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hypercalcemia/phosphatase

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Infusions of ovine prolactin for 10 days induced hypercalcemia in unfed American eels, Anguilla rostrata LeSueur, that tentatively was related to stimulation of branchial Ca2+-uptake mechanisms. Analysis of ATPase activities in the plasma membranes of the branchial epithelium in prolactin treated

Hypercalcemia and an elevated alkaline phosphatase level.

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Hypercalcemia induced by metastatic bone cancer in a patient with chronic renal failure.

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We present a diagnostically challenging case of hypercalcemia in a 50-year-old Japanese woman with chronic renal failure due to chronic interstitial nephritis. She had a history of a radical mastectomy for breast cancer at the age of 30. Despite her chronic renal failure, serum levels of calcium and

Genetic hypercalcemia.

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A genetic disorder should be suspected in patients with hypercalcemia, notably those who are young; have family members with hypercalcemia; or have had a tumor of the endocrine pancreas, thyroid, pituitary, adrenal gland, or jaw bone. All forms of hypercalcemia should be interpreted according to the
Parathyroid hormone (PTH) stimulates bone resorption as well as bone formation in vivo and in organ culture. The catabolic actions of PTH have been recognized in patients with hyperparathyroidism, or with acute infusion of the N-terminal 1-34 fragment of human PTH (hPTH1-34). Whereas the anabolic
The objective of the present work has been to study some aspects of bone and intestinal compartments in rats with Walker 256 carcinosarcoma, an experimental model of humoral hypercalcemia of malignancy (HHM). The results have been compared to those obtained in control animals and, also, to those
Heterozygous inactivating mutations in the calcium-sensing receptor (CaSR) gene are known to cause familial hypocalciuric hypercalcemia (FHH), usually a benign form of hypercalcemia without symptoms of a disrupted calcium homeostasis. FHH can be mistaken for the more common primary

Persistent arthralgia, vomiting and hypercalcemia as the initial manifestations of hyperthyroidism: A case report.

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A 53-year-old woman presented with persistent edema and pain of the metacarpophalangeal and proximal interphalangeal joints and the wrist, knee and ankle joints, with more recent intermittent nausea and vomiting. Treatment for rheumatoid arthritis and osteoarthritis was ineffective. No clinical

Post-partum hypercalcemia in hereditary hyperphosphatasia (juvenile Paget's disease).

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Hereditary hyperphosphatasia is a rare bone disorder characterized by increased bone turnover, elevated alkaline phosphatase (ALP) and bone deformity. We describe a patient with a mild form of hereditary hyperphosphatasia who was initially hypercalcemic in childhood with remission after puberty.
A 24-year-old black man presented with diffuse musculoskeletal pain and shotty lymphadenopathy. Laboratory studies revealed hypercalcemia and hyperphosphatemia, very high serum alkaline phosphatase activity, diffuse but intense uptake of radionuclide on a bone scan, urinary N-telopeptide excretion
BACKGROUND Hypercalcemia of immobilization, while rare, may occur in adolescent boys after fracture. Although not fully understood, the mechanism appears to be related to bone turnover uncoupling, in part mediated by upregulation of RANKL. Animal studies suggest that parathyroidectomy suppresses

Effect of gallium nitrate on tamoxifen induced hypercalcemia in rats bearing mammary tumor.

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OBJECTIVE To study the effect of gallium nitrate in the treatment of flare hypercalcemia in rats, bearing mammary tumor with bone metastasis. METHODS Female Sprague-Dawley albino rats were used in the study. Animals were divided into 5 groups: normal control; hypercalcemic rats bearing DMBA-induced

Interleukin-6 enhances hypercalcemia and bone resorption mediated by parathyroid hormone-related protein in vivo.

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Tumors frequently induce the multifunctional cytokine IL-6, which has been linked to several paraneoplastic syndromes, most notably cachexia. IL-6 stimulates osteoclast formation, causes mild hypercalcemia, and is produced by bone cells in vitro upon exposure to systemic hormones. Since IL-6 is
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