Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The peripheral levels of pregnenolone (delta5-P), 17-hydroxypregnenolone (17-delta5-P), progesterone (P), 17-hydroxyprogesterone (17-P), testosterone (T), 5alpha-dihydrotestosterone (DHT), androstenedione (A), dehydroepiandrosterone (DHEA), its sulfate (DHEA-S), estrone (E1), estradiol-17beta (E2), and cortisol (F) were measured prior to and 1 1/2 and 9 months after removal of a right adrenal "compact cell" adenoma in an amenorrheic patient with a virilizing adrenal adenoma, under the following conditions: 1) control for 2 days, 2) dexamethasone, 0.5 mg, every 6 hours for 2 days, and 3) dexamethasone, 2 mg, every 6 hours for 2 days. Except for E1, E2, and F, the control levels of all steroids measured were elevated, markedly so for delta5-P, 17-delta5-P, DHEA, A, and DHEA-S. Dexamethasone treatment had no detectable effect on the steroid levels. Following removal of the adrenal adenoma, the levels of all steroids returned to normal. The patient became eumenorrheic, with marked improvement of her hirsutism and virilization.
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PMID:Peripheral steroid levels in a patient with virilizing adrenal adenoma. 12 56

The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 +/- 1.86 microgram/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone. Upright PRA was suppressed in 9/16 patients with a mean of 4.9 +/- 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated. From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed. From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.
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PMID:Plasma renin activity and urinary aldosterone in Cushing's syndrome. 20 67

In a middle-aged woman with virilizing adenoma, 2 mg dexamethasone increased urinary excretion of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids, whereas 8 mg dexamethasone increased urinary excretion only of 17-KS. With discontinuation of dexamethasone, 17-KS excretion returned to the predexamethasone level. Dexamethasone depressed the basal level of cAMP synthesis and basal testosterone production by the normal adrenal tissue in vitro. Dexamethasone also depressed the increase of cAMP produced by ACTH in the normal tissue. In contrast, dexamethasone increased basal cAMP synthesis and stimulated testosterone secretion in the tumor tissue. ACTH and dexamethasone were additive in their effects on cAMP and testosterone in the tumor tissue. It is suggested that dexamethasone acted directly on the adrenal tumor to stimulate steroid secretion in this patients.
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PMID:Virilizing adrenal adenoma stimulated by dexamethasone in a middle-aged woman. 21 5

Thirty-eight hypertensive, hypokalemic patients underwent adrenalectomy for primary aldosteronism. Thirty-one patients were found to have an adenoma and seven patients "idiopathic" hyperplasia. The diagnosis was made by finding low plasma renin activity, which could not be stimulated, and unsuppressable elevated plasma or urine aldosterone. The distinction between adenoma and hyperplasia and the localization of an adenoma were accomplished by adrenal venography, adrenal vein blood analysis, and iodocholesterol scanning. Venography was accurate in 87%; adrenal vein blood analysis in 91%; and iodocholesterol scanning in 72%. Dexamethazone suppressed scanning heightened discrimination to 91%. The adenomas were equally distributed between the right and left adrenal gland, with one patient having bilateral adenomas. All but two patients underwent adrenalectomy from a posterior lumbar incision. Postoperative recovery was uncomplicated. Eighteen months after operation 77% of patients with an adenoma were normotensive.
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PMID:Primary aldosteronism: experience with thirty-eight patients. 47 33

Dexamethasone-suppression (DS) adrenal scintigraphy localizes an aldosteronoma, but with false-negative results, i.e. 2 of 19 cases in our study. Our aim was to clarify the clinical meaningfulness of this test. Adrenal iodomethyl-norcholesterol (NP-59) uptake on the adenoma side correlated with the estimated adenoma volume (n = 15, r = 0.843, P less than 0.001). Accordingly, the uptake ratio on the adenoma side to that on the opposite side depended on the adenoma volume (r = 0.683, P less than 0.01). This explains the false-negative results (uptake ratio less than 2) in two cases with small adenomas. The NP-59 uptake correlated weakly with the plasma aldosterone level (r = 0.516, P less than 0.05). This result indicates the low correlation between NP-59 uptake and the ability to secrete aldosterone. NP-59 accumulation in the surgically removed gland was analyzed by autoradiography in six cases where DS scintigraphy was done just before surgery. The density was higher in the adenoma cells than in the adjacent cortical cells in five cases, but the difference was rather small, i.e., within a 2-fold difference in four cases. In one case, almost the same density was observed in both types of cells. Thus, the laterality of NP-59 uptake primarily depends on the adenoma volume although NP-59 uptake somewhat reflects the adenoma's ability to secrete aldosterone or the adenoma cell's activity in accumulating NP-59. Care must be taken in interpreting the findings from DS scintigraphy where the adenoma is small or adrenal uptake is low.
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PMID:Iodomethylnorcholesterol uptake in an aldosteronoma shown by dexamethasone-suppression scintigraphy: relationship to adenoma size and functional activity. 240 12

We describe thirty-one patients with Cushing's syndrome, with the object of evaluating the relative merit of the Dexamethasone suppression test, Metyrapone test and Corticotrophin Releasing Factor (CRF) test in classifying the syndrome. Bilateral adrenocortical hyperplasia (Cushing's disease) was present in sixteen patients. Three had bilateral macrodular hyperplasia of the adrenal cortex, six had adrenocortical adenoma, four had adrenocortical carcinoma, and two patients presented ectopic ACTH-syndrome. The diagnosis was surgically verified in every case. The Metyrapone test was found to give the safest classification in patients with Cushing's syndrome. The Dexamethasone test will diagnose Mb. Cushing reliably when suppression of serum cortisol is present following the large dose of Dexamethasone, but failure to suppress does not exclude the diagnosis. The CRF test is easy to perform and distinguished reliably between Mb. Cushing and other causes of the syndrome in eight out of ten patients in whom it was performed. Outpatient examination including the CRF test and CT-scanning of the pituitary and adrenal glands is advocated as a preliminary step in the classification of biochemically and clinically suspected cases of Cushing's syndrome.
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PMID:[Investigation of Cushing's syndrome. The diagnostic value of the dexamethasone suppression test, the metopirone test and the CRF test]. 255 27

Endocrine hypertension secondary to disorders of the adrenal glands is uncommon, but by no means rare. The importance of correct biochemical diagnosis and subsequent localization of the responsible lesion(s) lie in the fact that many of these syndromes occur in younger patients, may exhibit familial patterns of inheritance and are frequently amenable to surgical cure. The radiopharmaceuticals (131)1-6 beta-iodomethyl-19-norcholesterol (NP-59), a marker of adrenocortical cholesterol uptake, and (131)1- and (123)1-metaiodobenzylguanidine (MIBG), a norepinephrine (NE) analog and marker of energy-dependent NE storage vesicle accumulation, can be shown to accurately localize adrenal cortex and sympathoadrenal dysfunction, respectively. In Cushing's syndrome (CS) not only does the pattern of NP-59 uptake depict the adrenal dysfunction and its pathophysiologic basis, but the level of NP-59 accumulation reflects the degree of adrenocortical hyperfunction. Adrenocorticotrophin-independent CS is uniformly and accurately localized, especially in bilateral cortical nodular hyperplasia where even high resolution computed tomography (CT) may fail to depict the often subtle, asymmetric anatomic abnormalities. Dexamethasone suppression NP-59 adrenal scintigraphy has been shown to be highly sensitive and specific, and exceeds the efficacy of CT in the differentiation of adenoma and bilateral hyperplasia in primary aldosteronism. MIBG is useful as a sympathoadrenal imaging agent whose clinical utility has been demonstrated in the localization of pheochromocytoma, especially as a modality to screen the body for multiple and extraadrenal, recurrent, or metastatic lesions. Moreover, the extent of metastatic involvement from neuroblastoma can also be accurately depicted using MIBG. In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. This approach, which is complementary to other anatomical modalities of imaging, can be used to advantage in the localization of functioning cortical and medulla adrenal diseases and other neoplasms of adrenergic origin.
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PMID:Scintigraphic studies in adrenal hypertension. 265 11

Synthetic ovine corticotropin-releasing factor (o-CRF) stimulated adrenocorticotropin (ACTH) release at the concentration of 10(-10) M or more in monolayer culture of rat anterior pituitary cells. Dexamethasone, 10(-7) M, inhibited this effect. In 5 healthy human subjects, o-CRF, 1 microgram/kg iv bolus, increased plasma ACTH levels from less than 10 pg/ml to 40.4 +/- 11.0 (mean +/- SD) after 30-60 min, and plasma cortisol from 12.8 +/- 2.8 micrograms/dl to 23.6 +/- 3.1 after 45-60 min. Of 7 patients with Cushing's disease (CD), five showed an exaggerated response of plasma ACTH and cortisol, one an exaggerated response of plasma ACTH but low response of plasma cortisol and the other no response of both hormones. The significant positive correlation between the inhibition of plasma cortisol by dexamethasone and the response of plasma ACTH and cortisol to o-CRF in CD was seen. No response of plasma ACTH and cortisol to o-CRF was seen in each one patient with Cushing's syndrome due to an adrenocortical adenoma, ectopic ACTH syndrome (but low response at retesting), isolated ACTH deficiency and Sheehan's syndrome. In one patient with Addison's disease an exaggerated response of plasma ACTH but no response of plasma cortisol was seen. In 4 of 5 healthy subjects and 5 of 7 patients with CD, plasma ACTH and cortisol levels showed a second peak at 120--210 min after o-CRF administration. To clarify the prolonged effect of o-CRF in human in vivo, the disappearance rates of injected o-CRF were evaluated by radioimmunoassay in 3 patients with cured Cushing's syndrome. A biexponential decay curve showed t1/2 values of 9.3 +/- 0.4 min and 79.6 +/- 0.7 min (mean +/- SE). From the chromatographic profile, a portion of injected o-CRF was thought to be bound to macromolecule (s). o-CRF, as a specific secretagogue of ACTH, is thought to be useful tool in evaluating patients with hypothalamo-pituitary-adrenal disorders.
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PMID:[Studies for clinical application of ovine corticotropin-releasing factor]. 298 91

We studied diurnal variation and the responses of plasma corticoids to dexamethasone and ACTH before and after adrenal surgery in 11 patients with primary aldosteronism. Diurnal variation of plasma corticoids was examined in all cases. Before adrenal surgery, plasma aldosterone (Ald) was higher at all times, deoxycorticosterone (DOC) was high value at 5:00 and then normal value, 11-deoxycortisol (S) was high value at 5:00 and 9:00, thereafter normal value, while corticosterone (B) and cortisol (F) were almost normal value at all times. The circadian rhythm was observed in these corticoids. Dexamethasone (2 mg/day) was administered to 8 patients for 10 days. Plasma Ald and DOC were significantly suppressed only at 5:00, while B, S and F almost suppressed at all times. After dexa suppression, the circadian rhythm of Ald still observed, while the diurnal variation of the other corticoids was even. ACTH (1 microgram) was injected intravenously to 9 patients. Responses of DOC, B and Ald were higher, and of S and F were almost normal. Diurnal variation of plasma corticoids was observed after 1 month of adrenal surgery. Ald was lower, the other corticoids were normal values. ACTH (1 microgram) was injected to the same case before surgery. Responses of these corticoids to ACTH were slightly lower. Contents of Ald in adenoma tissues were higher than those in adjacent and normal adrenal tissues, and the contents of the other corticoids in adenoma tissue were almost normal value. As these results showed, before surgery these corticoids were secreted from adenoma without ACTH, although these were responsible to ACTH, and the presence of regulative factor of circadian rhythm except ACTH was suggested. After surgery, not only the responses to ACTH of mineralocorticoids but these of glucocorticoids decreased.
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PMID:[Diurnal variation and responses of corticoids to dexamethasone and ACTH before and after adrenal surgery in primary aldosteronism]. 304 Apr 83

Pituitary thyrotrope tumours are a rare cause of hyperthyroidism. Prior in vitro studies of these tumours have revealed various patterns of differentiation and secretory activity. We have characterized the histological, biochemical, molecular and physiological features of a thyrotrope adenoma in order to define its origin and autonomy. Histochemical and electron micrograph findings confirmed the diagnosis of a thyrotrope cell adenoma. Immunostaining was positive for TSH and GH in the cytoplasm of the adenoma cells. Tissue extracts contained TSH-IR which co-eluted with authentic hTSH when analysed by gel filtration. Tumour fragments studied in a tissue culture system secreted TSH, alpha-subunit and GH. TRH (30 nmol/l) stimulated TSH and GH secretion. T3 (1.5 nmol/l) inhibited GH release and had no effect on TSH secretion. GnRH (50 nmol/l), dexamethasone (10(-4) mol/l), SRIH (1 mumol/l) and TRH-glycine, a tetrapeptide precursor of TRH, stimulated TSH release. Dexamethasone inhibited GH and alpha-subunit secretion. Stable transcripts for alpha- and beta-subunits of TSH and GH messenger RNAs were detected by molecular hybridization in cytosolic fractions. Immunohistochemistry, in vitro secretory function, and mRNA analysis suggest multidirectional differentiation of the tumour cells. TRH-glycine may have a direct stimulatory effect upon pituitary thyrotropes.
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PMID:Hormonal control of thyrotropin and growth hormone secretion in a human thyrotrope pituitary adenoma studied in vitro. 317 17


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