Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031511 (pheochromocytoma)
 14,622 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since adrenocortical hormones and the renin-angiotensin system are capable of inducing defined pathophysiologic changes in the cardiovascular system, similar to those observed after nicotine, experiments were performed in rats to investigate the effect of chronic nicotine administration on the plasma concentrations of aldosterone (PAC) and corticosterone (PCC) and on the plasma renin activity (PRA). The administration of nicotine (0.5 or 1.0 mg/kg s.c. twice daily) over a period of 8 weeks did not significantly affect PCC. However, PAC showed a marked decrease, which did not appear to be the result of a nicotine-induced ACTH inhibition, since a similar decrease in PAC was observed after suppression of ACTH by dexamethasone. PAC in rats with hereditary diabetes insipidus was depressed by nicotine to the same extent as in control rats. This argues against nicotine-induced stimulation of ADH leading to extracellular volume expansion, the cause of the observed decrease in PAC. Further experiments were carried out in which nicotine was administered chronically over 4 weeks (implanted osmotic minipumps infusing 0.17 mg/kg) in rats in which the endogenous activity of the renin-angiotensin system was modified by either a low- or high-salt diet. Nicotine did not influence PRA in the low-sodium group, whereas in the high-sodium group PRA increased after nicotine. The data show that chronic nicotine administration in rats does not activate salt- and volume-retaining endocrine systems. Plasma aldosterone even decreased, except in animals kept on a high-sodium diet, in which an increase of PRA under nicotine was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of chronic subcutaneous nicotine administration on aldosterone and corticosterone plasma concentrations and the plasma renin activity. 638 53

Secondary polycythemia has been noted in association with various neoplasms. An erythropoiesis stimulating factor (erythropoietin) has been demonstrated in the fluid or tissues obtained from most of these neoplasms and erythropoietin levels were found to be elevated in the serum and returned to normal after resection of these tumors. Recently, the potential of pheochromocytoma to produce a wide variety of hormones and neurotransmitters such as growth hormone, motilin, ACTH, atrial natriuretic factor (ANF) and others has been shown. Although elevated hematocrit has been observed in association with pheochromocytomas, the occurrence of absolute polycythemia in such cases is very rare. In this report, we describe a patient with a long history of hypertension and cardiac dysrhythmia as well as polycythemia which was secondary to pheochromocytoma. The patient's blood pressure normalized and the polycythemia regressed after resection of the tumor. Increased release of erythropoietin is the most favored explanation for this rare association. Pheochromocytoma should be included in the differential diagnosis of secondary polycythemia.
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PMID:Pheochromocytoma associated with polycythemia: case report. 750 17

The expression of H19 and insulin-like growth factor-II (IGF-II) genes is important for fetal growth, and the misexpression of these genes may also be involved in the development of some tumors. In human fetal adrenals, H19 and IGF-II expression levels are very high. We show here that H19 is strongly expressed (approximately 50% of the expression in fetal adrenals and 6-fold higher than that in adult liver) in normal adult adrenals (n = 9), adrenocortical adenomas (n = 28), and hyperplastic adrenals (n = 11). In four hormonally active adrenocortical carcinomas, very low levels of H19 ribonucleic acid (RNA) were detected, whereas IGF-II was highly expressed. In cultured adrenocortical cells, ACTH, (Bu)2cAMP, and cholera toxin increased H19 RNA accumulation 2- to 5-fold (P < 0.01), but had no significant effect on IGF-II messenger RNA levels. In pheochromocytomas (n = 22), H19 expression was variable, on the average, about 13% of the expression in the adjacent adrenal cortex. In primary cultures of pheochromocytoma cells, H19 RNA was not detectable via Northern blot analysis. Our data show that H19 expression is maintained at high levels in adult human adrenals and benign neoplasms. H19 RNA is up-regulated by ACTH in adult adrenocortical cells. The very low levels of H19 expression in hormonally active adrenocortical carcinomas suggest that loss of H19 expression may be associated with malignancy in these neoplasms.
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PMID:H19 and insulin-like growth factor-II gene expression in adrenal tumors and cultured adrenal cells. 753 13

The potent hypotensive peptide, adrenomedullin (AdM), originally isolated from a human pheochromocytoma is present in a variety of rat and human tissues. We examined its potential effects in anterior pituitary gland, reasoning that it may be a feedback regulator of adrenocorticotropin (ACTH) secretion. Rat AdM11-50 inhibited basal ACTH secretion from dispersed, rat anterior pituitary cells in a significant, dose-related fashion (maximum inhibition at 10(-9) M). Rat AdM11-50 also inhibited, in a dose-related fashion, corticotropin releasing hormone (CRH)-stimulated ACTH secretion, but did not block the ability of CRH to stimulate cAMP accumulation in these cells. These findings suggest that in addition to peripheral actions in the vasculature and kidney, adrenomedullin may act within the anterior pituitary gland to control fluid and electrolyte homeostasis.
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PMID:A novel vasoactive peptide, adrenomedullin, inhibits pituitary adrenocorticotropin release. 772 Jun 84

Pheochromocytoma is a rare cause of ectopic Cushing's syndrome. We report on such a patient in whom ectopic ACTH secretion displayed a cyclic pattern. A 35-year-old woman was referred to us with a diagnosis of ACTH-dependent Cushing's syndrome. A 3.3 cm left-sided adrenal mass was noted at abdominal computerized tomography. At admission, clinical and hormonal data were unrewarding, so it was decided to continue to observe the patient. Four months later, she became symptomatic with hypertensive and psychotic crises and glycemic decompensation. By that time, a full-blown Cushing picture was evident. Severe hypercortisolism was documented with urinary free cortisol ranging 1500-2200 micrograms/24 h, serum cortisol 143-160 micrograms/dl and plasma ACTH 167-218 pg/ml. Neither ACTH nor cortisol values were significantly modified after high-dose dexamethasone, oCRH or metyrapone. Urinary catecholamine and vanilyl mandelic acid excretion were moderately elevated. Chest CT and total body MIBG scan were negative and magnetic resonance of the sella region was inconclusive. No center to periphery ACTH gradient was observed by inferior petrosal sinus catheterization, whereas a significant left to right gradient was found on selective adrenal vein catheterization. A left adrenalectomy was performed and a 4 cm medullary neoplasia was removed. The cells were immunostained for ACTH, neuron-specific enolase and A chromogranin. Signs and symptoms of Cushing's syndrome resolved with normalization of basal and dynamic endocrine evaluations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclic Cushing's syndrome due to ectopic ACTH secretion by an adrenal pheochromocytoma. 774 35

Adrenomedullin, a novel hypotensive peptide, was discovered in human pheochromocytoma. Although adrenomedullin exists also in normal adrenal medulla and several other organs, its effect on steroidogenesis in adrenal cortex has not been studied. We examined the effect of adrenomedullin on aldosterone secretion by the dispersed rat adrenal zona glomerulosa cells. Adrenomedullin (10(-12)-10(-7) M) did not affect basal aldosterone secretion. Adrenomedullin dose dependently inhibited aldosterone secretion stimulated by 10(-9) M angiotensin II and 10 mM potassium, whereas 10(-9) M ACTH-stimulated aldosterone was not significantly inhibited by adrenomedullin. N6,O2'-dibutyryladenosine 3':5'-cyclic monophosphate (db-cAMP, 10(-5)-10(-3) M) and Ca+ ionophore A23187 (10(-8)-10(-6) M) stimulated aldosterone secretion dose dependently, and A23187-stimulated secretion was significantly inhibited by adrenomedullin (10(-8) M), but db-cAMP-stimulated secretion was not inhibited by adrenomedullin. Our data suggest the possibility that adrenomedullin is a novel inhibitory peptide of aldosterone secretion induced by increasing concentration of intracellular free calcium.
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PMID:Effect of adrenomedullin on aldosterone secretion by dispersed rat adrenal zona glomerulosa cells. 783 Apr 99

A pheochromocytoma from a 59-year-old woman was found to be immunoreactive to adrenocorticotropin (ACTH), chromogranin, neurofilament-200, neuron-specific enolase and S-100 protein. Northern blot analysis showed that both proopiomelanocortin (POMC) and corticotropin-releasing hormone (CRH) genes were expressed in the pheochromocytoma but not in the surrounding adrenal cortex. In primary culture, the POMC and CRH mRNAs were increased by dexamethasone (500 micrograms/l for 3 days) up to 10- and 15-fold of the control, respectively. The secretion of ACTH also was stimulated eightfold with the same treatment. The stimulatory effect of dexamethasone on POMC gene expression was inhibited 70% by nerve growth factor (NGF, 200 micrograms/l), 30% by 12-O-tetradecanoyl phorbol 13-acetate (TPA, 160 nmol/l) (a protein kinase-C activator) and 30% by (Bu)2cAMP (1 mmol/l). On the other hand, NGF alone increased the CRH mRNA accumulation up to 10-fold, and further enhanced the stimulatory effect of dexamethasone on the CRH mRNA twofold, and TPA inhibited (30%) the dexamethasone-induced CRH mRNA accumulation. Furthermore, the conditioned medium of the pheochromocytoma cells increased secretion of corticosterone fourfold in the primary culture of rat fetal adrenal cells. Our results indicate abnormal expression and regulation of POMC and CRH genes in this pheochromocytoma.
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PMID:Pheochromocytoma expressing adrenocorticotropin and corticotropin-releasing hormone; regulation by glucocorticoids and nerve growth factor. 792 Dec 4

The anesthetic management of a hemodialyzed patient with a dopamine producing pheochromocytoma is described. A 56-years old man underwent surgical procedure the day after hemodialysis. Prior to intervention adrenal cortex hormones were normal as well as other endocrine variables (T3-T4-TSH-cortisol-ACTH-parathyroid hormone); epinephrine and norepinephrine, were in a normal range while dopamine was elevated (185 pg/ml). Preoperatively the patient was alpha-blocked with oral phenoxybenzamine (20 mg/day). A balanced anesthesia was performed (isoflurane and fentanyl). Plasma catecholamines were determined. During the induction of anesthesia and before tracheal intubation phentolamine and labetalol were injected till 3.4 mg and 50 mg total dose respectively. During surgical manipulation a nitroglycerin infusion was started (1.5 gamma/kg/min) and after tumor resection dopamine was given till 15 gamma/kg/min. Hormonal values increased in presence of unchanged hemodynamic parameters, likely due to alpha and/or beta blockade. In this case report our problem was especially fluid replacement after tumor resection, because of renal failure. On the basis of CVP and PCWP values, fluid treatment and dopamine infusion allowed to achieve an adequate preload. A sufficient level of analgesia and an efficient alpha blockade may assure hemodynamic stability also in a so compromised patient status.
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PMID:Anesthetic management of pheochromocytoma in a long term hemodialysed patient. 820 20

Pheochromocytoma is a tumor displaying a considerable degree of clinical polymorphism both with respect to its location and the secretion of different types of catecholamines and its capacity to synthesize several ectopic hormones. The present work reports on a case of pheochromocytoma with secretion of ACTH that exhibited several clinical and biological peculiarities. Firstly, the clinical picture of the patient was characterized by a predominance of manifestations of adrenal hyperfunction as compared with those of the original tumor. Secondly a striking finding was an important degree of neutrophilia without band forms and a marked hypokalemia produced by the joint secretion of catecholamines and steroid hormones, as demonstrated later. Finally, the images obtained with computerized tomography were very characteristic, such that together with the above data it was possible to establish a preoperative diagnosis.
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PMID:[Pheochromocytoma with ectopic secretion of ACTH]. 823 79

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


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