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)

Glucose and arginine infusion tests were performed on 12 healthy volunteers (8 males, 4 females) before and after serotoninergic activation [oral administration of L-5-hydroxytryptophan (5-HTP-) for 6 days] and serotoninergic inhibition (oral treatment with D,L-p-chloropenylalanine for 6 days). 5-HTP treatment markedly increased urinary 5-hydroxyindoleacetic acid excretion, increased the mild hyperglycemic effect of arginine infusion, and lowered the glucose disposal rate constant. The adverse effect of serotoninergic activation on glucose tolerance is not sufficiently explained by the observed changes in insulin and glucagon secretion during the fasting state and after intravenous glucose and arginine infusions. Serotoninergic inhibition did not affect the carbohydrate tolerance of normal individuals. The results of this work supports the idea that excessive indoleamine production is probably the main cause for carbohydrate intolerance in carcinoid tumors.
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PMID:Serotoninergic activation and inhibition: effects on carbohydrate tolerance and plasma insulin and glucagon. 14 82

The levels of TRP, 5-HTP, 5-HT and 5-HIAA were measured in the proximal colon of the rabbit using ion exchange chromatography and spectrofluorimetry. Assays were performed on fragments of the intact colonic wall, on the muscle layers containing nerve plexuses, and on the mucosa-containing enterochromaffin cells. In spite of identical TRP concentration, 5-HT levels were higher in the mucosa than in the muscle containing nerve plexus. In the muscle, the ratio 5-HIAA/5-HT was about 1, i.e., comparable to that of the brain, whereas the ratio was very low in the mucosa, suggesting a weak 5-HT catabolism in the enterochromaffin cells. When the mucosa was severed from the muscle, 5-HT synthesis was increased. In this case, 5-HT and 5-HIAA concentrations in the reconstituted wall (muscles + mucosa) were higher than in the intact wall. In in vitro studies, levels of newly synthesized (3H)5-HT from (3H)TRP were 3 times higher in the reconstituted wall than in the intact one, and the conversion index of TRP to 5-HT was higher in the mucosa and in the reconstituted wall respectively. These results suggest that enterochromaffin cells do synthesize 5-HT from TRP when the mucosa is divided from the muscle. (3H)5-HT was taken up by both nerve plexuses and mucosa, with a high affinity mechanism. Results from tryptophan loading experiments indicated that 5-HTP decarboxylase in the gut might be involved in the regulation of 5-HT synthesis. The mucosa severed from the muscles might represent a good model for the study of carcinoid tumour development.
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PMID:5-HT metabolism in the intestinal wall of the rabbit. 616 29

A case of sporadic, histamine-producing gastric carcinoid with liver metastases is reported. The patient was treated with somatostatin analogue (octreotide) combined with cortisone and blockade of histamine receptors prior to surgery, which included subtotal gastrectomy, excision of lymph node metastases and superficial liver metastases. Residual liver metastases were injected with ethanol. These interventions markedly reduced the urinary excretion of the main histamine metabolite (MelmAA). Eighteen months later combined immuno- and chemotherapy was initiated due to tumour progression and recurrent hormonal symptoms with good clinical results over 12 months. Scintigraphy, using 111In-DTPA-D-Phe1-octreotide, visualized somatostatin receptors (sstr) in primary tumour, lymph node metastases and liver metastases. The tissue/blood 111In concentration ratios of tumour biopsies were very high. Northern analyses confirmed expression of all subtypes of sstr1-5. Immunocytochemically, tumour cells were strongly positive for chromogranin A, histamine and vesicular monoamine transporter (VMAT) 2 (histamine transporter), but negative for VMAT 1, suggesting an origin from gastric enterochromaffin-like cells. In primary tumour cell cultures, histamine, 5-HTP and 5-HIAA, but not 5-HT, could be detected in conditioned culture medium, indicating a defective decarboxylation of the tryptamine precursor. This rare case of histamine-producing gastric carcinoid demonstrates that excellent symptom relief can be achieved despite disseminated disease, if active, multimodal treatment strategy is instituted. The presence of high numbers of sstr in tumour tissue also raises the possibility of receptor-guided radiotherapy.
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PMID:Gastric carcinoid with histamine production, histamine transporter and expression of somatostatin receptors. 958 30

Carcinoid tumors account for less than 1% of all malignancies. The majority arise in the gastrointestinal system (GI carcinoids). The diagnosis of GI carcinoids is often made late, the protean symptoms are easy to overlook. Diagnosis, prognosis and treatment options are based on biochemical markers and imaging investigations. A high concentration of urinary 5-HIAA or an elevated serotonin level in plasma help to establish the diagnosis of GI carcinoid. Plasma chromogranin A has poor specificity (68%); its level depends on disease involvement and therapeutic response. Octreoscan is the best imaging technique to detect GI carcinoids, but CT scan and MRI are superior for the detection of metastasis. 18F-DOPA or 11C-5-HTP/PET, imaging fusion as of octreoscan or PET scan with CT or MRI, improve the results of metabolic imaging. Coronal contrast-enhanced CT or MRI angiogram can evaluate mesenteric vessel spread before surgery. Upper endoscopy or colonoscopy, can be performed to detect foregut carcinoid in MEN, or hindgut carcinoid. Echoendoscopy visualizes abdominal wall and local node involvement. Enteroscopy and capsule endoscopy localize 66% of midgut carcinoids. Although there have been considerable advances in diagnostic modalities, the diagnosis of carcinoid tumors is still, all too often, late.
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PMID:[Gastrointestinal carcinoid tumors: a multi-technique diagnostic approach]. 1792 31

Many neuroendocrine tumors (NET) are small and may escape localization by conventional imaging techniques. In such cases, 11C-5-hydroxy-tryptophan (11C-5-HTP) positron emission tomography (PET) has been tested as an additional diagnostic tool. Nine patients with clinically, biochemically and/or histologically confirmed NET and negative computerized tomography (CT) or magnetic resonance imaging (MRI), and 111In-pentetreotide (Octreoscan) scintigraphy underwent imaging with 11C-5-HTP-PET/CT in order to: 1) detect the primary tumor lesion in three patients; 2) detect residual disease in two patients with appendiceal carcinoid, one with rectal carcinoid, one with midgut carcinoid, and one with ectopic ACTH secretion (EAS) due to residual pulmonary carcinoid; and 3) restage a patient with medullary thyroid carcinoma (MTC) and hepatic metastases. 11C-5-HTP-PET/CT detected lesions in the mediastinum in a patient with EAS due to a pulmonary carcinoid, further hepatic metastases in a patient with carcinoid syndrome (CS) from a NET of unknown primary, further hepatic metastases in the patient with MTC, and hepatic metastases in the patient with midgut carcinoid. The 11C-5-HTP-PET/CT findings contributed to radical cure of the patient with recurrent EAS, and pointed towards bilateral adrenalectomy in the patient with EAS without evident primary tumor. In addition, 11C-5- HTP-PET/CT directed towards combined surgical and medical treatment in the patient with CS and multiple rather than single hepatic metastases and in the patient with midgut carcinoid, and towards continuation of medical treatment in the patient with MTC. 11C-5-HTP-PET/CT is a useful imaging technique, providing additional information for the diagnosis, staging and decision-making regarding management of patients with NET.
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PMID:The value of 11C-5-hydroxy-tryptophan positron emission tomography in neuroendocrine tumor diagnosis and management: experience from one center. 2033 8