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)

Plasma cortisol profiles were studied by the frequent sampling method in 5 patients with Cushing's disease (CD), 7 patients with Cushing's syndrome due to adrenocortical adenoma (AA), and one patient with bronchogenic carcinoma. Plasma ACTH was measured by radioimmunoassay at 10 min intervals in 2 of the subjects. In CD, there was distinct episodic secretion of cortisol and ACTH; the coefficients of variation about the mean plasma cortisol concentration ranged from 24 to 27%; plasma ACTH ranged from zero to 455 pg/ml with a mean of 94 pg/ml. In AA, the tumour secreted cortisol at a constant rate with little fluctuation; the coefficients of variation of plasma cortisol concentration ranged from 8 to 14%; plasma concentrations of ACTH were always near zero. In the patient with bronchogenic carcinoma, the coefficient of variation of cortisol was 14%. These results were apparent even in profiles of plasma cortisol concentrations measured over only a 6 h period. It is concluded that characteristics of plasma cortisol and ACTH secretory patterns are helpful in differentiating Cushing's syndrome of differing aetiology.
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PMID:Plasma cortisol profiles in Cushing's syndrome. 22 57

Simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in the peripheral plasma was carried out on normal subjects and in patients with adrenocortical disorders. The mean plasma levels of 18-OH-DOC at 0800h in normal males and in the follicular and luteal phases of normal females were 8.2 +/- 3.9 ng/100 ml (Mean +/- SD), 7.8 +/- 2.6 ng/100ml and 11.5 +/- 2.8 ng/100ml, respectively. The corresponding levels of 18-OH-B in normal males and in the follicular and luteal phases of normal females were 10.3 +/- 4.2 ng/100ml, 12.4 +/- 4.5 ng/100ml and 13.8 +/- 4.1 ng/100ml, respectively. No differences between the sexes nor the phases of the menstrual cycle were confirmed. ACTH stimulation increased plasma concentrations of 18-OH-DOC and 18-OH-B by 5.1 and 4.4 times respectively, while dexamethasone markedly decreased these 2 steroids. An upright posture increased these steroids significantly. In patients with Cushing syndrome, plasma levels of these 2 steroids were rarely high in cases with adrenocortical hyperplasia and adrenocortical carcinoma, while they were usually within the normal range in adrenocortical adenoma. These 2 steroid levels were increased in primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency. They were decreased in Addison's disease and the salt-loosing type of congenital 21 alpha-hydroxylase deficiency. Patients with congenital 21 alpha-hydroxylase deficiency (simple form) showed elevated levels of 18-OH-DOC and normal levels of 18-OH-B. In vitro production of 18-OH-DOC and 18-OH-B was studied by tissue slices of the normal adrenal cortex, adrenocortical carcinoma causing Cushing syndrome, aldosteronoma and nodular hyperplasia with hyperaldosteronism. In the normal adrenal cortex, the mean production rates of 18-OH-DOC and 18-OH-B were 31 and 26 ng/g tissue/hr, respectively. ACTH and angiotensin II significantly increased the production of both 18-OH-DOC and 18-OH-B. In adrenocortical carcinoma, the production of these steroids was markedly diminished and not stimulated with either ACTH or angiotensin II. Aldosteronoma tissue produced these 2 steroids 20 to 40 times that of the normal adrenal tissue and was significantly increased with the addition of ACTH and angiotensin II. Nodular hyperplasia with hyperaldosteronism produced much 18-OH-DOC and 18-OH-B, but did not respond to ACTH and angiotensin II.
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PMID:[In vivo and in vitro studies on 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone in normal subjects and in those with various adrenocortical disorders (author's transl)]. 22 27

Adrenal venous aldosterone/cortisol ratios were determined in 14 patients with primary aldosteronism. Of 12 patients diagnosed as having an adrenal adenoma, ten underwent surgery in which an adenoma was found. Bilateral adrenal hyperplasia was thought to have developed in two other patients. Measurement of adrenal vein cortisol and establishment of aldosterone/cortisol ratios were done to correct for catheter placement and dilute adrenal efflux. Determination of steroids after ACTH stimulation was helpful in distinguishing quiescent from suppressed adrenal in two patients and in confirming the diagnosis of the others.
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PMID:Preoperative diagnosis and localization of aldosteronomas by measurement of corticosteroids in adrenal venous blood. 22 11

Acute and prolonged alpha 1-24 corticotropin stimulation was performed on a treated chromophobe adenoma patient with partial ACTH deficiency and extreme hyperprolactinemia. Cortisol and aldosterone stimulated normally. However, the basal concentrations of androstenedione (A) and dehydroepiandrosterone (DHA) were low, and that of DHA-sulfate (DHAS) was undetectable. Furthermore, A and DHA did not stimulate normally, and DHAS did not stimulate at all. It has been claimed that adrenal androgen production is increased in hyperprolactinemia. However, the inability of prolactin (Prl) to maintain adrenal androgen (AA) secretion, with and without added ACTH, is demonstrated in this patient.
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PMID:Lack of adrenal androgen stimulation by ACTH in extreme hyperprolactinemia. 22 82

To elucidate the control mechanism of aldosterone production in primary aldosteronism, in vivo and in vitro studies were done in 7 patients with aldosterone-producing adenomas. In the in vivo study, plasma aldosterone was stimulated more significantly by (Formula: see text), synthetic ACTH than by angiotensin II or furosemide. Diurnal variations of plasma aldosterone, which were studied in 4 patients, were similar to those seen in normal controls. In agreement with the results in the in vivo study, the in vitro study also revealed ACTH stimulated aldosterone and deoxycorticosterone (DOC) from the adenoma more markedly than angiotensin II or III. There was no adenoma which was more sensitivie to angiotenion II or III than to ACTH. From these results it is considered that changes in plasma aldosterone induced by the exogenous administration of angiotensin II or ACTH in patients with aldosterone-producing adenoma are mainly based on changes in aldosterone production in the adenoma. Furthermore, in patients with an aldosterone-producing adenoma in whom diurnal variations of plasma aldosterone similar to those in normal subjects are observed, responses of aldosterone to angiotensin II are supposed to be less than those to ACTH.
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PMID:Responses of aldosterone-producing adenomas to ACTH and angiotensins. 23 71

Glucocorticoids, mineralocorticoids, and adrenal androgens were studied in 3 groups of patients: control subjects (group I), hyperprolactinemic subjects (group II) and miscellaneous patients including chromophobe adenomas and normalized hyperprolactinemic subjects treated with Bromocriptine (group III). All the patients were studied in the basal state and under various conditions: Metyrapone, ACTH, TRH for glucocorticoids, ACTH, TRH, saline perfusion for mineralocorticoids, ACTH and TRH for androgens. It is concluded that: the adrenal secretion of glucocorticoids, mineralocorticoids and androgens is not altered under basal conditions in chronic hyperprolactinemia nor during dynamic tests in chronic hyperprolactinemia (prolactin adenoma) nor in acute hyperprolactinemia (induced by TRH).
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PMID:[Adrenocortical function in hyperprolactinemia. The study of glucocorticoids, mineralocorticoids and androgens in chronic and acute hyperprolactinemias (author's transl)]. 23 34

Cerebrospinal fluid (CSF) and serum concentrations of TSH, ACTH, FSH, LH, GH and PRL were measured simultaneously in 34 subjects divided into 3 groups: I-12 normal subjects (6 males and 6 females); II-12 prolactin adenomas (3 males and 9 females); III-5 empty sella syndromes, 3 hypothalamic disorders, 1 chromophobe adenoma, 1 pituitary dwarfism. It is concluded that: 1) pituitary hormones are the normal constituents of CSF but the level can be undetectable and in any case lower than the serum level. 2) there is a positive correlation between serum and CSF concentration of PRL when serum PRL is higher than 20 ng/ml, indicating that the CSF level is influenced by serum level. 3) in prolactin adenomas, only prolactin is elevated in the CSF. 4) there is no correlation between the high level of CSF-PRL and a suprasellar extension of the adenoma.
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PMID:[Determination of 6 pituitary hormones in the cerebrospinal fluid. Control subjects, prolactin adenomas, empty sella syndrome and hypothalamic disorders (author's transl)]. 51 22

A series of 7 patients (all females) with Cushing's syndrome are presented. The syndrome was due to an adenoma of the cortex in 4 cases, to a carcinoma in 1 and to bilateral adrenal hyperplasia in another. In the 7th patient the cortical hyperplasia was due to a bronchogenic carcinoma (ectopic production of ACTH). Surgery was performed in all patients except 1. In 5 patients (adenoma, carcinoma) the diseased adrenal was removed. In 1 patient a left total and a right subtotal adrenalectomy were performed. Out of those 7 patients 4 survived and 3 died. 1 died a few hours after surgery, another 3 months after operation and the last one was never operated on.
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PMID:Diagnostic and therapeutic problems in Cushing's syndrome. Series of 7 cases. 62 22

Two cases of Nelson's syndrome (macroscopic cortico-melanotropic pituitary adenoma developing after bilateral total adrenalectomy for Cushing's disease) are reported. The unusual feature was spontaneous necrosis of the adenoma, as indicated by the rapid disappearance of melanoderma, the normalisation or decrease in plasma ACTH level, retraction in the diaphragm of the sella at air encephalography and autopsy findings in one case.
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PMID:[Corticotrophic adenomas with melanoderma (Nelson's syndrome). Two cases clinical and laboratory studies before and after spontaneous intercurrent necrosis (author's transl)]. 66 43

Cushing's syndrome may be caused by pituitary ACTH, ectopically produced ACTH, adrenocortical tumor or medication. Cushing's disease, due to excessive pituitary ACTH resulting in adrenocortical hyperplasia, remains a complex endocrine disorder for which no single treatment is wholly satisfactory. Twenty-two patients with surgically treated Cushing's syndrome are presented: Four with benign adrenocortical adenoma, two with adrenocortical carcinoma and 16 with adrenocortical hyperplasia. The four benign adenomas were excised with the one death due to respiratory failure and sepsis. Both patients with carcinoma and liver metastases died of their tumors. Of the 16 patients with adrenocortical hyperplasia and Cushing's disease, eight underwent subtotal adrenalectomy and thereafter eight had total intra-abdominal adrenalectomy with autotransplantation of adrenal tissue to the thigh. There was one operative death. Total adrenalectomy has now replaced subtotal resection in most clinics. All eight of the patients who had adrenal autotransplantation exhibited biopsy or functional evidence of some degree of graft survival. On patient stopped steroid replacement permanently and another developed recurrent Cushing's syndrome from the grafts. Of a total of 26 reported patients with adrenal autotransplants surveyed, 22 exhibited evidence of graft survival, 16 were able to discontinue steroid replacement therapy and three eventually developed recurrent Cushing's syndrome from the transplants. There is now strong evidence that most patients with Cushing's disease harbor a pituitary basophil ademona, and in the future the initial surgical attack may be directed to the pituitary rather than to the adrenals.
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PMID:Surgical management of Cushing's syndrome with emphasis on adrenal autotransplantation. 68 95


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