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)

Three cases of carcinoid tumour of the stomach associated with primary hyperparathyroidism had the clinical and pathological features of a pluriglandular syndrome. Two of the patients showed multiple small polypoid carcinoids in the non-antral stomach, in conjunction with a parathyroid adenoma in one and parathyroid hyperplasia in the other case. One of these patients was also suffering from pernicious anaemia. A third patient had a large metastasising carcinoid arising in the gastric body and a parathyroid adenoma. Immunohistochemical stains for PGP 9.5 were positive in the carcinoids of all three cases. In all cases the carcinoids showed immunoreactivity for gastrin. A positive family history of endocrine hyperplasia and neoplasia was established in one case. It is suggested that patients with gastrointestinal carcinoids and their families should be evaluated for hyperparathyroidism, and patients with hyperparathyroidism presenting with upper gastrointestinal symptoms should undergo endoscopy to rule out gastric carcinoid tumours.
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PMID:Carcinoid tumour of stomach and primary hyperparathyroidism: a new association. 295 64

Although enterochromaffin-like (ECL) cells form the major endocrine cell population of the non-antral stomach, they have been largely overlooked in the study of gastric disease. In the human, their product and functions are unknown, but they are associated with histamine secretion in rodents. The cells are controlled by neural and hormonal factors, the most significant of the latter being gastrin. Interest in ECL cells has been stimulated by the observation that hyperplasia of these cells, sometimes leading to formation of gastric carcinoid tumours, occurs in conditions of persistent hypergastrinaemia - for example, in response to the achlorhydria of individuals with pernicious anaemia. The advent of new highly potent inhibitors of gastric acid secretion is allowing more information to be obtained on the physiology and functions of the ECL cell. However, there is clearly a great deal more to be discovered about this enigmatic endocrine cell type.
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PMID:Review: the enterochromaffin-like cell, intragastric acidity and the trophic effect of plasma gastrin. 297 52

We have described a 40-year-old woman whose classic adrenal insufficiency, achlorhydria, and hypergastrinemia was complicated by the development of a gastric carcinoid. There is now evidence that patients with elevated serum gastrin levels are at increased risk for this rare tumor.
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PMID:Gastric carcinoid associated with achlorhydria, hypergastrinemia, and Addison's disease. 305 27

Recently, the gastric endocrine system has been recognized as the origin of benign and malignant tumors in pernicious anemia. It has also been found that the gastric endocrine cells respond to permanent elevation of serum gastrin levels induced by changes in acid secretion in response to surgical procedures, drug therapy and age. Therefore, a definition of nonantral gastric endocrine hyperplasia (simple or diffuse, linear or chain-forming, micronodular, adenomatoid), dysplasia (enlarging or fusing micronodules, microinvasion, nodular growth) and neoplasia (intramucosal carcinoid, invasive carcinoid) is presented. The individual entities are illustrated, together with the literature discussed and the techniques for their identification presented.
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PMID:Histopathological classification of nonantral gastric endocrine growths in man. 307 29

Clinical and experimental evidence indicates that carcinoid tumours of the stomach fundic mucosa represent another example of hormone-dependent neoplasm, gastrin being the hormone involved in tumour induction. In this context hyperplasia of fundic endocrine cells associated with chronic atrophic gastritis (CAG) and hypergastrinaemia is regarded as the most frequent preneoplastic lesion. However, the cell type involved in this hyperplasia has not been clarified. To elucidate this problem fundic endocrine cells were characterized ultrastructurally in 9 patients from which endoscopic gastric biopsies were obtained. ECL cells were the most frequent cell type in 8 cases, in 4 of which they were more numerous than all other cell types taken together. D1 cells were the most frequent type in one case while they were inconspicuous in the other cases. P cells were found with a frequency in each case intermediate between that of ECL cells and that of D1 cells. These results indicate that fundic endocrine cell hyperplasia occurring in hypergastrinaemic CAG is in most cases cytologically similar to that found in other hypergastrinemic conditions, in which the gastrin-dependent ECL cells were already found to prevail. They also explain why fundic carcinoids arising in CAG are mostly composed of ECL cells. The relation between ECL, D1 and P cells, if any, remains obscure.
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PMID:Ultrastructural characterization of fundic endocrine cell hyperplasia associated with atrophic gastritis and hypergastrinaemia. 308 27

Neuroendocrine tumours of upper gastrointestinal tract fall into two main categories. First carcinoid tumours of the stomach and duodenum and secondly endocrine pancreatic tumours. The endocrine tumours of the gastric mucosa include two main types, so called ECL-oma of the corpus and fundic region and gastrin producing carcinoids or hyperplasia of the antrum and duodenum. The endocrine tumours of pancreas include entopically secreting insulinomas, glucagonomas, somatostatinomas, PP-omas, and ectopically secreting tumours, such as gastrinomas and tumours producing ACTH, GHRH, and calcitonin. The diagnosis of a neuroendocrine tumour of the upper gastrointestinal tract is based on the recognition of certain clinical syndromes and the determination of certain humoral products. A broad battery of radioimmunological assays for determination of different peptides is mandatory for the diagnosis and follow up of these patients. The diagnosis is also based on histological and immunocytochemical investigation of tissue specimens obtained at operation or by biopsy. Ultrasound investigation is the best non-invasive technique to detect metastases from neuroendocrine gut and pancreatic tumours, but angiography might unveil metastases down to a size of less than 5 mm. Surgery is still the primary treatment procedure but other treatments are needed because many patients have metastases already at the time of diagnosis. Chemotherapy with streptozocin combined with 5-fluorouracil or adriamycin and human leucocyte interferon has demonstrated objective response rate of about 70%. The new somatostatin analogue SMS 201-995 is an important adjunct in controlling clinical symptoms in patients with neuroendocrine gut and pancreatic tumours. A combination of different treatment procedures is needed for long-term management of these patients.
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PMID:Neuroendocrine tumours of the upper gastrointestinal tract and pancreas. 329 22

Immunohistochemical, histochemical, and morphometrical studies of six gastric carcinoid tumors and their possible precursor lesions in gastric mucosa are reported. All tumors, presenting successively at our institute, occurred in the corpus mucosa of 45- to 78-year-old patients. Two neoplasms had already metastasized. Three tumors contained gastrin- and/or serotonin-positive cells. Two groups of carcinoids, one with atrophic gastritis type A [AGA (four cases)], and one without AGA (two cases) were discerned. Only cases with AGA showed antral G cell hyperplasia consistently as well as fundic endocrine cell proliferation and sometimes multifocal tumors. This confirms previous reports that hypergastrinemia might be a predisposing condition for the development of gastric carcinoids in AGA. Fundic endocrine cell increase, verified by quantitative methods, was either diffuse or nodular. Diffuse endocrine cell hyperplasia comprised G, EC, and ECl cells. The observation that endocrine cell nodules comprised a similar mixture of endocrine cells, sometimes communicating with glands of pseudopyloric metaplasia and proving to be reversible in one case, provides evidence that these nodules are hyperplastic, but finally may lead to gastric carcinoid tumors in AGA. Size less than 150 micron, basal location, and mixed hormone content may be helpful criteria for the distinction of hyperplastic endocrine cell nodules from small carcinoid tumors.
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PMID:Gastric endocrine cell hyperplasia and carcinoid tumors in atrophic gastritis type A. 331 12

Among 196 patients examined in 1972-1985 because of pernicious anemia (PA), 105 patients under the age of 76 years were invited for gastroscopic screening, and 71 patients (68%) participated. Gastroscopy revealed carcinoid tumor(s) in 5 patients (7%) but no case of carcinoma. In addition, one patient with gastric carcinoid, 5 patients with adenocarcinomas and one with a concomitant carcinoid and carcinoma had already been diagnosed earlier in the overall PA group on the basis of clinical symptoms. Thus, within a follow-up of 0-20 years (mean 7 years) the total frequency of gastric carcinoid tumors was 4% and that of carcinoma 3%. Patients with carcinoid tumors had a long duration of PA and young age of onset; these cases were not necessarily those with the highest serum gastrin levels. Even though most gastric carcinoids are small subclinical tumors of uncertain clinical significance, their unexpectedly high frequency, combined within the risk of carcinoma in PA, might indicate the need for gastroscopic follow-up, at least in cases of juvenile onset PA.
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PMID:Gastroscopic screening for gastric carcinoids and carcinoma in pernicious anemia. 338 91

The usefulness of radio-metaiodobenzylguanidine (MIBG), a specific radiopharmaceutical agent for scintigraphic imaging and treatment of phaeochromocytoma and neuroblastoma, has been extended to the location of carcinoid tumors. Scintigraphic evaluation with I-123 MIBG in a patient with a histologically proven endocrine tumor (apudoma) of unknown origin with liver and bone metastases is reported. Elevated plasma hormone levels of gastrin, pancreatic polypeptide, and serotonin were found. Tumoral content of these hormones was immunocytochemically confirmed on liver biopsy. I-123 MIBG uptake could be seen in those areas of the liver with deficient lesions in the Tc-99m colloid image with a maximal uptake in a large mass at the level of the left liver lobe. No abnormal uptake could be observed at any other level, which was in contrast with autopsy findings of generalized metastatic disease.
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PMID:Iodine-123 MIBG imaging in a generalized pancreatic polypeptide-gastrin-serotonin secreting tumor. 339 Sep 81

There is a recognised association between pernicious anaemia and the development of gastric carcinoma, endocrine cell hyperplasia, and carcinoid tumour. Multiple endoscopic biopsies from the body mucosa of seven patients with pernicious anaemia showed small intestinal metaplasia with varying degrees of inflammation, fibrosis, and expansion of the lamina propria. Using conventional silver and lead stains, endocrine cells were inconspicuous. Staining for the general neural and neuroendocrine markers NSE and PGP 9.5 revealed a proliferation of endocrine cells in the epithelium and isolated clumps of endocrine cells in the lamina propria. The clumps were composed of two cell types, either small or large. Some of these endocrine cells showed gastrin, 5HT, VIP and substance P immunoreactivity of varying intensity. Ultrastructurally nine morphologically distinct types of granules were found some of which correlated with the immunohistochemistry. Some separate islands were composed solely of endocrine cells while others had a definite neural component, suggesting that the former arise from 'budding off' of enteroendocrine cells and the latter originate from the neuroendocrine cells of the lamina propria plexus. Thus there may be a dual origin of carcinoid tumours. Carcinoid tumours associated with pernicious anaemia tend to be multifocal and are infrequent. Less than 50 such cases have hitherto been reported. Our findings of endocrine cells proliferations in seven cases of pernicious anaemia indicate that this may be an adaptive change that occurs frequently and provides the basis on which carcinoids, less frequently, develop.
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PMID:Pernicious anaemia and mucosal endocrine cell proliferation of the non-antral stomach. 352 38


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