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 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

A 41-yr-old female with presumed Cushing's syndrome was found to have a diurnal cortisol rhythm characterized by low values of 8:00 a.m. and consistently high values at 4:00 p.m. and midnight. Hourly sampling of plasma cortisol over 24 hr confirmed this rhythm, as did measurement of urinary free cortisols in samples collected every 6 hr over 24 hr. Hypercortisolemia was not suppressed by 2 mg of dexamethasone given every 6 hr for 24 hr. The adrenal tissue was responsive to ACTH. Iodocholesterol scanning revealed unilateral activity, and the patient's syndrome was cured by resection of an adrenal adenoma. In this patient a diurnal cortisol secretory pattern was present due to the secretory activity of the adenoma. The cause of the abnormal but persistent diurnal pattern is unknown.
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PMID:Cushing's syndrome due to adrenal adenoma with persistent diurnal cortisol secretory rhythm. 20 99

Bilateral malignant polyadenomas of adrenals seem to be rare. They involve either a double primary adrenal tumour, or a metastasis of a controlateral tumour. In the observation reported here, the evolution is characterized by periods of central stimulation with partial autonomy, and periods of tumoral autonomy with central inertness. Pathological findings consist of coexistence of various histological aspects (atrophy, hyperplasia, benign adenoma, carcinoma) suggesting the successive steps of a very particuliar adrenal carcinogenesis. Such findings allow to discuss the following physiopathological mechanism: a stimulation by ACTH might have resulted initially in a preneoplasic hyperplasia, then in an incompletely autonomous tumour, and finally in an autonomous tumour. Accordingly, from a practical and therapeutic point of view, it would be suitable, after removal of an adrenal tumour, especially of one with demonstrated ACTH-dependance, to suppress totally endogenous ACTH by cortisol or cortisone therapy, in order to reduce the occurence of corticotropin stimulation of possibly remaining malignant adrenal cells.
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PMID:[Partially hormone dependent bilateral malignant polyadenomatous hyperplasia]. 20 15

In one case of pituitary basophil adenoma, the majority of the cells contains numerous small granulations which, by using immunohistoenzymatic technique, react with alpha, 17-39 ACTH and beta, MSH antisera. The reaction with anti beta, 1-24 ACTH is negative. The radioimmunoassay of ACTH reveals an increase of plasmatic ACTH, but the cortisol cycle stays low. This data suggests that this functional adenoma releases a product of which has an immunological relationship with ACTH, without biological activity.
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PMID:[Pituitary adenoma with alpha, 17-39 ACTH and beta, MSH cells, without hypercorticism (author's transl)]. 20 17

A 48-year-old hypertensive diabetic woman rapidly became virilized. Urine 17-oxo-and oxogenic steroids and plasma testosterone, androstenedione, DHEA, DHEA-sulphate and androstenediol were greatly elevated. Plasma cortisol was constantly high and was not suppressed by dexamethasone. Circulating immunoreactive ACTH was consistently detectable at 18-24 ng/l. A 450 g carcinoma arising from a nodular hyperplastic right adrenal gland was resected. Production by the tumour of 17a-hydroxypregnenolone, 17a-hydroxyprogesterone and five C-19 steroids, but very little prenenolone, progesterone or cortisol, was shown by blood sampling, tumour culture and dramatic falls after operation. The plasma cortisol fell to half, with no diurnal variation, consistent with persistent Cushing's syndrome, and the plasma ACTH rose to 55 ng/l. She died 3 months later from a myocardial infarction. Autopsy revealed a pituitary basophil adenoma at a site where radiologically there had been an indentation in the fossa floor for at least 7 years. The left adrenal gland showed nodular hyperplasia. Therefore we conclude that mild pituitary-dependent Cushing's syndrome may have been present for many years before development of a virilizing carcinoma. This case demonstrates that adrenal carcinoma in man can sometimes develop as a consequence of nodular adrenal hyperplasia which may in turn be due to long-standing trophic hyper-stimulation.
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PMID:Cushing's syndrome, nodular adrenal hyperplasia and virilizing carcinoma. 20 18

In 31 patients with primary aldosteronism routine clinical and laboratory data, the effect of orthostasis on plasma aldosterone (PA), plasma renin activity (PRA) and cortisol (PC), effect of fludrocortisone or high sodium intake on basal PA and night-day fluctuations of basal PA and PC with and without suppression of pituitary ACTH by dexamethasone were determined to differentiate patients with a unilateral aldosterone producing tumour (adenoma, APA, n=20; carcinoma, CA, n=1) from those with idiopathic bilateral adrenal hyperplasia (IAH, n=10). Mean systolic and diastolic blood pressure, age, serum potassium and urinary excretion of sodium and potassium were not significantly different in both groups of patients. Normokalaemic primary aldosteronism occurred both in patients with APA (n=2) and in patients with IAH (n=1). Mean basal PA and mean urinary excretion rate of aldosterone-18-glucuronide were higher though not significantly different in patients with APA or CA than in those with IAH. A substantial number of the patients with APA (n=5) and with IAH (n=3) showed urinary excretion rates of aldosterone-18-glucuronide less than 13 microgram/24 h. Mean PA and PRA significantly increased (P less than 0.025) in patients with IAH in response to posture. However, these changes also occurred at times in some patients with APA. Both fludrocortisone and high sodium intake produced a variable and no group-specific effect on basal PA. Night-day variations in PA were positively correlated with those in PC in all patients with APA (n=12) and in 5 of 8 patients with IAH. A dissociation of PA and PC, however, was only observed in patients with IAH. Finally, the effect of dexamethasone on plasma aldosterone curves was variable in both groups of patients. Our results indicate that under the described conditions analysis of routine clinical and laboratory data and of peripheral PA, PRA and PC are of limited value in differentiating patients with APA or CA from those with IAH.
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PMID:Primary aldosteronism: inability to differentiate unilateral from bilateral adrenal lesions by various routine clinical and laboratory data and by peripheral plasma aldosterone. 21 20

The low sensitivity of adrenocortical adenoma to ACTH, documented in vivo, and in vitro, results from decreased cAMP generation in response to ACTH while distal steps of biosynthesis of cortisol are even more active in these tumoral cells than in normal adrenocortical cells.
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PMID:[Response to ACTH of human adrenocortical cells isolated from normal glands and from adrenocortical adenoma (author's transl)]. 21 94

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

The responses of the cyclic AMP-generation system and corticosteroids biosynthesis to ACTH and angiotensin II and cholesterol and other lipid contents in adrenal tissues were estimated in the in vitro experiments in 3 cases of Cushing's syndrome due to ACTH-responsive and unresponsive adenomas, one case of Cushing's disease (diffuse hyperplasia), one case of primary aldosteronism and one normal subject. The responses of cAMP accumulation and corticosteroids production to ACTH in in vitro studies were quite in good agreement with the in vivo responses of plasma cortisol by ACTH infusion test. The adenylate cyclase activity decreased and the phosphodiesterase activity increased in the case of hyperplasia and in one case of ACTH-responsive adenoma, whereas the basal cyclic AMP content was slightly more in ACTH-responsive adenoma and maximal in hyperplasia compared with that of the normal adrenal tissue. The characteristic features observed in ACTH-unresponsive adenoma were the largest amount of the basal corticosteroids production and esterified cholesterol content, and the lowest content cAMP. These results indicate that there was not always the consistent correlation between the cAMP-generation system, corticosteroids and aldosterone production, and conversion of cholesterol to pregnenolone by the stimulation of ACTH and angiotensin II in adrenal tumors.
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PMID:Comparative study of cyclic AMP-generation system, steroid biosynthesis and lipid metabolism in vitro in ACTH responsive and unresponsive adrenal tumors. 22 40

A 50-yr-old woman with Addison's disease from the age of 14 yr was diagnosed as empty sella turcica in 1974 (Rev Clin Esp 139: 183, 1975). She subsequently continued with hyperpigmentation in spite of adequate hormone substitution therapy which permitted her to lead a normal life. When studied she showed an extreme elevation of plasma ACTH (1500--2000 pg/ml), and with dexamethasone (2 and 8 mg/day) continued to have levels of 900 pg/ml. With 60 mg hydrocortisone daily, effects of overdosage were observed (swelling and Cushingoid facies) associated with depigmentation. However, she continued to manifest levels of plasma ACTH of 700 pg/ml and an absence of circadian rhythm. It seems likely that this patient represents a case of pituitary ACTH secretory adenoma (corticotropinoma) secondary to the preexisting Addison's disease. The circulating levels of other pituitary hormones were normal.
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PMID:Probable pituitary adenoma with adrenocorticotropin hypersecretion (corticotropinoma) secondary to Addison's disease. 22 93


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