Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the group of 1635 patients with nephorolithiasis the authors found 16% with idiopathic hypercalciuria. They administered thiazide diuretics for 8 days as a test for the detection of masked hyperparathyroidism in idiopathic hypercalciuria. In 6 cases which were diagnosed in this manner, the existence of a parathyroidadenoma could be demonstrated by surgical operation. The hypercalciuria persisted after exstirpation of the tumor, in some cases the nephrolithiasis also remained active. the various pathogenetic mechanisms connected with these common diseases are discussed in relation to these results.
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PMID:[Nephrolithiasis in hypercalciuria and hyperparathyroidism]. 81 7

We report a 14-year-old boy with severe hypertension who was cured by surgical removal of a pheochromocytoma. The tumor was shown biochemically and morphologically to secrete predominantly noradrenaline. The metabolic effects noted in this patient were raised free fatty acid levels and depressed insulin levels, hyperreninemia, hypercalcemia, and hypercalciuria with normal parathyroid function. All these abnormalities returned to normal after removal of the tumor. It is suggested that these effects were mediated via beta-adrenergic stimulation of the excess noradrenaline.
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PMID:The metabolic effects of excess noradrenaline secretion from a pheochromocytoma. 90 78

Hypercalciuria has been reported in rats with mild hyperprolactinemia due to implantation of anterior pituitary glands under the kidney capsule and in rats bearing transplantable tumors that secrete large amounts of prolactin (PRL) and growth hormone (GH). We studied Buffalo rats implanted subcutaneously with the new MMQ pituitary tumor line that secretes only PRL. Urinary calcium excretion increased as the tumors grew. Three weeks after tumor implantation in female rats, the urinary calcium excretion was 1.102 +/- 0.092 mg/100 g body weight (BW).24 hours compared with controls, 0.296 +/- 0.079, P less than .0005. Male tumor-bearing rats also had increased urinary calcium excretion compared with male controls. In tumor-bearing rats the urinary calcium excretion factored for urinary sodium excretion, dietary calcium intake, or urinary creatinine excretion was elevated. Urinary calcium excretion was correlated with serum PRL levels and with estimated tumor volume. Serum calcium, immunoassayable parathyroid hormone, and urinary cyclic adenosine monophosphate (cAMP) excretion were normal in the tumor-bearing rats. There was some evidence of loss of bone calcium in rats bearing the MMQ tumor, and serum levels of calcitonin were decreased. These results are similar to those found in anterior pituitary-grafted hypercalciuric rats. It is unlikely that parathyroid hormone (PTH) abnormalities are responsible for the hypercalciuria in the MMQ-bearing rats. The pituitary gland may have an effect on the distal renal tubule to decrease calcium reabsorption.
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PMID:Hypercalciuria in a new rat model of hyperprolactinemia. 184 86

Hypercalcemia occurred in a patient with leiomyosarcoma when multiple lung metastases developed. Despite normal plasma parathyroid hormone (PTH) levels and low 1,25-dihydroxyvitamin D, this hypercalcemic patient had a marked hypercalciuria and phosphaturia associated with an increased excretion of nephrogenous cyclic AMP (NcAMP). Administration of cisplatin ameliorated both the hypercalcemia and hypercalciuria without any reduction in tumor size of NcAMP excretion. Terminally, acute pancreatitis occurred producing a profound hypocalcemia. In the extract of tumor tissue obtained post mortem, bioactivity stimulating the generation of cyclic AMP in osteogenic cells was demonstrated along with the immunoreactive PTH-related protein (PTH-rP). the first report of a solid non-epithelial malignancy producing PTH-rP and associated with humoral hypercalcemia of malignancy. The hypercalcemia in this case caused acute pancreatitis, which led to a profound hypocalcemia.
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PMID:A case of leiomyosarcoma associated with humoral hypercalcemia of malignancy: demonstration of biological and immunological activities of parathyroid hormone-related protein in the tumor extract. 255 69

A 41-year-old man with acromegaly was suffering from chronic, progressive backache and aware of reduction in his body height. Endocrine studies revealed increased glucose non-suppressible serum growth hormone (GH) and serum prolactin (PRL). Pituitary microadenoma was detected by a computerized axial tomogram and subsequently resected by trans-sphenoidal adenomectomy. The tumor proved to be a mixed GH- and PRL-secreting adenoma by electron microscopy and immunoperoxidase staining. Concurrent investigation of backache and reduced height disclosed markedly reduced radiodensity of the spinal bones, bilateral nephrocalcinosis, and hypercalciuria, which were ascribed to renal tubular acidosis (RTA) demonstrated by reduced urinary excretion of acids and insufficient reduction of urinary pH following oral administration of ammonium chloride. From the analogy to certain endocrinopathies, it appears likely that enhanced calcium metabolism and resultant hypercalciuria due to excess GH and PRL have led to the development of RTA, which further enhanced calciuria. Such enhanced calcium metabolism and consequent hypercalicuria conceivably led to accelerated demineralization of the spine and resulted in the reduced height of this patient in his early forties.
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PMID:A case of active acromegaly with reduced height and type 1 renal tubular acidosis. 289 4

The effect of a low calcium diet, mithramycin, or dichlorodimethylene bisphosphonate were evaluated in nude mice with humoral hypercalcemia of malignancy associated with the transplanted canine adenocarcinoma (CAC-8). Low calcium (0.01%) diet significantly reduced serum calcium levels in hypercalcemic nude mice and reduced urine calcium excretion to control levels. Mithramycin (8 mg/kg) decreased serum calcium concentration and urine calcium excretion to the range of control non-tumor-bearing nude mice at day 5 after a single injection, but there was no change in the number of tartrate-resistant acid phosphatase-positive osteoclasts in lumbar vertebrae. Osteoclasts from CAC 8-bearing nude mice after mithramycin administration were decreased in size, had small ruffled borders, and increased relative size of clear zones. Dichlorodimethylene bisphosphonate (Cl2MDP) (45 mg/kg) partially reduced serum calcium concentration of hypercalcemic tumor-bearing nude mice, decreased urine calcium excretion to control levels, and markedly reduced the numbers of tartrate-resistant acid phosphatase-positive osteoclasts in lumbar vertebrae. Osteoclasts from Cl2MDP-treated nude mice were smaller and had a reduced frequency of ruffled borders than saline-treated hypercalcemic nude mice. In vitro bone resorption induced by CAC-8 extract was significantly reduced by Cl2MDP and mithramycin. The results of these investigations suggest that the hypercalcemia and hypercalciuria associated with HHM in nude mice with CAC-8 are the combined result of altered calcium homeostasis in the bone, kidney, and intestine. Chemotherapeutic agents that specifically affect only bone or feeding a low calcium diet alone may not completely ameliorate the hypercalcemia of HHM.
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PMID:The effect of low calcium diet, mithramycin, and dichlorodimethylene bisphosphonate on humoral hypercalcemia of malignancy in nude mice transplanted with the canine adenocarcinoma tumor line (CAC-8). 297 5

Studies were conducted in a patient with idiopathic hypophosphatemic osteomalacia to delineate the roles of parathyroid hormone (PTH), vitamin D and renal tubular function. A 43-year-old woman presented with progressive skeletal pains resulting in severe incapacity. Workup revealed: hypophosphatemia with a low tubular maximal phosphate reabsorption per glomerular filtrate (TmP/GFR) of 1.05 mg/dl, normocalcemia, hypocalciuria, elevated alkaline phosphatase and glycinuria. PTH and urinary cyclic AMP (UcAMP) were normal, while calcitriol was low. Renal tubular acidosis or other transport defects were not present and no tumor was found. Biopsy was diagnostic for osteomalacia, and the patient responded to 1-alpha OHD3 and phosphate therapy. Hyperparathyroidism was ruled out by 1) normocalcemia persisting after 1-alpha OHD3 and calcium loading and 2) normal PTH and UcAMP challenged by phosphate supplements. Combined calcium and 1-alpha OHD3 administration resulted in hypercalciuria, decreased UcAMP and increased, but not corrected, TmP/GFR. These findings suggest that the osteomalacia was due to hypophosphatemia caused by a renal leak. PTH is only contributory to the phosphaturia. Low calcitriol level contributes to the osteomalacia directly and indirectly through impaired mineral absorption and, therefore, is also responsible for the hypocalciuria.
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PMID:Metabolic studies in a patient with idiopathic hypophosphatemic osteomalacia. 334 50

The effect of one single injection of two new bisphosphonates, 4-amino-1-hydroxybutylidene-1,1-bisphosphonate and 2-(2-pyridyl)ethylidene-1,1-bisphosphonate, and of dichloromethylenebisphosphonate on the hypercalcemia and hypercalciuria induced by the Walker carcinosarcoma 256/B in the thyroparathyroidectomized rat was evaluated. When given either before or after the development of hypercalcemia and hypercalciuria, 16.1 mumol/kg 4-amino-1-hydroxybutylidene-1,1-bisphosphonate or 2-(2-pyridyl)ethylidene-1,1-bisphosphonate totally inhibited hypercalciuria, whereas hypercalcemia was only partially reduced over the 14 days of the experiment. At 10 and 100 times lower doses, the effect was strongest the first days, but still partially present 14 days later. The difference of activity on calcemia and calciuria appears to be due to the fact that the tumor increased both bone resorption and renal reabsorption of calcium. Only the former was altered by the bisphosphonates. The two new compounds appeared to be of similar potency and more active than dichloromethylenebisphosphonate. These compounds could be promising for the treatment of malignant hypercalcemia and other conditions with increased bone resorption in humans, even when given only over short periods of time.
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PMID:Effect of a single injection of two new bisphosphonates on the hypercalcemia and hypercalciuria induced by Walker carcinosarcoma 256/B in thyroparathyroidectomized rats. 367 71

Line A Walker carcinoma differs from line B in that it does not elicit hypercalcemia and hypercalciuria when implanted in rats at various sites (s.c, i.m., intraaortically). However, Walker 256/A, unlike line B, may invade the tibia when implanted i.m. in the adjacent gastrocnemius muscle. This invasion was evaluated by measuring the increased weight of the bone and decreased calcium concentration per unit weight of the tibia, by reduced opacity to X-ray, and by the presence of tumor cells in the compact bone cortex. Ethane-1-hydroxy-1,1-bis(phosphonate), a diphosphonate derivative, at a dose of 10 to 30 mg/kg/day s.c., prevented cancer cell invasion of the tibia as judged by the above criteria. This inhibition was obtained with no apparent effect on the growth of Walker 256/A carcinoma.
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PMID:An experimental rat model of local bone cancer invasion and its responsiveness to ethane-1-hydroxy-1,1-bis(phosphonate). 392 Dec 38

We evaluated the effects of chronic massive elevations of serum GH and PRL on calcium metabolism in rats bearing the MStT/W15 and 7315a transplantable pituitary tumors. MStT/W15 tumor rats manifest elevated serum GH and PRL levels, hypercalcemia, hypercalciuria, and elevated serum levels of PTH and 1,25-dihydroxyvitamin D. The hypercalcemia was not reversed by dexamethasone or propranolol treatment, but was ameliorated by starvation. Parathyroidectomy produced hypocalcemia in the MStT/W15 tumor rats, confirming the parathyroid dependence of the hypercalcemia. The 7315a tumor produced a milder degree of hypercalcemia, along with elevated serum levels of PRL, ACTH, and corticosterone; serum GH was normal. In high concentrations, PRL and/or GH may stimulate the secretion of PTH as well as enhance dietary calcium absorption, in part through the mediation of 1,25-dihydroxyvitamin D.
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PMID:Hypercalcemia in rats bearing growth hormone- and prolactin-secreting transplantable pituitary tumors. 402 91


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