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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The estrogen-induced hamster renal carcinoma contains appreciable amounts of all cytosolic steroid receptor classes sedimenting as 7 to 8S moieties following sucrose gradient centrifugation. Their relative concentrations, expressed in fmol/mg protein +/- S.E. are progesterone (1496 +/- 23) greater than estradiol (218 +/- 3) greater than 5 alpha-dihydrotestosterone (154 +/- 7) greater than dexamethasone (138 +/- 3) greater than aldosterone (40 +/- 2). No cross-competition is apparent for either estrogen or progesterone receptors, but progesterone competes for both androgen and adrenocorticoid binding. These hormone-receptor complexes undergo nuclear translocation using purified tumor nuclei and in tissue minces at elevated temperatures. Salt-extractable nuclear receptors for estrogen (5S), androgen (3.2S), progesterone (2.7S), and corticosteroid (3.5S) have been identified. The existence of five specific steroid receptors within a single tissue is unique and provides a novel model for studying the interrelated actions of all steroid hormones and their therapeutic responses in a hormone-dependent neoplasm.
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PMID:Nuclear retention of all steroid hormone receptor classes in the hamster renal carcinoma. 44 67

Hypertension, hypokalemia, suppressed plasma renin activity and increased plasma aldosterone were found in a middle-aged woman. Following removal of the tumor in the left adrenal gland these abnormalities disappeared. Concurrently, however, the plasma cortisol level did not show normal diurnal change, although the value at 6 A.M. was within the normal range. Administration of 2 mg dexamethasone failed to depress the plasma cortisol level and urinary 17-OHCS concentrations. Postoperatively, plasma cortisol and urinary 17-OHCS were below normal. Histologic examination of the tumor indicated the presence of two types of adenoma cells; one was a large watery clear cell with rich lipid and possibly with aldosterone secretion and the other was an acidophilic cell with poor lipid and possibly with cortisol secretion. It is suggested that, in addition to oversecretion of aldosterone, the tumor autonomously secreted cortisol, although the amount of cortisol secreted was not large enough to produce typical Cushing's syndrome.
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PMID:Concurrent hypersecretion of aldosterone and cortisol from the adrenal cortical adenoma. 47 99

Adrenal steroids and compenents of the renin-angiotensin system were measured before and after adrenalectomy in a woman with Cushing's syndrome and hypertension from a functioning adrenocortical adenoma. Aldosterone, deoxycorticosterone and cortisol were produced in excess by the adenoma, and were measured in tumor tissue. High plasma renin substrate concentrations, and normal basal and furosemide-stimulated plasma renin activities and plasma renin concentrations which were present before surgery, decreased after adrenalectomy, and the hypertension diminished. The inappropriately normal levels of renin and potassium in this patient, despite autonomous aldosterone overproduction, suggest an ineffective mineralocorticoid action of aldosterone, possibly from interaction with her other adenoma-produced steroids. The decrease in components of the renin-angiotensin system suggests a partial renin-dependence of her hypertension.
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PMID:Hypertension and aldosterone overproduction without renin suppression in Cushing's syndrome from an adrenal adenoma. 47 1

Described herein is an autopsy case of a 16-year-old female with severe hypertension, hyperreninemia and secondary aldosteronism. She had had a progressively growing tumor of her right orbita from the age of 4. The tumor was partially excised 13 months before death. A high content of a renin-like material was detected in the excised tumor, which was histologically a hemangiopericytoma. Bowie stain revealed some granules in small number of tumor cells and electron microscopic study showed some cytoplasmic granules. Following the operation, hypertension was somewhat improved, but the levels of plasma renin activity and plasma aldosterone concentration remained elevated, because the tumor was partially resected. At autopsy, the tumor invaded into the cranial base and right frontal lobe, and metastasized to the lungs. In the present case, renal renin-secreting tumor, malignant hypertension and renovascular hypertension were ruled out by the clinical and pathological studies.
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PMID:Extrarenal renin-secreting tumor associated with hypertension. 91 Jun 30

The dexamethasone-modified adrenal scintiscan, a noninvasive procedure, is described for the preoperative distinction between primary aldosteronism (aldosterone-producing ademona) and idiopathic aldosteronism (bilateral hyperplasia) and for the preoperative localization of aldostersone-producing adenomas. This procedure has been carried out on 17 subsequently proved cases of primary aldosteronism and nine cases (four unexplored) of idiopathic aldosteronism. In the tumor cases, it indicated correctly the side of the tumor in 88 per cent. It was correct in predicting the existence of bilateral hyperplasia in all of the five cases explored. It produced the same response in four more cases believed to have bilateral hyperplasia, in which surgical exploration has not been carried out. Many of the same patients had, in addition, standard adrenal scintiscans (SS), adrenal venography, and determinations of aldosterone in adrenal venous blood. These results are compared with those of the dexamethasone scintiscan (DS). In tumor localization, the 88 per cent figure for the DS was only moderately better than that of the other three (71 per cent, SS; 80 per cent, venography; 80 per cent, adrenal venous aldosterone levels). However, in predicting bilateral hyperplasia, the DS was 100 per cent correct, as were the levels of aldosterone in adrenal venous blood. The SS and adrenal venography failed in bilateral hyperplasia and gave many false-positive results indicating tumor. The DS, a relatively simple outpatient procedure, appears to be at least as effective, both in lateralizing tumors and distinguishing between tumor and bilateral hyperplasia, as the more difficult, expensive, and sometimes hazardous invasive procedure of bilateral adrenal vein catheterization.
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PMID:The dexamethasone-modified adrenal scintiscan in hyporeninemic aldosteronism (tumor versus hyperplasia). A comparison with adrenal venography and adrenal venous aldosterone. 97 47

A woman with a benign tumor of the left adrenal cortex had a six-year history of hypertension. Serum potassium level and plasma renin activity were low. Plasma aldosterone and cortisol levels were low normal, and plasma desoxycorticosterone (DOC) level was extremely high. Iodine 131-labeled cholesterol accumulated in the tumor in the left upper quadrant of the abdomen. At laparotomy, a benign adrenal tumor was excised; thereafter, the blood pressure and plasma DOC levels returned to normal. We believe that this is the first case of a benign DOC-producing adrenal tumor.
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PMID:Benign desoxycorticosterone-producing adrenal tumor. 98 80

A young woman with mild to moderate hypertension and normal PRA, serum potassium levels, and urinary aldosterone excretion rate was found to have a renal tumor by selective renal arteriogram. Renal vein renin activity indicated an increased production of renin from the kidney containing the tumor. At surgery, a clear cell carcinoma of the kidney was found that contained renin activity in excess of the surrounding kidney tissue. The renin activity appeared identical to human kidney renin. Previous renin-producing tumors have been associated with severe hypertension, elevated plasma renin activity, hypokalemia, and elevated urinary aldosterone excretion. This case should call attention to the renin-secreting tumor as a cause of even mild hypertension.
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PMID:Renin-secreting clear cell carcinoma of the kidney. 113 Sep 32

Our experience indicates that although adrenal carcinoma is not a common cause of primary aldosteronism, 4 to 5% of patients in a single large series may have a malignant adrenocortical tumor. The magnitude of the hypokalemia and the hyperaldosteronuria tends to be greater in patients with malignant tumors, but these patients cannot be clearly separated from those with benign tumors or hyperplasia on this basis. Patients who have malignant tumors may have no chemical evidence of adrenocortical dysfunction other than excessive aldosterone secretion. Finally, a good response to spironolactone for months does not exclude adrenal carcinoma as the cause of primary aldosteronism.
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PMID:Primary aldosteronism and malignant adrenocortical neoplasia. 117 89

Hyperaldosteronism due to aldosteronoma is a rare but potentially curable form of pediatric hypertension. We have presented a patient who had symptoms of enuresis and fatigue, and in whom the diagnosis was suggested by low serum potassium and persistent hypertension. Diagnosis was confirmed by increased plasma and urinary aldosterone and decreased plasma renin. The tumor was localized with the aid of adrenal venography and catheterization, which showed greatly increased plasma aldosterone levels in the right adrenal vein. The pathologic findings were totally reversed by right adrenalectomy. The clinical picture and results following surgical removal of aldosterone-producing tumors in six children are reviewed.
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PMID:Aldosteronoma in a child with localization by adrenal vein aldosterone: collective review of the literature. 120 77

We used 131I-19-iodocholesterol as an adrenal-imaging agent in 27 hypertensive patients who had biochemical evidence of abnormalities in the renin-angiotensin-aldosterone system. In 10 of 12 patients in whom the biochemical findings suggested the presence of an aldosterone-producing adenoma the adrenal uptake was asymmetric. The adenoma was subsequently confirmed in all eight patients in this group who underwent operation. In contrast, the adrenal uptake was asymmetric in only one of 13 patients with biochemical evidence of iodopathic hyperaldosteronism or low-renin essential hypertension. Two patients with adrenal carcinoma causing primary aldosteronism did not concentrate the isotope in their tumors. When metabolic studies suggest an aldosterone-producing adenoma, adrenal imaging with 131I-19-iodocholesterol may locate the tumor before operation.
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PMID:Location of aldosterone-producing adenomas with 131I-19-iodocholesterol. 124 8


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