Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of adrenal scintiscans, venograms and venous aldosterone levels are compared with the histologic findings in 33 patients submitted to operations for primary aldosteronism. Standard and suppression scintiscans were performed 2-14 days following intravenous administration of 2mCi of 131I-19-iodocholesterol. The adrenal lesions were histologically classified into four categories: 25 patients had adenomas, 6 had macronodular hyperplasia, 1 had microscopic hyperplasia and 1 had an adenocarcinoma. Asymmetrical uptake between the two adrenals seen on standard scintiscans did not differentiate between a tumor or asymmetrical hyperplasia, unless the tumor was greater than 2 cm in diameter. During suppression scintiscans, unilateral uptake visible within five days of tracer injection was consistent with adenoma. Patients with nodular hyperplasia demonstrated early uptake in both adrenal glands during suppression scintiscans, while the patient with microscopic hyperplasia did not. The type of adrenal lesion was correctly identified in 20/26 (77%) of patients by suppression scintiscans; 21/28 (75% of patients by venograms and 12/16 (75%) of patients who had adrenal venous aldosterone measurements attempted. The majority of surgically correctible lesions could be identified on suppression adrenal scintiscans. Adrenal vein catheterization can be reserved for those patients in whom the results of suppression scintiscans are inconsistent with the clinical degree of aldosteronism.
 ...
PMID:Adrenal imaging with 131I-19-iodocholesterol in the diagnostic evaluation of patients with aldosteronism. 124 93

A 66-year-old female was admitted to Chiba University Hospital for the evaluation of a left adrenal mass which was incidentally discovered by computerized tomography. The patient had no clinical signs of Cushing's syndrome. Although the plasma ACTH level was suppressed, serum cortisol and urinary 17-OHCS levels were normal. Serum cortisol was not suppressed by dexamethasone and loss of diurnal rhythm of cortisol was observed. Uptake of 131I-aldosterone in the left adrenal gland was noted, but no accumulation was observed in the right one. Left adrenalectomy was performed. The tumor resected was 20 x 22 x 26 mm in size. Pathological diagnosis was adreno-cortical adenoma. Whether slight abnormality of adrenocortical function without clinical symptoms observed in the present case would develop into a clinically typical Cushing's syndrome remains to be solved.
 ...
PMID:[A case of pre-Cushing's syndrome]. 132 52

Exciting developments in knowledge of primary aldosteronism include description of new subtypes and elucidation of the genetic basis of one variety. Furthermore, relatively simple biochemical screening (aldosterone/renin ratio) has disclosed that primary aldosteronism is more common than previously thought, by diagnosing patients at an earlier, normokalaemic stage. The mutant gene discovered in the glucocorticoid-suppressible variety (FHI) codes for an aldosterone biosynythetic enzyme normally controlled by angiotensin II, and now controlled by corticotropin. The zona fasciculata is hyperplastic and makes aldosterone and "hybrid steroids" 18-oxocortisol and 18-hydroxycortisol in excess, in response to ACTH but not to angiotensin II. Adrenal tumours have not yet been described in this condition. Aldosterone-producing adenomas (Conn's syndrome) are also commonly composed of zona fasciculata-like cells, make "hybrid steroids" in excess and are very sensitive to ACTH but not to angiotensin II. We have described a new variety of aldosterone-producing adenoma which is responsive to angiotensin II (AII-responsive APA), consists of at least 20% zona glomerulosa-like cells, and does not make "hybrid steroids" in excess. We have also described a new familial variety of primary aldosteronism that includes tumours and is not glucocorticoid-suppressible (FHII). We propose that primary aldosteronism is a spectrum of genetic diseases expressed as either hyperplasia or neoplasia, and that morphological and genetic diversity explains biochemical and clinical behaviour.
 ...
PMID:Primary aldosteronism: hypertension with a genetic basis. 135 75

In a 21-year-old Caucasian women with von Hippel-Lindau disease, norepinephrine-producing adrenal pheochromocytoma was identified as the underlying cause of severe hypertension. She was found to have extremely elevated levels of circulating renin and aldosterone, and she was markedly hypokalemic. Administration of captopril further enhanced renin secretion, while her blood pressure improved. The patient became normokalemic following tumor removal, and her blood pressure decreased to normal levels with reestablishment of normal circadian blood pressure rhythm. This case demonstrates that, in the absence of renovascular or malignant hypertension, pheochromocytoma can be the underlying cause for the clinical syndrome of hypertension associated with severe hypokalemia and hyperreninemic hyperaldosteronism.
 ...
PMID:Hyperreninemia and secondary hyperaldosteronism in a patient with pheochromocytoma and von Hippel-Lindau disease. 143 50

Compound 1 [3-(4-aminophenyl)-3-cyclohexylpiperidine-2,6-dione] is a highly potent nonsteroidal aromatase inhibitor of the aminoglutethimide (AG)-type containing an asymmetric carbon atom. 1 and its enantiomers (+)-1 and (-)-1 inhibited human placental aromatase by 50% at 0.3, 0.15, and 4.6 microM, respectively (IC50 AG = 37 microM). A competitive type of inhibition was observed for 1 and (+)-1 (Ki 1 = 3.9 nM, Ki (+)-1 = 2.0 nM, Ki AG = 408 nM). Using solubilized high spin aromatase, 1 showed a type II difference spectrum indicating the interaction of the amino nitrogen with the central Fe(III)-ion of the cytochrome P450 heme component. 1 and (+)-1 inhibited cholesterol side chain cleavage enzyme (desmolase) by 50% at 67 and 82 microM, respectively (IC50 AG = 29 microM). In ACTH-stimulated rat adrenal tissue in vitro, 1 was less active in inhibiting aldosterone and corticosterone production compared to AG (IC50s, 1, 130 and 140 microM, AG, 80 and 50 microM, respectively). In vivo, 1 was superior to AG, too: it showed a stronger inhibition of the plasma estradiol concentration of pregnant mares' serum gonadotropin-primed SD rats, the activity residing mainly in the (+)-enantiomer [ovarian vein: (+)-1, 0.31 mg/kg: 81% inhibition, (-)-1, 0.31 mg/kg: 6%, AG, 1.25 mg/kg: 35%]. Furthermore 1 was much more active in inhibiting the testosterone-stimulated tumor growth of the ovariectomized 9,10-dimethyl-1,2-benzanthracene tumor-bearing SD rat (postmenopausal model). Up to a dose of 600 mg/kg of 1 no central nervous symptom depressive effects were observed in the motility test and the rotarod experiment, whereas AG exhibited ED50s of 62 and 164 mg/kg, respectively.
 ...
PMID:Evaluation of the racemate and the enantiomers of a new highly active and selective aromatase inhibitor of the aminoglutethimide type. 147 56

The usefulness of ultrasonography (US) in the diagnosis of aldosterone-producing adenoma(s) (APA) was compared with computed tomography (CT) and adrenal scintigraphy in 13 patients. The initial examination with US could demonstrate four of seven right APA. Repeat examinations later in two patients whose tumors were initially not detectable did reveal a tumor in one patient. On the other hand, two left APA were delineated on the initial trial. The other seven left APA, except two small APA in one patient, could be delineated during repeat US examinations performed on other days. With CT, all APA were detected during the first or second trial except for the smallest one. The rate of localization by adrenal scintigraphy with dexamethasone pretreatment was 11 of 13 patients. CT had the highest localization rate. However, US was shown to be useful in the localization diagnosis of APA on repeat examinations with a high delineation rate comparable to CT.
 ...
PMID:Ultrasonography in the diagnosis of aldosterone-producing adenoma: is it useful? 150 19

19-Nor-deoxycorticosterone (19-nor-DOC), a hypertensinogenic mineralocorticoid, equipotent with aldosterone and independent of the renin-angiotensin system, is synthesized in the kidney and excreted in excess in the urine of patients with aldosterone-producing adenomas. This current study evaluated the adrenal and renal venous levels of aldosterone and 19-nor-DOC after adrenal and renal venous catheterization and blood sampling in five patients with aldosterone-producing adenomas. Aldosterone (mean +/- SEM) in the adrenal vein ipsilateral to the tumor (469 +/- 293 ng/dl) was higher than in the contralateral vein (70 +/- 59 ng/dl). 19-Nor-DOC (mean +/- SEM) was also higher in the ipsilateral (548 +/- 286 ng/dl) than in the contralateral (51 +/- 14 ng/dl) adrenal vein. In the renal veins, ipsilateral aldosterone (2.2 +/- 0.8 ng/dl) and 19-nor-DOC (12.2 +/- 2.4 ng/dl) were respectively similar to contralateral aldosterone (1.5 +/- 0.5 ng/dl) and 19-nor-DOC (14.6 +/- 1.3 ng/dl), whereas 19-nor-DOC was higher than aldosterone in each renal vein. The present study demonstrates that 19-nor-DOC is produced, not only from the kidneys, but also from the ipsilateral adrenal of patients with aldosterone-producing adenomas. The ipsilateral adrenal 19-nor-DOC production is comparable to that of aldosterone, suggesting that 19-nor-DOC may be contributing to the hypertension and hypokalemia in this disease. In the contralateral adrenal, aldosterone is suppressed to a greater extent than 19-nor-DOC, suggesting that these two steroids are under the influence of two different regulatory mechanisms.
 ...
PMID:19-Nor-deoxycorticosterone production from aldosterone-producing adenomas. 155 68

The present study was undertaken to investigate our recent finding that the peripheral levels of prolactin are elevated after the treatment of intact tumor-bearing rats with antiprogestins, like ONAPRISTONE (ON) and MIFEPRISTONE (MI). In ovariectomized rats, s.c. administration of ON (10 mg/kg/day for 5 days) induced a significant increase in the peripheral levels of prolactin without stimulating uterine growth or suppressing LH secretion. Additionally, treatment with ON enhanced the estradiol-induced increase in the serum prolactin levels, suggesting different mechanism(s) for the effects of ON and estradiol on prolactin secretion. In the castrated animals treated with ON we also found a significant increase in the serum levels of aldosterone and corticosterone, but no measurable amount of estradiol and no significant change in the levels of serum androstenedione. Accordingly, we supposed that the effect of ON on prolactin secretion may be induced by suppression of the known activity of adrenal corticosteroids in inhibiting the prolactin secretion. In a further study using ovariectomized and adrenalectomized rats we, in fact, found no appreciable effect of ON on the serum prolactin levels at all. By contrast, dexamethasone (DEX) (0.15 mg/kg for 5 days, s.c.) significantly decreased the prolactin levels which were elevated after adrenalectomy. This effect of DEX was partially reversed by a simultaneous application of ON. From the present observations, it is anticipated that the increase in the peripheral prolactin levels found after treatment with ON is partly due to the antiglucocorticoid effect of the compound.
 ...
PMID:Involvement of the adrenal glands in the prolactin rise induced in the female rat by an antiprogestin, onapristone. 156 60

Increased function of the adrenal cortex is a normal response in times of physiologic and psychologic stress. Adrenal cortical secretions (e.g., glucocorticoids, aldosterone) orchestrate a multitude of internal processes aimed at maintaining homeostasis and psychologic integrity. Many patients admitted to a critical care unit will manifest some increase, even minor, in adrenal function. However, excessive secretions of these hormones can have a lethal effect of fluid and electrolyte balance, energy metabolism, and immune function. Cushing's syndrome denotes a disorder characterized by increased circulating levels of glucocorticoids (primarily cortisol). An easily recognizable disorder, it may arise from pathology of the adrenal cortex or the anterior pituitary glands, ectopic secretions from a nonendocrine tumor, or from excessive doses of exogenously administered glucocorticoids. Cushing's syndrome is rarely an admitting diagnosis to critical care but is a disorder that can seriously affect recovery from coexisting illnesses if not treated. Aldosteronism, although rare, will often be diagnosed after admission to a critical care unit for management of troublesome hypertension, hypokalemia, congestive heart failure, and various dysrhythmias. Suspicion of the diagnosis should always arise when these manifestations occur, particularly when hypokalemia is refractory to potassium supplementation. Without timely diagnosis and treatment, these patients will succumb to lethal dysrhythmias.
 ...
PMID:Endocrinopathies of hyperfunction: Cushing's syndrome and aldosteronism. 157 32

In the 1950s, after years of suspicion and work by many investigators regarding a potent mineralocorticoid hormone from the adrenal cortex, aldosterone was at last isolated and chemically identified [40, 41]. Soon after, Jerome Conn was the first to report [11] the clinical correlate of excessive secretion of aldosterone from a benign adrenocortical tumor manifested by hypertension and hypokalemia with the increased urinary excretion of aldosterone. This tumor is often called as aldosteronoma, and the disorder produced by it has been called primary aldosteronism by Conn. In the vast majority of patients harboring such tumors, the hypertension is cured by the resection of the tumor [12, 51], although some suggest that the hypertension may recur in a proportion of apparently cured patients [3, 36]. Thus, primary aldosteronism represents one of a few potentially curable forms of hypertension. Since aldosterone is elaborated normally by the zona glomerulosa cells of the adrenal, it has been assumed that all aldosteronomas originate from the cells of the glomerulosa zone. A clonal origin of aldosteronomas has also been suggested [28]. Some earlier and recent developments, however, indicate that functionally there may be more than one type of aldosteronomas and that their cellular origins might be different.
 ...
PMID:Cellular origin of aldosteronomas. 160 Mar 48


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>