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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient presented with mediastinal metastases from renal adenocarcinoma. Palliative therapy included Gelfoam and steel coil embolization of the right renal artery. Six weeks later he was found to have developed severe hypertension. Arteriogram revealed collateral vessels which supplied the tumor; the renal vein renin activity was four times higher on the right than on the left. We suspect that infarction of the kidney was not complete because of collateral arterial supply, and renin-dependent hypertension was the result. Thus, it may be hazardous to embolize large hypernephromas without subsequent nephrectomy.
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PMID:Hypertension with renal carcinoma. An effect of arterial embolization. 685 May 39

Evaluation for hypertension revealed a hypernephroma in two patients and increased plasma renin concentrations (PRC) of 2.8 and 3.1 GU . 10(-4)/ml, respectively. In one of the patients, bilateral renal venous catheterization showed lateralization of PRC toward the tumor side in the ratio 10:3. She had secondary hyperaldosteronism with a plasma aldosterone concentration (PAC) of 738 pmol/l, and hypokalemia with a serum potassium level of 3.0 mmol/l. In the other patient, who had malignant hypertension, PAC was not measured but serum potassium was subnormal (3.3 mmol/l). After nephrectomy, blood pressure (BP), PRC and serum potassium returned to normal in both as did PAC in one of the patients. At regular follow-ups through one year after nephrectomy, BP, PRC, PAC and serum potassium remained normal and metastases were not discovered. The increased incidence of hypernephroma in hypertensive patients underscores the importance of acknowledging this possibility during evaluation for hypertension.
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PMID:Hypernephroma and hypertension. Two case reports. 701 Sep 27

Adrenocortical carcinomas are very rare tumors. The diagnosis and therapeutic results in 5 female patients are reported. In 4 cases the tumor displayed biochemical and clinical features of Cushing's syndrome, while one was an adrenocortical carcinoma with hypersecretion of aldosterone only. The mean age was 53.6 +/- 8.2 years. In all four cases with Cushing's syndrome the diagnosis was established by measurement of urinary free cortisol extraction rates and excretion rates of 17-ketogenic steroids (mean 1794.5 +/- 1968 micrograms/24 h for free cortisol and 50.5 +/- 24.9 mg/24 h for 17-ketogenic steroids), while the excretion of 17-OH-steroids was in the normal range in one case with hypercortisolism. The patient with mineralocorticoid excess showed markedly elevated plasma aldosterone levels (840 pg/ml) and undetectable plasma renin activity (less than 0.2 ng/ml/3 h), but normal urinary excretion rates of 17-hydroxy- and 17-ketosteroids. The adrenal lesions were localized by intravenous pyelography or sonography and by angiographic procedures, while radioscanning by 131I-cholesterol showed no uptake of activity. Unilateral adrenalectomy was performed in four cases. After appearance of hormonally active metastases o,p'DDD was administered as an antitumor agent in 3 patients. Two of these patients died 10 and 25 months after surgery. One patient with multiple lung metastases is still alive, with a postoperative course of more than 80 months.
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PMID:[Diagnosis and therapy of hormonally active cancer of the adrenal cortex. Study of 5 cases]. 726 61

The adenovirus (Ad) E1 region genes, E1A and E1B, are well known cooperatively to transform primary rodent cells and activate a number of cellular promoters, including nuclear oncogenes such as N-myc and c-jun, in transfected cell lines. However, there is still less information available on the in vivo mechanism(s) by which the E1 region gene, when chromosomally integrated in the living animals, exerts its effect on nuclear oncogene activation coupled with transformation. To investigate such in vivo activity of E1A we have used a series of microinjection experiments into fertilized eggs to generate three transgenic mice carrying the Ad12-type E1A/E1B genes under the control of the human renin gene. This transgene caused an early onset of bowel cartinoid tumors that express neural cell adhesion molecules, but do not metastasize to any region. Northern blot analysis revealed that the transgenes were considerably expressed in the tumors, but not in other tissues at detectable levels. Interestingly, the levels of N-myc and c-jun mRNAs in the cartinoid tumors were elevated 19- and 8-fold, respectively, as compared with those found in the control intestine. In contrast, the major histocompatibility complex (MHC) class I mRNA level was not altered between the tumor and control intestines, suggesting that this unchanged expression may reflect the loss of tumor metastasis. These findings provide the first in vivo evidence that the expression of the Ad12 E1 region gene induces cartinoid tumors associated with the activation of the nuclear oncogenes N-myc and c-jun.
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PMID:Activation of the nuclear oncogenes N-myc and c-jun in carcinoid [correction of cartinoid] tumors of transgenic mice carrying the human adenovirus type 12 E1 region gene. 786 36

Malignant rhabdoid tumor is a rare, aggressive, invariably lethal tumor that is resistant to multimodal treatment. In this report, two patients with malignant rhabdoid tumor of the kidney (RTK) are described. The first patient is the first case of RKT with hyperreninemia, and the second case is also the first case with a specific chromosomal abnormality, del 11p13. The first patient presented with hematuria and a mass in the left kidney. Plasma renin, angiotensin, and aldosterone levels were elevated and paralleled the tumor progression. The karyotype of the tumor cells was normal (46,XX). In the second patient, who presented with a mass in the right kidney, the concentration of plasma tissue polypeptide antigen was elevated and paralleled the tumor progression. The karyotype of the tumor cells was 46,XX, del(11)(pter-p13::p12-qter). RTK with a cytogenetic abnormality of del(11p13), which is usually found in aniridia-Wilms' tumor syndrome, has not been known. Both patients died of metastatic disease within 7 months of diagnosis in spite of the multimodal therapy. The clinicopathology of RTK and the differences between Wilms' tumor and RTK raise compelling questions which should be the subject of future studies.
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PMID:Rhabdoid tumor of the kidney: a report of two cases with respective tumor markers and a specific chromosomal abnormality, del(11p13). 869 95

Adrenal masses are more and more frequently detected by adrenal ultrasound, computed tomography or nuclear magnetic resonance carried out for a reason other than the suspicion of adrenal disease (incidentalomas). The findings of an incidentaloma still leaves many diagnostic and therapeutic questions open. We report the results of a multicentric retrospective evaluation of patients with adrenal incidentalomas, performed by a Study Group of the Italian Society of Endocrinology. According to the definition of incidentaloma, exclusion criteria a priori were: severe or paroxysmal hypertension, frank hypokalemia and clinical signs of hypercortisolism or hyperandrogenism. 29 centers participated in the study and the data obtained by questionnaire were collected in 2 centers for final elaboration. Center 1 carried out the epidemiological and clinical evaluation. Basal and dynamic hormonal evaluation of 786 among the 1013 cases recruited were performed in our center (center 2). Functional studies included: diurnal rhythm of cortisol, urinary free cortisol (UFC), ACTH, DHEAS, 17-OH progesterone, testosterone, androstenedione, supine and upright plasma renin activity (PRA) and aldosterone, urinary aldosterone, urinary catecholamines and VMA. The hormonal dynamic evaluation included the overnight dexamethasone suppression test (1 mg), CRH test and ACTH test. In our study, 89% (702 patients) of adrenal incidentalomas were non-hypersecretory masses; 6.2% (49 patients) showed a preclinical Cushing's syndrome (PCS) (at least two altered parameters of pituitary-adrenal axis); 3.4% (27 patients) were pheochromocytomas; 0.89% (7 patients) were aldosteronomas. One tumor was a masculinizing adrenocortical carcinoma. Two hundred sixty patients underwent surgical exploration and the histological diagnosis showed: 138 adenomas (53%), 32 carcinomas (12%), 26 pheochromocytomas (10%). 16 myelolipomas (8%), 13 cystic lesions (5.5%), 7 tumors of neuronal lineage (3%). 12 metastases (4%), 13 others (5%). The 138 patients with adenomas had the following hormonal diagnosis: 103 nonfunctional adenomas (74%), 31 PCS (23%) and 4 cases of hyperaldosteronism (3%). In the patients with PCS an abnormal dexamethasone suppression test was found in 86% of cases (37/41 patients). Values for ACTH were low in 78% (32/41 patients). UFC was elevated in 64% of patients, the diurnal rhythm of cortisol evaluated in 14 patients was absent in 7. Only in 50% of cases DHEAS values (12/24 patients) were decreased, whereas they were normal in the other 50%. Interestingly, 8 patients with normal DHEAS and normal UFC showed nonsuppressible cortisol by dexamethasone test (1 mg). Blunted ACTH response to CRH was detected in 9 of 14 patients (64%). Thus our data suggest that the best parameter for evaluating subclinical hypercortisolism seems to be the overnight dexamethasone suppression test. In 27 patients with pheochromocytoma 24-hour urinary catecholamine and VMA levels were elevated in 86 and 46% of cases respectively. In 7 patients with hyperaldosteronism upright PRA was suppressed in 100% of cases and aldosterone plasma levels were elevated in 6 patients (86%); serum potassium level was slightly decreased in 60% of cases. In 86 of 138 histologically proven adenomas, DHEAS levels were: normal in 59% of patients, decreased in 36% and elevated in 4.6%, whereas in 22 of 32 cortical carcinomas evaluated. DHEAS levels were normal in 63% of cases, decreased in 18% and elevated 18%. Post-ACTH 17-OH progesterone levels were elevated in 52% (62/118 patients) of non-functioning adenomas and in 2 of 4 carcinomas. Not enough data are yet available postoperatively. In summary, endocrine evaluation can lead to the identification of a nonnegligible number of cases of clinically unsuspected pheochromocytomas and subtle hypercortisolism (about 3.4 and 6.2%, respectively of all adrenal incidentalomas), while cases of primary subclinical aldosteronism are rarely found. (ABSTRACT TRUNCATED)
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PMID:Adrenal incidentaloma: an overview of hormonal data from the National Italian Study Group. 916 66

To evaluate whether low DHEA-S levels are predictors of cortical origin, benignity and hormonal activity in incidentally detected adrenal masses, thirty-five patients with adrenal incidentalomas were studied. All patients were operated on and the diagnosis was histologically confirmed. Basal endocrine workup included plasma determination of cortisol before and after dexamethasone (1 mg overnight), plasma ACTH (08:00 h), 17-OH-progesterone, testosterone and potassium, standing plasma renin activity and aldosterone, supine and standing plasma noradrenaline and adrenaline. If necessary, we performed dexamethasone suppression tests at low (2 mg) and high (8 mg) doses, or the loperamide test (16 mg os) for evaluation of glucocorticoid activity and the glucagon test (1 mg i.v.) for exploring adrenal medulla function. Plasma DHEA-S was measured in all patients and the results were compared to those obtained in controls matched for age, sex and menopausal status. Suppression of DHEA-S was found in 11 out of 35 patients (31.5%). However, this hormonal finding occurred in 50% of the extracortical adrenal lesions, while in proven cortical adenomas (no. = 19) it was detected in only 5 patients (26.3%). Sensitivity, specificity, diagnostic accuracy and positive predictive value of low DHEA-S in indicating a cortical origin of the mass were 0.27, 0.0, 0.25, and 0.80. In malignancies (no. = 6) low DHEA-S levels were found in 1 out of 2 metastases and never in cortical carcinomas. Sensitivity, specificity, diagnostic accuracy and positive predictive value of low DHEA-S in indicating a benign form were 0.34, 0.83, 0.42, and 0.91. Six out of 19 patients with cortical adenomas showed signs of hypothalamic-pituitary adrenal (HPA)-axis dysfunction. Low DHEA-S levels were found in 50% of adenomas with HPA-axis abnormality and in 15.3% of adenomas without hormonal activity. Sensitivity, specificity, diagnostic accuracy, and positive predictive value of low DHEA-S levels in indicating hormonal activity of the mass were 0.50, 0.84, 0.73, and 0.60. Our data indicate that the association between low DHEA-S levels and adrenal incidentalomas is frequent. Low DHEA-S appears to be a poor predictor of hormonal activity with low sensitivity and specificity in respect of cortical origin and benignity of the mass. In conclusion, our results show that DHEA-S measurement does not offer relevant clinical information in the management of adrenal incidentalomas.
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PMID:Utility of plasma dehydroepiandrosterone sulphate determination in adrenal incidentalomas. 969 28

Incidentally discovered adrenal masses, or adrenal incidentalomas, have become a common clinical problem owing to wide application of radiologic imaging techniques. This definition encompasses a heterogeneous spectrum of pathologic entities, including primary adrenocortical and medullary tumors, benign or malignant lesions, hormonally active or inactive lesions, metastases, and infections. Once an adrenal mass is detected, the clinician needs to address two crucial questions: is the mass malignant, and is it hormonally active? This article provides an overview of the diagnostic clinical approach and management of the adrenal incidentaloma. Mass size is the most reliable variable to distinguish benign and malignant adrenal masses. Adrenalectomy should be recommended for masses greater than 4.0 cm because of the increased risk of malignancy. Adrenal scintigraphy has proved useful in discriminating between benign and malignant lesions. Finally, fine-needle aspiration biopsy is an important tool in the evaluation of oncological patients and it may be useful in establishing the presence of metastatic disease. The majority of adrenal incidentalomas are non-hypersecretory cortical adenomas but an endocrine evaluation can lead to the identification of a significant number of cases with subclinical Cushing's syndrome (5-15%), pheochromocytoma (1.5-13%) and aldosteronoma (0-7%). The first step of hormonal screening should include an overnight low dose dexamethasone suppression test, the measure of urinary catecholamines or metanephrines, serum potassium and, in hypertensive patients, upright plasma aldosterone/plasma renin activity ratio. Dehydroepiandrosterone sulfate measurement may show evidence of adrenal androgen excess.
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PMID:Adrenal incidentaloma. 1100 18

We studied 4 new cases of juxtaglomerular cell tumor and compared their morphologic and immunohistochemicalfeatures with 2 renal hemangiopericytomas and 5 cutaneous glomus tumors. The juxtaglomerular tumors were resectedfrom 2 males and 2 females (mean age at diagnosis, 23 years). Three patients manifested with severe hypertension. Tumors ranged from 2.2 to 8.0 cm and were well circumscribed. The tumors consisted of solid sheets and nodules of variably sized tumor cells with round, oval, and spindled nuclei alternating with edematous microcystic foci. Nuclear atypia, present in all tumors, was a prominent feature in 2. Mitotic activity was not identified. All cases showed hemorrhage, numerous mast cells, and thick-walled blood vessels. Unusual features included coagulative tumor necrosis, a hemangiopericytoma-like vascular pattern, and hyalinized stroma. All tumors were immunoreactive for CD34 and actin. Ultrastructural analysis revealed the presence of rhomboid-shaped renin protogranules. Patients were treated by partial or radical nephrectomy and followed up for 14 to 48 months. There were no recurrences or metastases. The characteristic clinical and morphologic features of juxtaglomerular cell tumor permit distinction from renal hemangiopericytoma and other renal tumors.
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PMID:Juxtaglomerular cell tumor: a clinicopathologic study of four cases and review of the literature. 1204 49

The incidental finding of an unsuspected adrenal mass ranges from 0.5% to 5% in abdominal CT series. The optimal diagnostic approach to such masses is to diagnose malignant or secretory tumors requiring excision and to otherwise avoid unnecessary surgery. Physical examination generally contributes little. A standard biochemical evaluation should include the measurement of 24 hour urinary catecholamines and metanephrine, urinary free cortisol and plasma cortisol levels at 8 a.m. and 8 p.m. combined with an overnight low-dose dexamethasone suppression test, serum potassium assay, and determination of upright plasma aldosterone to plasma renin activity. These tests will serve to screen for pheochromocytoma, subclinical Cushing's syndrome, and primary hyperaldosteronism respectively. Imaging characteristics suggestive of malignancy include: size greater than 4 cm., heterogeneous lesion and/or density greater than 20 Hounsfield Units on CT scan, slow enhancement with delayed washout after intravenous contrast injection on CT scan, and slightly decreased signal intensity in out of phase (fat suppressed) MR acquisition. Fine-needle aspiration biopsy should be performed only if metastatic disease is suspected. Adrenal scintigraphy with iodocholesterol may be useful where adenoma with subclinical Cushing's syndrome or solid tumor is suspected. In summary, the following strategy is recommended for the management of adrenal incidentalomas : mass lesions larger than 4 cm. and hormone-secreting tumors should be removed. All non-secreting adrenal incidentalomas smaller than 4 cm. in diameter should be followed by serial imaging at regular intervals (6, 12, and 36 months) and by endocrine reevaluation at one year.
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PMID:[Diagnostic and therapeutic strategy for an incidental finding of an adrenal mass]. 1241 Jan 36


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