Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007095 (carcinoid)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

3 cases of pernicious anaemia in association with gastric carcinoid (in 1 case multiple) are described. All tumours were rich in argyrophil cells with the Sevier-Munger and Grimelius staining techniques, indicating that they might be of the enterochromaffin-like cell type. The possible causal relationship between pernicious anaemia and this type of argyrophil carcinoid is discussed.
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PMID:Pernicious anaemia in association with argyrophil (Sevier-Munger) gastric carcinoid. 9 57

An unusual case of a gastric carcinoid tumour producing multiple biogenic amines is described in a patient with pernicious anaemia. Electron microscopy demonstrated two distinct types of secretory granules.
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PMID:Multiple biogenic amine-secreting 'carcinoid' tumour of the stomach: a case report. 59 35

A clinical case of a patient with pernicious anaemia and a carcinoid tumor of the gastric fundus is described. In the context of the case the relationship between pernicious anaemia, achlorhydria, atrophic gastritis and gastric carcinoid is discussed. The gastric neuroendocrine tumours and their structural and functional characteristics were reviewed in an attempt to clarify the nomenclature and the diagnostic and therapeutic approach in these situations.
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PMID:[Gastric carcinoid associated with pernicious anemia]. 149 6

The aim of the study was to evaluate what family characteristics and what morphological, functional and immunological changes of the gastric mucosa precede the development of gastric malignancy in a follow-up of 11-14 years. The material consisted of 301 first-degree relatives of gastric carcinoma patients, 183 relatives of pernicious anaemia patients, and of 358 control relatives of probands computer matched from the general population by age and sex for the carcinoma probands. All subjects were endoscopically examined in 1973-1976 and followed up to the end of 1987. According to cancer registry data, 11 cases of malignant gastric tumours (9 carcinomas, one carcinoid tumour and one anaplastic tumour with suspicion of Hodgkin's disease) had been diagnosed during the follow-up: 6 belonged to gastric carcinoma, 2 to pernicious anaemia and 3 to control families. The occurrence of malignancy was significantly related to the presence of advanced gastritis with atrophy and of intestinal metaplasia before the start of the follow-up. In relatives with achlorhydria and low serum pepsinogen I levels the incidence of malignancy did not significantly differ from that in controls of similar age and sex distribution. The risk of getting malignancy was about four-fold in female members of gastric carcinoma and pernicious anaemia families but was not increased in control families. The risk was increased only in female members and concerned only gastric malignancy being the expected one or even lower than the expected in regard to malignancies of other location.
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PMID:Characteristics of gastric mucosa which precede occurrence of gastric malignancy: results of long-term follow-up of three family samples. 175 23

The relevance of enterochromaffin-like (ECL) cells in gastric pathobiology has generated considerable interest particularly since the recent description of a pathological state characterized as gastric argyrophilic carcinoidosis. The morphological and biofunctional properties of these cells are distinct from other gastric endocrine cells. It is probable that ECL cells have a major role in the regulation of parietal cell function. Other possible functions may include a trophic regulatory influence. Of particular interest is the recent observation that agents which result in profound and sustained acid inhibition may cause ECL cell hyperplasia. This phenomenon has also been noted in human disease states in which a significant decrease in acid section is evident (pernicious anemia/atrophic gastritis). In patients with gastrinomas of the multiple endocrine neoplasia type I group, therapeutically induced acid inhibition may result in gastric ECL hyperplasia and even neoplasia (gastric carcinoid or ECLoma). Similarly, in the rodent species mastomys, which is genetically predisposed to the formation of gastric carcinoids, exposure to acid inhibitory agents results in rapid (90-120 days) development of gastric carcinoids. The pathobiological relevance of ECL cells and the mechanisms of their inducible hyperplasia and neoplasia may be of considerable significance in understanding the regulatory role of gastric endocrine cells.
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PMID:Enterochromaffin-like cells and gastric argyrophil carcinoidosis. 185 6

Several previous reports suggest an association between treatment of patients with interferon-alpha (IFN-alpha) and development of autoantibodies and autoimmune disease. We here summarize the experience from a group of 135 patients with midgut carcinoid tumors treated with natural leukocyte IFN-alpha or recombinant IFN-alpha (rIFN-alpha). An unusual high incidence of antimicrosomal antibodies (MsAb) or anti-thyroglobulin antibodies (TgAb) and thyroid disease manifested as hyperthyroidism, hypothyroidism or a biphasic Hashimoto-like disease was seen, with female predominance. The incidence of antinuclear antibodies (ANA) was also increased, but equally in both sexes. Antibodies to parietal cells were found in 5 cases and 4 patients with pernicious anemia were detected. Two patients developed vasculitis of leukocytoclastic type and one a syndrome resembling systemic lupus erythematosus. Some patients treated with rIFN-alpha develop anti-IFN antibodies. Such antibodies may also be autoantibodies reacting with autologous IFN-alpha. They can neutralize the biologic activity of administrated IFN preparation and cause therapeutic failure. The implications of the various autoimmune manifestations during IFN-alpha treatment are discussed.
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PMID:Autoimmune phenomena in patients with malignant carcinoid tumors during interferon-alpha treatment. 185 11

Gastric enterochromaffin-like cell carcinoids have been detected in rats exposed lifelong to omeprazole. By inhibiting acid secretion, omeprazole causes hypergastrinemia which, with prolonged exposure, exerts a trophic effect on enterochromaffin-like cells with eventual enterochromaffin-like cell carcinoid formation in some animals. This mechanism seems to explain the appearance of enterochromaffin-like cell carcinoids in human hypergastrinemic states, whether associated with hyperchlorhydria, eg, Zollinger-Ellison syndrome, or with hypochlorhydria, eg, pernicious anemia (nonantral atrophic gastritis). Omeprazole produces modest serum gastrin elevations in humans when monitored over a 24-hr period. Gastrin levels are markedly lower and less sustained than in the above hypergastrinemic states. Extensive gastric biopsy data from patients enrolled in long-term studies indicate that omeprazole administration is not associated with clinically significant changes in the human oxyntic endocrine cell population. Man and rat differ markedly both in their gastrin response to a given level of acid inhibition and in their response to the trophic influence of gastrin on enterochromaffin-like cells. The rat model is a false indicator of risk in man.
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PMID:Omeprazole. Gastrin and gastric endocrine cell data from clinical studies. 186 13

Multifocal gastric carcinoid tumors occasionally develop in patients with pernicious anemia, associated with hyperplasia of endocrine cells in the atrophic and metaplastic gastric body mucosa. This constellation of findings probably requires a trophic drive from hypergastrinemia associated with antral G cell hyperplasia, a consequence of achlorhydria in these patients. We report a case in which antrectomy was performed on such a patient in order to abrogate the trophic stimulus. Antrectomy was followed by resolution of hypergastrinemia and a decrease in the size of polyps endoscopically. Nine months later, the gastric remnant was resected. Using morphometric techniques, endocrine cells in the initial antrectomy specimen (which included body mucosa at the resection line) were compared with those in the subsequently removed gastric body. Antrectomy resulted in striking decreases in number (137 versus 34/mm2; P = 0.0001) and size (93 versus 56 microns2; P = 0.0001) of endocrine cells of body mucosa. The findings suggest that antrectomy may be useful in the management of endocrine cell hyperplasia, and possibly also associated carcinoid tumors, in pernicious anemia.
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PMID:Reversal by antrectomy of endocrine cell hyperplasia in the gastric body in pernicious anemia: a morphometric study. 223 80

A total of 71 patients has been reported in the English literature to have developed carcinoid tumors in the fundus of the stomach in association with chronic atrophic gastritis secondary to pernicious anemia. The tumors appear to develop from argyrophilic cells in response to hypergastrinemia produced by hyperplastic G cells in the antrum of the stomach. We report a similar patient who, in addition, had a neuroendocrine tumor develop in the neck of the pancreas, which obstructed the pancreatic duct and resulted in severe chronic pancreatitis in the body and tail of the gland. There was an associated splenic vein thrombosis with left-sided portal hypertension. The pancreatic neoplasm was treated by excision, including the caudal 85 per cent of the pancreas and spleen. The gastric carcinoids appeared to diminish in size in response to a octreotide acetate (Sandostatin, Sandoz Pharmaceuticals; Hanover, NJ) administered to promote closure of a low-volume postoperative pancreatic fistula. The gastric lesions may require surgical treatment in the future. We were unable to find other examples of pancreatic neuroendocrine tumor occurring in association with pernicious anemia in a search of the English literature.
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PMID:Neuroendocrine tumor of the pancreas in a patient with pernicious anemia. 235 Jan 7

Thirty-six patients with malignant carcinoid tumors were treated with human leukocyte interferon (IFN) im at doses of 3-6 megaunits/day. The origins of the primary tumors were as follows: mid-gut (29 patients); pulmonary (four); rectal (one); ovarian (one); and unknown (one). Nineteen of the 36 patients had previously been treated with cytotoxic agents, streptozocin plus 5-fluorouracil or doxorubicin, but showed progressive disease. With IFN objective tumor responses were seen in 17 of the 36 patients (47%): in 14 of the 29 patients with mid-gut carcinoids (48%) and in three of the four patients with lung carcinoids (75%). The median duration of response was 34 months. Stable disease was noted in 14 of 36 patients (39%), all presenting mid-gut carcinoids. The median duration of stable disease was 25 months. Progressive disease from the start of IFN therapy was seen in five patients (14%). All responders except one had a greater than 50% reduction of urinary 5-hydroxyindoleacetic acid or alpha-human chorionic gonadotropin, whereas four patients also had a significant reduction of tumor size on computerized tomographic scan or at laparotomy. Two patients achieved complete remission. Improvement of clinical manifestations of the carcinoid syndrome was seen in all patients with objective response. Adverse effects including influenza-like syndrome, reduction of blood cells, chemical signs of liver dysfunction, and disturbed lipid metabolism occurred but were reversible or could be circumvented by dose reduction. Autoimmune phenomena were also noted such as development of thyroid autoantibodies with thyroiditis, SLE syndrome with antinuclear factors, and parietal cell antibodies with pernicious anemia. IFN therapy seems to be very effective in controlling tumor-secreted substances and thus giving relief of clinical symptoms. It also arrests tumor growth for extended time periods (median, 2 years). The adverse effects are surmountable and less severe than with cytotoxic therapy.
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PMID:Treatment of malignant carcinoid tumors with human leukocyte interferon: long-term results. 242 64


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