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)

We evaluated plasma growth hormone (GH) and plasma prolactin (PRL) levels in ten patients with metastatic carcinoid tumors and the carcinoid syndrome ("active tumors") and seven patients with metastatic carcinoid tumors without the carcinoid syndrome ("inactive tumors"). The patients with active tumors had elevated serum serotonin levels and increased urinary 5-hydroxyindoleacetic acid (5-HIAA) while these values were normal in patients with inactive tumors. Forty-five per cent of patients with active tumors had elevated fasting plasma GH levels that were either not suppressed or showed a paradoxical increase in response to I.V. glucose. There was a positive correlation between the plasma GH levels and serotonin production by the tumor. Twenty-eight per cent of patients with inactive tumors had elevated fasting plasma GH levels. GH levels were decreased by the administration of serotonin antagonists in some but not all of the patients. Parachlorophenylalanine (PCPA) an inhibitor of serotonin synthesis caused a paradoxical rise in GH levels. GH release in response to insulin hypoglycemia was normal. Plasma prolactin levels were normal in most of the patients with metastatic carcinoid tumors. PCPA administration did not systematically alter plasma prolactin levels. We conclude that elevated plasma GH levels are frequently present in patients with the carcinoid syndrome. Both serotonin produced by the tumors and the tumor itself may be responsible for the elevated GH levels.
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PMID:Growth hormone and prolactin secretion in the carcinoid syndrome. 12 43

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 urinary excretion of 5-hydroxyindoleacetic acid, 5-hydroxytryptophan, serotonin, tryptamine, and tyramine and the serum serotonin concentration were determined in 38 consecutive patients with metastatic carcinoid tumors. Four of the 23 patients with the carcinoid syndrome (15%) had markedly elevated excretion of 5-hydroxytryptophan. None of the patients had markedly elevated excretion of tryptamine or tyramine; a substantial number of patients had moderately low urinary excretion of these amines. All of the patients with the carcinoid syndrome had elevated urinary 5-hydroxyindoleacetic acid excretion; 2 of these patients had normal serum serotonin concentrations, suggesting that quantitative 5-hydroxyindoleacetic acid excretion is the most reliable test for the carcinoid syndrome. Although tryptamine secretion by carcinoid tumors is rare, 5-hydroxytryptophan secretion may be more common than is recognized.
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PMID:Serotonin metabolism in patients with carcinoid tumors: incidence of 5-hydroxytryptophan-secreting tumors. 30 17

To determine if patients with chronic hyperserotoninaemia from the carcinoid syndrome have increased basal adrenocortical function, I have determined the urinary free cortisol excretion of seventeen patients with carcinoid tumours and the carcinoid syndrome, twelve patients with carcinoid tumours without the carcinoid syndrome and seventeen normal subjects. There was no significant difference in the urinary free cortisol excretion of the patients with carcinoid tumours and the carcinoid syndrome (133 +/- 20.0 nmoles/24 h), patients with carcinoid tumours without the carcinoid syndrome (115 +/- 29 nmoles/24 h) and the normal subjects (96 +/- 9 nmoles/24 h). There was no correlation between the urinary free cortisol secretion and urinary 5-hydroxyindoleacetic acid or serum serotonin concentration in the patients with the carcinoid syndrome. There was a suggestion that patients with 5-hydroxytryptophan (5-HTP) secreting carcinoid tumours had higher urinary free cortisol excretion than patients with predominantly serotonin (5-HT) secreting carcinoid tumours. This may be due to the fact that the non-polar 5-HTP molecule penetrates the blood-brain barrier more effectively than the polar 5-HT molecule. 5-HTP is then converted to 5-HT within the brain. None of the twenty-nine patients with carcinoid tumours had clinical or laboratory evidence of the ectopic ACTH syndrome.
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PMID:Urinary free cortisol excretion in patients with hyperserotoninaemia from the carcinoid syndrome. 31 72

Results of evaluations of adrenal function in 11 patients with carcinoid tumors are presented. Nine patients had tumors that made and secreted serotonin resulting in elevated 5-hydroxyindoleacetic acid (5-HIAA), elevated serum serotonin, and the carinoid syndrome; while two patients had tumors that did not make serotonin and that did not cause elevated 5-HIAA excretion or elevated serum serotonin. All of the patients had normal 24-hr 17-hydroxycorticosteroid excretion. In the group of patients with tumors actively secreting serotonin, the correlation between 17-hydroxycorticosteroid and 5-HIAA excretion (r = 0.44) was not significant. Six of these patients pretreated with cyproheptadine (CYPRO), a serotonin antagonist, experienced a 36% mean decrease in 17-hydroxycorticosteroid excretion, a finding that was not present when three of them were treated with triprolidine (TPRO), an antihistamine. Serum cortisol at 8 a.m. was normal in all patients except two whose values were mildly elevated, and these two patients showed evidence of suppression of ACTH secretion secondary to dexamethasone treatment. There was a significant positive correlation between serum-cortisol concentrations and 5-HIAA excretions (r = 0.73, p less than .05). Normal diurnal variation was present in six patients in whom it was determined. The serum-cortisol response to insulin-induced hypoglycemia in six patients who had carcinoid tumors actively secreting serotonin was not statistically different from that of 12 normal volunteers. Comparisons between these two groups were difficult because the carcinoid patients' fall in blood sugar was 50%, whereas that of the control group was to 38% of the fasting glucose concentration. Six patients with actively secreting carcinoid tumors responded to standard metyrapone testing with a mean increment of 22.8 +/- 2.5 mg/day in 17-hydroxycorticosteroids. This response was statistically different from the increment of 13.8 +/- 5.3 mg/day in 17-hydroxycorticosteroid excretion found in 34 age-matched hospitalized control patients. When the tests were repeated in four of the patients with carcinoid tumors after pretreatment with CYPRO, the increment in 17-hydroxycorticosteroid excretion was reduced well below the mean increment of the control group. Peak serum 11-deoxycortisol (Compound S) values during the test were also reduced. This decrease in the metyrapone response after CYPRO pretreatment was not due to changed peripheral cortisol metabolism, altered adrenal responsiveness to ACTH, interference with recovery of 17-hydroxysteroids by the Porter-Silber reaction, altered metyrapone metabolism, or reduced renal clearance of Compound S. These changes in adrenal response to metyrapone were not seen when the patients were pretreated with TPRO. Our data suggest that the alterations in adrenal function in our patients may be related to elevated serum serotonin. If CYPRO acts by antagonizing serotonin, these data may give support to the idea of serotoninergic control of cortisol secretion.
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PMID:Adrenal function in the carcinoid syndrome: effects of the serotonin antagonist cyproheptadine. 117 50

Carcinoid patients are diagnosed biochemically on the basis of increased urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA); urinary and platelet serotonin concentrations are considered to provide complementary information. Using established HPLC methods with fluorometric detection, we evaluated the clinical usefulness of measurements of urinary 5-HIAA and urinary, plasma, and platelet serotonin in 30 consecutive patients with histologically proven carcinoid tumors of fore-, mid-, and hindgut origin before treatment. Ten patients showed no signs of serotonin overproduction; 14 had increased concentrations of urinary 5-HIAA and platelet serotonin; and platelet serotonin, but not urinary 5-HIAA, was increased in 6. None had increased urinary 5-HIAA excretion without an increase in platelet serotonin content. In cases with high rates of tumor serotonin secretion, platelet serotonin reached a maximum and did not correlate with serotonin secretion rate, whereas urinary 5-HIAA was correlated. Increased platelet serotonin was correlated with increased plasma serotonin and with occurrence of carcinoid syndrome. Increased urinary serotonin, allegedly caused by increases in circulating 5-hydroxytryptophan, almost invariably coincided with increased platelet serotonin, but not necessarily with above-normal urinary 5-HIAA excretion. From these results and long-term monitoring of three patients during treatment, we conclude that platelet serotonin is more sensitive than urinary 5-HIAA for detecting carcinoids that secrete only small amounts of serotonin.
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PMID:Improved diagnosis of carcinoid tumors by measurement of platelet serotonin. 137 75

24 patients with malignant carcinoid tumours received octreotide and interferon alfa (IFN-alpha). All the patients initially received octreotide 50-100 micrograms, twice daily. When progressive symptoms or increasing biochemical markers were observed, the daily dose was raised to a median 300 micrograms. If the initial dose proved ineffective or if no improvement was seen after escalation, IFN-alpha was added (median 9 MU subcutaneously per week). After the addition of IFN-alpha, 17 of the 22 patients (77%) with elevated urinary 5-hydroxyindoleacetic acid showed a significant (> 50%) reduction. Only 1 patient progressed and 4 had continuously stable biochemical disease. No significant reduction in tumour size was noted; in 5 patients, the tumour continued to grow despite decreasing hormone levels. 18 patients had carcinoid syndrome when IFN-alpha was added in 10 (56%) symptoms ameliorated. Thus, the addition of IFN-alpha is beneficial for patients with malignant carcinoid tumours that progress and/or who do not respond to octreotide.
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PMID:Octreotide and interferon alfa: a new combination for the treatment of malignant carcinoid tumours. 138 92

14 patients with metastatic carcinoid tumour were treated with recombinant interferon alfa 6-30 x 10(6) IU weekly for 3-25 (median 6.5) months. A decrease in the 24-h urinary 5-hydroxyindoleacetic acid (5-HIAA) level to less than 50% of the pretreatment value was observed in 5 of the 10 cases with an elevated urinary 5-HIAA level. In 4 of the 5 remaining patients, the 5-HIAA level decreased 30-50% from the pretreatment value. 5 of the 9 evaluable patients with carcinoid syndrome experienced symptomatic relief, but none became symptom-free. Severe toxicity was not observed. The median time to progression was 4.5 months, and, in patients with a greater than 50% decrease in 24-h urinary-5-HIAA, it was 17 months. Objective regression in tumour size could not be demonstrated in any of the patients.
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PMID:Treatment of metastatic carcinoid tumour with recombinant interferon alfa. 138 93

From 1970 until 1990, 8,958 cases of primary carcinoma of the lung were diagnosed at the Duke University Medical Center. During the same period, 126 patients (mean age, 53 +/- 13 years) were diagnosed with bronchial carcinoid. The overall survival was 78% for 5 years and 71% for 10 years. Surgical treatment in 106 patients included pneumonectomy (15), lobectomy (63 with 9 bronchoplastic procedures), stapled wedge resection (22), and bronchoscopic laser resection (6). The method of diagnosis was chest roentgenography (121), chest computed tomography (77), mediastinal tomography (31), bronchoscopy (81), bronchoscopic brushing and washing (50), bronchoscopic biopsy (40), transthoracic needle biopsy (27), thoracotomy (100), and autopsy (5). Univariate analysis of the medical history, presenting signs and symptoms, diagnostic test results, and pathologic data predicted improved survival (p less than 0.001) for: female sex (n = 58), asymptomatic presentation (n = 47), normal serum serotonin or urinary hydroxyindoleacetic acid levels (n = 76), peripheral location of the primary tumor (n = 50), pathologic stage I or II (n = 91), negative lymph nodes (n = 80), primary tumor 2 cm or less in diameter (n = 67), and typical histology (n = 80). No significance (p greater than 0.1) was observed for age, smoking history, race, family history of carcinoid, environmental exposure, or hemoptysis. The most important factors affecting survival defined by multivariate analysis were (p less than 0.01) pathologic stage, atypical histology, and asymptomatic presentation. Bronchial carcinoid tumors are unique, making up 1% to 2% of primary lung neoplasms and having an excellent prognosis after resection with a 95% 5-year and 93% 10-year survival for pathologic stage I disease.
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PMID:Bronchial carcinoid tumors: a retrospective analysis of 126 patients. 161 Feb 54

Eight patients with metastatic carcinoid tumor, seven of whom had symptoms of the carcinoid syndrome, were treated with either human leukocyte interferon (seven patients) or recombinant alpha-interferon (IFN alpha-2b) (one patient) at doses of 4.5 to 21 x 10(6) IU weekly for 1 to 21 (mean, 8.5) months. Tumor regression on computed tomography (CT) scan was found in one patient, the CT findings remained unchanged in three, and the tumor progressed in four patients. A clearcut and continuing decrease in urinary levels of 5-hydroxyindoleacetic acid (5-HIAA) was observed in one patient and a transient one in four patients. The symptoms improved in only two of seven patients. Four patients had leukopenia develop, which was circumvented by reducing the dose. The authors conclude that interferon therapy of the carcinoid tumor is not as successful as has been suggested in previous reports.
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PMID:Is the treatment of metastatic carcinoid tumor with interferon not as successful as suggested? 185 91


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