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)

An 11-year-old spayed cat was presented with clinical signs suggestive of hyperadrenocorticism. Adrenocortical function was assessed by dexamethasone suppression and by stimulation with ACTH and the results provided a tentative diagnosis of adrenocortical tumour. Via laparotomy (paracostal approach), the enlarged right adrenal gland was removed. Histopathological diagnosis was adrenocortical adenoma.
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PMID:Cushing's syndrome due to adrenocortical adenoma in a cat. 70 43

Pituitary function was studied in nine patients who had recovered from pituitary apoplexy. All the patients recovered spontaneously; none required immediate surgery. Four of the patients had acromegaly, two had pituitary-dependent Cushing's syndrome, and a "functionless" pituitary adenoma was found in three. Low serum growth hormone concentrations were observed in three patients with acromegaly whereas the concentration remained increased in the fourth one. Of the two patients with Cushing's syndrome, a selective ACTH-deficiency developed in one and Nelson's syndrome appeared with excessive secretion of ACTH in the other. Transient or persistent hypofunction of the anterior pituitary occurred in al patients. Three patients underwent hypophysectomy after respective intervals of three, eight and 12 months after pituitary apoplex. The operation revealed a hemorrhage in one functionless adenoma and a large cyst in another one. In the third patient who had acromegaly, no signs of the pituitary apoplexy were observed at operation.
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PMID:Pituitary function after pituitary apoplexy. 70 35

A case of Cushing's syndrome associated with a bronchial adenoma treated eight years before with bilateral adrenalectomy was cured by surgical excision of the bronchial adenoma. A discussion of clinical and hormonal features of this lesion is presented. It is concluded that this tumor manifested a capability of synthesizing and releasing substances which are chemically and biologically similar to adrenocorticotropic hormone andmelanocyte-stimulating hormone (MSH). Stimulation of the adrenal cortex by this material results in hyperplasia and hypersecretion, and stimulation of the melanocytesy MSH resulted in excessive pigmentation. Acknowledgment: We are indebted to Doctors Wendell Nicholson, David N. Orth, and Grant W. Liddle of Vanderbilt University for determinations of ACTH and MSH levels and to Mrs. E.P. Jessup for assistance in preparation of statistical data for this manuscript.
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PMID:Cushing's syndrome associated with bronchial adenoma. 83 99

Plasma aldosterone concentration was consistently decreased by 50% or more in 6 patients with aldosterone-producing adenoma on the first day of dexamethasone administration, only to rise subsequently with continued use of dexamethasone while plasma cortisol concentration remained suppressed. The secondary rise in plasma aldosterone was not related to measured changes in known stimuli of aldosterone secretion. It is probable that the observations result from intrinsic alteration of aldosterone synthesis in the adenoma during prolonged ACTH suppression.
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PMID:Transient fall and subsequent return of high aldosterone secretion by adrenal adenoma during continued dexamethasone administration. 84 88

Hypertension and hypokalemia occur in patients with Cushing's syndrome whereas aldosterone production is normal and plasma renin activity is usually normal or increased. A normal aldosterone level in the face of suppressed plasma renin activity is unusual and suggests excess mineralocorticoid hormone activity. Our patient, who had Cushing's syndrome due to adrenocortical adenoma, can be classified as having low renin hypertension (suppressed renin and normal aldosterone levels). The mineralocorticoid hormone in excess was deoxycorticosterone which suppressed renin. The aldosterone production was normal and was produced solely by the adenoma. Contralateral adrenal gland suppression of both the zona glomerulosa by deoxycorticosterone via renin, and of the fasciculata by cortisol via ACTH was demonstrated after removal of the adenoma. Normal adrenal function was gradually restored.
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PMID:Concurrent hypercortisolism and hypermineralocorticoidism. 87 Nov 29

The effect of circadian rhythm and alterations in posture on plasma aldosterone concentration was studied in 13 patients with primary aldosteronism (six adenoma, five idiopathic hyperplasia, two carcinoma) to define the regulatory mechanism in each of these pathologic subtypes. Blood samples for aldosterone, cortisol, renin, and potassium concentrations were obtained every 4 h during prolonged recumbency (32 h) and upright posture (16 h). During recumbency, aldosterone and cortisol followed a normal circadian pattern in patients with adenoma and hyperplasia, with peak values at 0400-0800 h and the nadir at 1600-2400 h. Normalized aldosterone and cortisol values correlated significantly in both groups (adenoma r=+0.66, P less than 0.001; hyperplasia r=+0.42, P less than 0.01). With upright posture, aldosterone levels declined parallel to the normal circadian fall in cortisol in patients with adenoma (r=+0.68, P less than 0.001); whereas aldosterone levels increased in patients with hyperplasia parallel to small increments in renin (r=+0.65, P less than 0.001) and potassium (r=+0.64, P less than 0.001). During the administration of dexamethasone, aldosterone no longer correlated with cortisol in patients with adenoma but continued to correlate with renin during upright studies in patients with hyperplasia (r=+0.77, P less than 0.01). Aldosterone circadian rhythm was abnormal in patients with carcinoma and no effect of posture was noted. Unilateral adrenalectomy restored the normal postural relationship in four patients with adenoma. These studies suggest that aldosterone secretion is under continuous ACTH control regardless of posture in patients with adenoma, whereas persistent adrenal responsiveness to small increments in renin and/or potassium mediate the postural increase in plasma aldosterone in patients with hyperplasia. True adrenal autonomy occurs only in patients with adrenal carcinoma and when ACTH is suppressed in those with adenoma.
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PMID:Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism. 94 31

Four women with secondary amenorrhea associated with hyperprolactinemia were studied. Baseline hormonal evaluation, including serum FSH, serum LH, TSH, T3, T4, and plasma cortisols were normal. Plain sella turcia x-rays were also normal. Prolactin-secreting pituitary microadenomas were found in all of the patients only after further diagnostic studies were done. These studies included polytomography of the sella turcia, dynamic pituitary testing of growth hormone reserve, ACTH reserve, gonadotropin reserve, and prolactin suppression with L-dopa. The early diagnosis of a small prolactin-secreting adenoma may be possible if several diagnostic criteria are ulilized. The most sensitive techniques available are: (1) polytomography, (2) the magnitude of plasma prolactin evaluation, and (3) the failure of suppression of prolactin secretion with L-dopa. Our findings emphasize the importance of an extensive evaluation of all women with amenorrhea associated with hyperprolactinemia.
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PMID:Diagnosis of prolactin-secreting pituitary microadenoma. 103 71

In a prospective study of 7 patients with aldosterone-producing adenoma (APA), long-term (6-72 months) preoperative stimulation of plasma renin activity (PRA) by diuretic therapy (spironolactone plus hydrochlorothiazide) did not prevent selective aldosterone deficiency postoperatively. In all patients aldosterone excretion rate (AER) fell to subnormal values (from a mean of 97 to 2.6 mug/24 h) following removal of APA, although PRA remained elevated. Generalized adrenocortical insufficiency was excluded by the demonstration of normal baseline plasma cortisol and urinary 17-OHCS and the appropriate response to ACTH stimulation. In 6 of 7 patients studied 1-3 months postoperatively, short-term (4 days) sodium deprivation evoked normal increases in PRA, but AER response was blunted (except in 1). Restudy of 3 of 6 patients after 6-12 months revealed that aldosterone production had returned to normal. These results indicate that renin deficiency is not the principal cause of postoperative selective hypoaldosteronism in these patients. On the other hand, they appear to substantiate the possibility raised by in vitro and in vivo studies that spironolactone can directly inhibit aldosterone biosynthesis.
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PMID:Selective hypoaldosteronism despite prolonged pre- and postoperative hyperreninemia in primary aldosteronism. 115 65

Plasma aldosterone, plasma renin activity and plasma cortisol were determined in patients with primary aldosteronism in response to posture and at short-time intervals overnight while the patient were supine. In the 5 patients with an aldosterone-producing adenoma postural changes in plasma aldosterone were paralleled by those in cortisol while plasma renin activity was generally undetectable indicating an ACTH-dependent secretion of aldosterone. This concept was supported by the observation that in 3 of these patients who were tested overnight 1. episodic secretion of plasma aldosterone was paralleled by those of cortisol and 2. episodic secretion of plasma aldosterone could be blunted by dexamethasone. In the patient with idiopathic adrenal hyperplasia concomittant changes in plasma aldosterone and plasma renin activity occurred. The assumption that in this patient the fluctuations in plasma aldosterone were mediated through changes in renal renin secretion was supported by the finding that episodic secretion of plasma aldosterone persisted under suppression of ACTH-secretion by dexamethasone. Our results indicate, that the described procedures may all serve as diagnostic criteria to differentiate between aldosterone-producing adenoma and idiopathic adrenal hyperplasia.
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PMID:Regulation of aldosterone secretion in primary aldosteronism. 118 23

Diagnostic and therapeutic problems in a patient with ectopic ACTH syndrome caused by a malignant bronchial adenoma are discussed. Persistent Cushing's syndrome was present following apparent total adrenalectomy, but radioactive scanning with 131I-19-iodocholesterol showed the presence of residual adrenal tissue in the right suprarenal bed. Amelioration of the hypercortisolism occurred after removal of the bronchial adenoma. A paradoxical elevation of adrenocortical activity followed administration of dexamethasone and data are presented which suggest that periodic secretion of ACTH accounted for this phenomenon.
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PMID:Cushing's syndrome associated with a bronchial adenoma. Possible periodic hormonogenesis. 118 65


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