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)

Several studies have demonstrated that the corticotropin-releasing factor test (CRF) is useful for the aetiological diagnosis of Cushing's syndrome: in Cushing's disease, as opposed to ectopic ACTH secretion syndrome, the hypothalamus-pituitary-adrenal (HPA) axis can still be stimulated by CRF. In the present study, we compared the CRF test with the reinforced dexamethasone suppression test in 18 patients: 11 with Cushing's disease, 6 with ectopic ACTH secretion and 1 with adrenal gland adenoma. We obtained 2 false-negative results with the CRF test and 1 false-positive result with the dexamethasone suppression test. Our study, together with published data, suggests that the CRF test is useful in the exploration of Cushing's syndromes of uncertain origin. However, the results obtained with this test must be compared with those of other methods used to explore the HPA axis and which are still necessary.
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PMID:[Value of the corticoliberine test in the etiologic diagnosis of Cushing's syndrome]. 215 88

1. Two patients with angiotensin-responsive aldosterone-producing adenoma (APA) and one with adrenal cortical carcinoma demonstrated autonomous secretion of cortisol as well as of aldosterone. 2. The response of cortisol and of aldosterone to ACTH did not differentiate between the two APA which secreted cortisol and the eight which demonstrated normal suppression with dexamethasone. 3. Concurrent autonomous secretion of cortisol as well as aldosterone may occur in patients who present clinically with primary aldosteronism. 4. Biochemical distinctions between adenomas may reflect differences in their cellular composition.
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PMID:Some aldosterone-producing adrenal tumours also secrete cortisol, but present clinically as primary aldosteronism. 216 Mar 40

The purpose of this study was to ascertain whether the pituitary-adrenal responses to human corticotropin-releasing hormone (hCRH) in "non-functioning" adrenocortical adenoma would uncover a functional activity in these adrenal nodules. Eleven patients with incidentally discovered "silent" adrenocortical adenoma and eleven controls were studied. The initial clinical and laboratory examination, including an overnight 1 mg dexamethasone suppression test, revealed no abnormalities in any of the subjects. IR-ACTH and serum steroids (F, S, P, 17OHP, 18OHB, and aldosterone) were normal in both controls and patients. After pulse IV injection of 100 micrograms hCRH, the cortisol response was significantly exaggerated (P = 0.01). Stimulated plasma ACTH levels were, however, significantly lower in patients than in controls (P = 0.01), indicating counter-feedback regulation of cortisol. The peak cortisol/peak ACTH ratio (Fmax/ACTHmax) in the patients was significantly elevated (26.8 +/- 4.37 nmol/ng vs. 14.6 +/- 2.16 nmol/ng, P = 0.02). Two further patients with incidentally discovered "pre-Cushing's" adrenocortical adenoma displayed an even higher ratio (43.5 and 45.5 nmol/ng). In established Cushing's syndrome due to an autonomous adrenocortical adenoma, suppression of ACTH and of the ACTH response to hCRH occurs with a very high basal cortisol/basal ACTH ratio. Our findings suggest some functional activity even in clinically "silent" adrenocortical adenoma. Response to hCRH uncovers a continuous spectrum between adrenocortical adenoma, "pre-Cushing's", and Cushing's syndrome.
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PMID:Endocrine activity of the "silent" adrenocortical adenoma is uncovered by response to corticotropin-releasing hormone. 216 44

This study explores the possibility of improving endocrinologic testing during petrosal sinus catheterization by determining both beta-endorphin and corticotropin (ACTH). We studied 14 patients with Cushing's disease, two with adrenal tumor, and three with ectopic tumors secreting ACTH. In patients with Cushing's disease, beta-endorphin concentrations paralleled those of ACTH in all basal plasma samples collected either from petrosal sinuses or peripheral veins. Individual responses of beta-endorphin and ACTH to corticotropin releasing hormone (CRH) were closely related to the presence of a corticotroph adenoma. In such patients, a consistently higher concentration of beta-endorphin over ACTH was observed in all samples collected either from petrosal sinuses or peripheral veins; the ratios were unchanged after the administration of CRH. In patients with ectopic ACTH secretion, the mean ratio of beta-endorphin over ACTH (with both values expressed in pmol/L) was significantly higher (3.5) than that of patients with Cushing's disease (2.9) or Cushing's syndrome due to adrenal tumor (2.7).
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PMID:Parallel assays of beta-endorphin and ACTH in Cushing's patients undergoing petrosal sinus sampling. 217 14

Fifty-seven patients with pituitary-dependent Cushing's syndrome and eight with Nelson's syndrome underwent transsphenoidal pituitary exploration, with removal of macroscopically abnormal tissue in 64 patients and detailed histology of this in 63. The cure rate by stringent criteria 1 month later was 48 (83%) of the 58 with assessable data, who were followed for 225 patient-years. Two patients relapsed later, a rate of one per 112 patient-years of follow-up. In 27% of patients, the macroscopically abnormal tissue removed was histologically indistinguishable from normal pituitary gland but the cure rate was 82%, and a quarter of the patients in this group assessable for recovery of normal ACTH function gained it. Another 53% of biopsies showed corticotroph adenomas, and the cure rate in these was 89% though rather more (69%) recovered normal ACTH function. The remaining 20% of biopsies were consistent with corticotroph hyperplasia. The cure rate varied little whether the lesion was diffuse or localized, whether or not it was in the invasion zone/interlobar cleft, whether or not there was pituitary enlargement, or whether the surgery was radical or selective. Six patients, of whom three are cured, showed surgical or radiological evidence of invasion outside the pituitary fossa. The data are consistent with the idea that pituitary adenoma is merely the end stage of some other process in the corticotrophs, and cure often follows removal of a lesion other than adenoma. Of patients who were permanently cured, 47% regained normal ACTH function within 3 years of operation (none later), 53% remaining ACTH-deficient at 3 years or more. Of all patients 48% acquired gonadotrophin deficiency, 28% have TSH deficiency and 25% permanent diabetes insipidus. All these pituitary function deficits were more common after radical surgery and in patients with normal histology, The literature contains so little objective data on these functions that we cannot say whether the endocrine damage in our patients is exceptional or not.
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PMID:Transsphenoidal surgery for Cushing's disease: does what is removed determine the endocrine outcome? 217 17

In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.
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PMID:Pituitary peptides other than ACTH may not be aldosterone secretagogue in primary aldosteronism. 217 3

The presence of adrenal nodules in patients with congenital adrenal hyperplasia seems to be relatively frequent but is seldom reported. We observed such nodular formations in 3 women and 2 men aged from 19 to 71 years. Four patients had enzyme deficiency revealed in childhood (3 were deficient in 21-hydroxylase and 1 in 11-hydroxylase); the fifth patient had a virilizing form of an unrecognized 21-hydroxylase deficiency. In 3 patients the nodular formations had a diameter of 10 millimetres or less. In the other 2 patients the diameter was greater than 30 millimetres, and an adrenocortical adenoma was found at surgery. In one case a preoperative increase of medical treatment resulted in partial regression of the nodules. Our findings show that young subjects may have adrenal nodules, and their dependence on ACTH is discussed. We also discuss the possible influence of these nodules on the difficulty of medical treatment, the need for a life-long therapy and the necessity to look for a congenital adrenal hyperplasia when confronted with an "incidentaloma".
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PMID:[Nodular adrenomegalies in congenital adrenal hyperplasia in adults. Implications]. 217 90

One third of a general population reacts to exogenously applied corticosteroids with an increase of intraocular pressure. In this study we investigated the influence of endogeneously elevated serum cortisol levels on the intraocular pressure and the presence of glaucomatous changes in the morphology of the optic disc and retinal nerve fiber layer. 15 patients with hypothalamic-pituitary Cushing's disease due to an ACTH producing adenoma of the pituitary gland and undergoing transphenoidal microsurgical exploration of the sella turcica were ophthalmologically examined pre- and post-operatively. Subjective symptoms had been noticed not earlier than four years before operation. Intraocular pressure was preoperatively and postoperatively within the normal range for all but one patient with readings of 23/23 mm Hg preoperatively. In the subgroup with endocrinological remission the intraocular pressure readings decreased postoperatively. Photography of the retinal nerve fiber layer, morphometry of 15 degree color stereo optic disc diapositives, and perimetry revealed no changes typical for glaucoma. In 4 patients the retinal nerve fiber bundles were remarkably well visible. We conclude that patients suffering from hypothalamic-pituitary Cushing's disease with endogeneously elevated serum cortisol levels and a duration of subjective symptoms of less than 4 years run a lower risk of developing glaucomatous damage than patients with topical administration of corticosteroids.
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PMID:[Glaucoma in central hypothalamic-hypophyseal Cushing syndrome]. 217 29

In 16 patients with high cortisol plasma levels MRI and CT investigation of adrenal gland region was performed; 13 also had the pituitary region examined. CT and MRI results in Cushing's Syndrome due to adrenal glands etiology (8 cases) are overlapping. The morphological criteria utilized consist in the radiological finding of bilateral adrenal hyperplasia or adrenal mass (adenoma, carcinoma). The great amount of retroperitoneal fat increases the normal contrast with both techniques. In the pituitary Cushing's Syndrome MRI was more sensible than CT as far as it concerns ACTH producing pituitary lesion assessment; this technique may show 5 mm diameter adenomas for their high signal intensity.
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PMID:[Comparison of MR and CT in a radiological study of Cushing's syndrome. A report on 16 cases]. 231 10

The immunohistochemical characterization of 92 surgically resected abnormal pituitaries showed 24 cases with ACTH immunoreactivity. These included two cases of nodular hyperplasias, 20 functional adenomas, and two silent corticotropic adenomas. Both patients with nodular hyperplasia and 19 patients with functional adenomas had Cushing's disease, while one patient with a functional adenoma had Nelson's syndrome. The two silent corticotropic adenomas were not associated with Cushing's disease, although both patients had slightly elevated serum prolactin levels. The tumors, which were stained for beta-endorphin (12 cases) and alpha and beta-MSH (five cases) were all positive for these peptides. These results show that immunohistochemical staining is indispensable in the diagnosis of nodular hyperplasia and silent corticotropic adenomas and that it is extremely helpful in confirming the diagnosis of ACTH-producing adenomas.
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PMID:The spectrum of ACTH-producing pituitary lesions. 242 63


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