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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catecholamines induce bone resorption and hypercalcaemia by the beta-adrenergic effect in bone and hypercalciuria by the alpha adrenergic effect in kidney. The interplay between the alpha-adrenergic hypercalciuria and beta-adrenergic hypercalcaemia explains why in some, but not all, phaeochromocytomas hypercalcaemia occurs. The hypothesis predicts hypercalciuria in both phaeochromocytoma and neuroblastoma. In hyperthyroidism, negative calcium balance and hypercalcaemia cannot be attributed to the direct effect of thyroid hormones on the bone but can be explained by augmentation of the catecholamine effects on bone and kidney by thyroid hormones. The hypothesis offers a solution for an apparent paradox in hyperthyroidism of increased urinary cAMP while nephrogenous cAMP is decreased. It also explains why propranolol corrects hypercalcaemia without influencing renal calcium loss.
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PMID:Catecholamines cause the hypercalciuria and hypercalcaemia in phaeochromocytoma and in hyperthyroidism. 33 Oct 32

Plasma 3-O-methylated catecholamines, i.e. 3-methoxytyramine, normetanephrine and metanephrine, were separated from catecholamines by passing through alumina and further purified by adsorbing on weakly acidic resin and Amberlite XAD-4. The amines were trifluoroacetylated and determined by gas chromatography or mass fragmentography. Tracer quantities of tritiated 3-MT, NMN or MN were used as internal standards for total recovery estimations. The contents of 3-O-methylated catecholamines in the plasma of normal persons and patients with hyperthyroidism, hypertension, neuroblastoma and pheochromocytoma were measured.
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PMID:Gas-liquid chromatographic and mass fragmentographic determination of 3-O-methylated catecholamines in human plasma. 117 84

Endocrine and neurological diseases are rare causes of arterial hypertension in childhood. They represent less than 5% of all cases of secondary hypertension. Inflammatory, traumatic, and tumorous disorders of the central nervous system rarely result in chronic hypertension but may frequently be associated with acute hypertensive crisis. The most important hypertensinogenic endocrine diseases are the catecholamine producing tumors pheochromocytoma and neuroblastoma and disorders of the adrenal cortex such as Cushing's syndrome, hyperaldosteronism, 11-hydroxylase deficiency and other mineralocorticoid excess syndromes. Renin producing tumors, hyperthyroidism and hyperparathyroidism are rare causes of hypertension in children. Neurogenic and endocrine forms of hypertension have contributed considerably to a better understanding of the pathophysiology of blood pressure regulation. They are of particular interest to the pediatrician since specific therapy may be available.
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PMID:[Endocrine and neurogenic hypertension in childhood]. 666 53

Circulating angiotensin is produced by the action of renin from the kidneys on circulating angiotensinogen. There are other renin-angiotensin systems in various organs in the body, and recent observations raise the intriguing possibility that angiotensin II is produced by a totally intracellular pathway in the juxtaglomerular cells, the gonadotrops of the anterior pituitary, neurons, in the brain, salivary duct cells, and neuroblastoma cells. Circulating angiotensin II levels depend in large part on the plasma concentration of angiotensinogen, which is hormonally regulated, and on the rate of renin secretion. Renin secretion is regulated by an intrarenal baroreceptor mechanism, a macula densa mechanism, angiotensin II, vasopressin, and the sympathetic nervous system. The increase in renin secretion produced by sympathetic discharge is mediated for the most part by beta-adrenergic receptors, which are probably located on the juxtaglomerular cells. Hyperthyroidism would be expected to be associated with increased renin secretion in view of the increased beta-adrenergic activity in this condition, and hypothyroidism would be associated with decreased plasma renin activity due to decreased beta-adrenergic activity. Our recent research on serotonin-mediated increases in renin secretion that depend on the integrity of the dorsal raphe nucleus and the mediobasal hypothalamus has led us to investigate the effect of the pituitary on the renin response to p-chloroamphetamine. The response is potentiated immediately after hypophysectomy, but 22 days after the operation, it is abolished. This slowly developing decrease in responsiveness may be due to decreased thyroid function.
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PMID:Thyroid hormones and renin secretion. 704 Aug 92

We present a series of nonectopic pituitary adenomas presenting as polypoid sinonasal or nasopharyngeal masses. Thirteen cases diagnosed by biopsies from the nasal cavity, sinuses, or nasopharynx were identified from a series of 1288 surgical pituitary specimens. The patients included 5 men and 8 women ranging from 29 to 69 years of age. The presentations included nasal obstruction (4 cases), headaches (3), visual defects (2), recurrent nose bleeds (1), rhinorrhea (1), sepsis (1), fatigue (1), and hyperthyroidism (1). All patients had large tumors involving the sella and extending inferiorly to involve the sphenoid sinus in 10 cases, ethmoid in 8, nasopharynx in 3, nasal cavity in 6, maxillary and frontal sinuses in 1 case each. In 3 patients, the biopsy was from the nasopharynx, in 4 from the nasal cavity, in 4 from the sphenoid sinus, and in 2 from the ethmoid sinus. The correct diagnosis of pituitary adenoma was initially made in 10 cases. In 3 cases the initial diagnosis was incorrect; 2 tumors were classified as olfactory neuroblastoma, one of those was reclassified as neuroendocrine carcinoma, and 1 case was initially diagnosed as neuroendocrine carcinoma with aberrant adrenocorticotrophic hormone expression. Clinical follow-up (2 to 25 y) and treatment information was available in 10 cases. All 10 patients were alive, either free of disease (4 cases) or with disease (6 cases). In 2 cases, the wrong diagnoses led to incorrect treatment with significant morbidity. These cases illustrate that pituitary adenomas can invade nasopharynx and sinonasal cavities and when they do, they present a possible diagnostic pitfall with potentially serious consequences. We demonstrate the need to always consider this entity when encountering a nasopharyngeal or sinonasal tumor with neuroendocrine features.
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PMID:Pituitary Adenomas Presenting as Sinonasal or Nasopharyngeal Masses: A Case Series Illustrating Potential Diagnostic Pitfalls. 2800 11