lesions, representing less than 2% of all carcinoid tumors and less than 1% of all stomach neoplasms. More recent studies have demonstrated that they may constitute as much as 10-30% of carcinoid tumors. Patients with conditions associated with hypergastrinemia, such as chronic atrophic gastritis, Zollinger-Ellison syndrome with multiple endocrine neoplasia type 1 (ZES-MEN-1), and pernicious anemia, display a markedly elevated incidence of gastric carcinoid tumor formation. A classification system distinguishing three types of gastric carcinoid tumor has been proposed: 1) tumors associated with chronic atrophic gastritis, 2) tumors associated with Zollinger-Ellison syndrome, and 3) sporadic lesions. Tumors that develop in association with hypergastrinemia are usually composed of enterochromaffin-like (ECL) cells, in contrast to sporadic lesions that contain a variety of endocrine cell types (enterochromaffin, ECL, X). In both intact animal models such as the rat and Praomys (mastomys) natalensis and in isolated purified ECL cell preparations, gastrin has been demonstrated to exert a powerful trophic effect on ECL cells, in addition to stimulating histamine secretion. It is apparent that hypergastrinemia-associated gastric carcinoids display relatively benign biological behavior. Sporadic lesions require aggressive surgical management on diagnosis. Type I and type II (hypergastrinemia-associated) lesions can be managed initially by endoscopic excision of accessible tumors, followed by endoscopic surveillance. If tumors recur, antrectomy and local excision may be used to remove the source gastrin, resulting in cure in the vast majority of patients.
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PMID:Gastric carcinoid tumors: the biology and therapy of an enigmatic and controversial lesion. 787 69

A patient with long-standing Zollinger-Ellison syndrome, treated for 14 years with antisecretory agents, underwent computed tomography and upper gastrointestinal examination because of upper gastrointestinal bleeding. Radiologic and pathologic examinations showed multiple nodular masses arising from the wall of the stomach that were determined to be mucosal carcinoid tumors. A gastrin-producing islet cell tumor of the pancreatic head was also present. Gastric carcinoid tumors occurred as a consequence of chronic hypergastrinemia.
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PMID:Gastric carcinoid tumors associated with chronic hypergastrinemia in a patient with Zollinger-Ellison syndrome. 888 25

Gastric carcinoid tumors arise from enterochromaffin-like (ECL) cells, these tumors represent 2-41% of all neuroendocrine tumors and 0.3% of malignant gastric neoplasias, being more common in men than in women, and commonly affecting people over 60 years old. These tumors arise from accelerated proliferation of the ECL cells as a consequence of the hypersecretion of gastrin, situation that can be present in atrophic gastritis and the Zollinger-Ellison syndrome. We report the case of a 51 year old hispanic female who presented with a 3 month history of abdominal pain, meteorism and constipation; she was treated with ranitidine and metoclopramide without clinical improvement, thus she underwent upper gastrointestinal endoscopy which showed an atrophic gastritis and gastric polyps. Histopathologic examination revealed a neuroendocrine gastric tumor which was positive to serotonine and gastrin stainings. Hormonal screening showed normal serum levels of LH, FSH, estradiol, ACTH, progesterone, calcitonin and cortisol. The serum level of gastrin was elevated with 500 pg/mL. Gammagraphic scanning with octreotide was negative for metastasis.
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PMID:[Gastric neuroendocrine tumor]. 1006 36

Gastric carcinoid tumours are rare neoplasms of neuroendocrine origin. They are believed to grow from enterochrommaffin-like (ECL) cells. Three different types of tumours can be distinguished: type I: hypergastrinaemic, induced by achlorhydria in chronic atrophic gastritis; type II: hypergastrinaemic, associated with Zollinger-Ellison syndrome and multiple endocrine neoplasia syndrome type 1; type III: sporadic. The trophic effect of gastrin on ECL cells is of crucial importance in the pathogenesis and treatment of hypergastrinaemic carcinoids. In these patients, hypergastrinaemia leads to ECL-hyperplasia, -dysplasia and -neoplasia. Hypergastrinaemic carcinoids often follow a very benign course, which makes it possible to avoid surgery, at least in patients at high surgical risk. The management of these three types is discussed.
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PMID:[Gastric carcinoid--pathogenesis and treatment]. 1042 89

Gastric carcinoid tumors are uncommon, but their percentage among all gastric malignancies has increased to 1.8%. Although they are most often discovered incidentally during endoscopy, gastric carcinoids can present with abdominal pain, bleeding, or symptoms related to the secretion of bioactive substances, most commonly histamine. Gastric carcinoids originate from the foregut and are derived from histamine-containing enterochromaffin-like (ECL) cells. Type I gastric carcinoid, the most common, exhibits slow growth and benign behavior. It occurs within the setting of chronic atrophic gastritis with achlorhydria-induced hypergastrinemia. Gastrin acts directly on ECL cells to induce hyperplasia, dysplasia, and, eventually, neoplasia. Type II gastric carcinoid, the least common type, occurs in patients with gastrinoma-associated multiple endocrine neoplasia syndrome-type 1 (MEN-1). The overall survival is related more to the underlying MEN-1 syndrome than to the gastric carcinoid. Rodents readily develop gastric carcinoid tumors in response to hypergastrinemia. However, in humans, other factors in addition to hypergastrinemia, such as pernicious anemia or MEN-1, must be present, implying that a genetic predisposition is necessary for the development of these tumors. Type III or sporadic gastric carcinoids exhibit a more malignant behavior, with overall 5-year survival rates of less than 50% and normal serum gastrin concentrations. Treatment of all types of gastric carcinoids is predicated upon accurate classification and staging. Radiolabeled somatostatin analogues are superior to conventional radiologic imaging techniques in detecting both primary and metastatic lesions. Treatment of choice for localized disease is excision, either endoscopically or surgically. Antrectomy, by eliminating the trophic effect of gastrin, can be useful for select type I carcinoids. Long-acting somatostatin analogues are excellent palliative agents.
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PMID:Treatment of gastric carcinoids. 1739 27

Gastric carcinoid tumors comprise 7% of all gastrointestinal carcinoids and have significantly increased in incidence over the past few decades. Seventy to 80% of gastric carcinoids are type I, which usually are clinically asymptomatic and found incidentally at endoscopic evaluation for abdominal pain or anemia. In this review, advances in understanding the pathophysiology of type I gastric carcinoid are highlighted. In addition, various current diagnostic and treatment options are discussed. Although type I carcinoids generally hold a benign course, rigorous investigation is needed to ensure accurate diagnosis and optimal treatment. This includes appropriate diagnostic procedures and imaging and accurate staging of tumor. Tumor size, depth of invasion, presence of metastasis, and the tumor's gastrin dependency dictate treatment options. Appropriate treatments can consist of endoscopic resection, antrectomy, medical management, or frequent follow-up. This article provides a systematic method of evaluating and treating type I gastric carcinoid.
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PMID:Review of the pathogenesis, diagnosis, and management of type I gastric carcinoid tumor. 2155 99