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)

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma. 2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated. 3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal. 4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.
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PMID:Free and conjugated catecholamines in human hypertension. 28 3

In mice having a high renin content in the submaxillary glands allo- and autotransplantation of the gland showed identical histological changes of the tissue, comprising disappearance of acini and intercalated ducts as well as a reduction in the number and size of granules in the granulated ducts. No structural signs of rejection were found. Adenomas, possibly originating in the granulated ducts, were frequently present in the transplanted glands. The renin content of autotransplanted glands was invariably much higher than in allotransplants, and after noradrenaline injection renin was released only from autotransplants, never from allotransplants. Blockade of the renin system was accordingly followed by a decrease in blood pressure only in mice with autotransplants.
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PMID:Structural changes and ability to release renin in auto- and allo-transplants of mouse submaxillary glands. 46 67

The sensitivity of the eccrine sweat glands to adrenaline and noradrenaline was examined in 9 patients with pheochromocytoma and 12 patients with primary aldosteronism by Wada's method for determining threshold concentrations of local sweat response to intradermal injection. In pheochromocytoma most of the patients characteristically showed considerably reduced sensitivity to catecholamines in the sweat glands. Sensitivity was rapidly restored after the extirpation of the tumor in all cases. In primary aldosteronism the sweat gland sensitivity varied over a very wide range from subnormal to supernormal levels. These were restored to normal range after extirpation of the adrenocortical adenoma. In both diseases it was found that the sensitivity of the sweat glands to catecholamines and the vascular system to noradrenaline altered almost in parallel.
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PMID:Eccrine sweat gland sensitivity to catecholamines in patients with pheochromocytoma and primary aldosteronism. 114 19

1. Serial observations of blood pressure after unilateral adrenalectomy for aldosterone-producing adenoma revealed an incidence of hypotension (systolic BP less than fifth percentile for age- and sex-matched normal population) of 27% at 2 years, more than 5 times that predicted. 2. Serial observations of volume regulatory hormones showed significantly raised mean levels of plasma renin activity consistent with hypovolaemia. Significantly reduced mean aldosterone levels despite significantly raised mean plasma renin activity levels may reflect reduced responsiveness of the remaining adrenal. 3. Reduction of significantly elevated preoperative ANP levels to significantly reduced levels postoperatively is also in keeping with postoperative hypovolaemia. 4. A 50% reduction in plasma adrenaline after unilateral adrenalectomy might contribute to reduced noradrenergic activity (prejunctional beta-receptor) and reduced blood pressure, but plasma noradrenaline did not fall significantly postoperatively. 5. Postoperative levels of renin, aldosterone, adrenaline and noradrenaline were not significantly different between those who did, and those who did not, become hypotensive.
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PMID:Unexpected incidence of low blood pressure 2 years after unilateral adrenalectomy for primary aldosteronism. 274 20

The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
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PMID:Sympatho-adrenal response to hypoglycaemia in infants. 285 Sep 15

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.
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PMID:Pheochromocytoma associated with adrenocortical adenoma: case report and literature review. 372 Jun 79

To determine the mechanism and the site of action of catecholamines as well as hormones including thyrotropin-releasing hormone (TRH)1 and somatostatin on pituitary hormone release in patients with acromegaly and in normal subjects, the effects of these substances on growth hormone (GH) and prolactin (PRL) secretion from adenomatous and nonadenomatous human pituitary cells in culture were examined. When dopamine (0.01-0.1 microM) or bromocriptine (0.01-0.1 microM) was added to the culture media, a significant inhibition of GH and PRL secretion from adenoma cells from acromegalic patients was observed. This inhibition was blocked by D2 receptor blockade with metoclopramide or sulpiride, but not by D1 receptor blockade. Similarly, dopamine suppressed GH and PRL release by nonadenomatous pituitary cells in a dose-dependent manner, which was again blocked by D2 receptor blockade. The minimum effective concentration of dopamine required for a significant inhibition of PRL secretion (0.01 microM) was lower than that for GH release (0.1 microM). Norepinephrine, likewise, caused a suppression of PRL secretion from adenomatous and nonadenomatous pituitary cells. This effect was blocked by sulpiride, phentolamine, however, was ineffective. When TRH was added to the media, both GH and PRL secretion were enhanced in adenoma cells, while only the stimulation of PRL release was observed in nonadenomatous pituitary cells. Coincubation of TRH and dopamine resulted in variable effects on GH and PRL secretion. Somatostatin consistently lowered GH and PRL secretion in both adenomatous and nonadenomatous pituitary cells and completely blocked the TRH-induced stimulation of GH and PRL secretion from adenoma cells. Opioid peptides (1 microM) failed to affect hormone release. These results suggest that no qualitative difference in GH and PRL responses to dopaminergic agonists or to somatostatin exists between adenoma cells of acromegalic patients and normal pituitary cells, and that the direct effect of catecholamines on GH and PRL secretion from human pituitary cells is mediated mainly through dopamine receptor activation.
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PMID:Direct effects of catecholamines, thyrotropin-releasing hormone, and somatostatin on growth hormone and prolactin secretion from adenomatous and nonadenomatous human pituitary cells in culture. 614 Feb 73

A 61-year-old woman with hyper-catecholaminemia and hyper-glucocorticoidemia due to a mixed tumor of the right adrenal gland is described. The patient, who had been medicated for hypertension since 1977, complained of thirst and general malaise in 1986. Body weight loss was remarkable. There was neither absolute truncal obesity nor moon face. In September 1986, her blood pressure was 180/110 mmHg and blood glucose level was 400mg/dl. Noradrenaline levels in plasma and in urine were remarkably elevated (1659 pg/ml and 120 micrograms/day, respectively), and adrenaline levels were also high (397 pg/ml in plasma, 34 micrograms/day in urine). Plasma cortisol and urinary 17-OHCS were elevated (39.2 micrograms/dl and 11.9 mg/day, respectively). Plasma ACTH was in the normal range (42.6 pg/ml). Oral administration of neither 1mg nor 8 mg of dexamethasone suppressed plasma cortisol or ACTH levels. Both 131I-metaiodobenzylguanidine and 131I-adosterol accumulated in the right adrenal gland. In 1987 the adrenal tumor (3.0 x 3.5 cm, 30 g) was resected. After the operation, her blood pressure and blood glucose level returned to normal, so that the medication became unnecessary. Histologically it was revealed that the tumor was a mixed adenoma consisting of adreno-medullary and cortical cells (corticomedullary adenoma). The literature on 21 cases of pheochromocytoma associated with Cushing's syndrome was briefly reviewed. Mathison (1969) reported the first case of a mixed tumor of adreno-medullary and cortical cells. So far as we know the present case is the second.
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PMID:[A case of adrenal mixed tumor of pheochromocytoma and adrenocortical adenoma presenting diabetes mellitus and hypertension]. 837 53

It is described the case of a patient with Ovarian Cystadenoma in whom a 3.5 cm nodular lesion was accidentally detected in her left suprarenal gland. She had no signs of hypercortisolism or any other suprarenal pathology and was symptomless. Determinations in the urine of 24 hours of Cortisol, Adrenaline and Noradrenaline, 17-ketosteroids and Tetrahydroaldosterone were normal. Daily rhythm and plasmatic determinations of ACTH, cortisol and 11-deoxycortisol were normal. The Dexamethasone suppression test was also normal. In the suprarenal gammagraphy it appeared an intense captation by left suprarenal without visualization of right gland. A left suprarenalectomy was performed and the anatomopathological analysis showed a clear cell corticoadrenal adenoma. Therefore the only data of the function of suprarenal adenoma was the one coming from gammagraphy. We thought that the adenoma was responsible of practically all the corticoadrenal function without reaching pathological levels, meeting the criteria of "pre-Cushing" syndrome or subclinical Cushing, due to the fact that the contralateral gland was not seen in the gammagraphy. Therefore in the characterization of certain tumors which appear clinically and biochemically as non functional, the suprarenal gammagraphy could be a technique of great usefulness for the diagnosis.
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PMID:[Gammagraphic diagnosis of a non-hyperactive suprarenal adenoma]. 851 7

A right adrenal tumor was found incidentally during abdominal computed tomography exam in a 51-year-old female patient, who had had diabetes and hypertension for more than 10 years. The computed tomography scan was arranged for possible pancreatic lesion by a neurologist. Norepinephrine level was high in the plasma and urine. Vanillylmandelic acid level was elevated in the urine. Diurnal cortisol rhythm, plasma adrenocorticotropic hormone and urine free cortisol were all normal,but the plasma cortisol concentration could not be suppressed after a standard low-dose dexamethasone suppression test. Therefore, adrenal cortical adenoma with subclinical Cushing's syndrome was highly suspected; however, further imaging studies, including magnetic resonance image and 131I-6beta-iodomethylnorcholesterol adrenal scintigraphy failed to discriminate an additional tumor. After right adrenalectomy, a small adrenal cortical adenoma and a large pheochromocytoma were noted. This is an extremely rare case of an adrenal incidentaloma consisting of both medullary and cortical tumors in the same gland.
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PMID:Pheochromocytoma and adrenocortical adenoma in the same gland. 1763 66


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