Cases reported "Bone Resorption"

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1/5. hyperparathyroidism, humoral hypercalcemia of malignancy, and the anabolic actions of parathyroid hormone and parathyroid hormone-related protein on the skeleton.

    So what have we learned from the Takeuchi case? It has been 80 years since malignancy-associated hypercalcemia was described. It has been 45 years since HHM was first described. It has been 15 years since PTHrP was identified, and 12 years since PTHrP immunoassays became available for clinical research. We now know almost everything about HHM in pathophysiological terms, and we can reproduce the cardinal features of the syndrome in laboratory animals and humans. The Takeuchi case reminds us that we still have a few things to learn about HHM. Specifically, "Why is the regulation of 1,25(OH)2D different in patients with HHM and HPT?" and "Why is normal osteoblast-osteoclast coupling dysregulated in HHM?" or more fundamentally, "What regulates osteoblast-osteoclast coupling, and why is it deranged in HHM?" Given the rate of accumulation of new information about HHM, about the anabolic effects of PTH and PTHrP, and about osteoblast-osteoclast coupling over the past 10 years, there is reason to be optimistic that the answers to these questions will soon become clear.
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2/5. Characterization of a renal cell carcinoma cell line derived from a human bone metastasis and establishment of an experimental nude mouse model.

    PURPOSE: We provide the necessary tools to study the biology of bone metastasis using renal cell carcinoma as a model. A relevant renal cell carcinoma cell line developed from a human bone metastasis is described and an experimental model in the nude mouse was established. MATERIALS AND methods: The novel cell line RBM1 was developed from bone metastasis from a patient with renal cell carcinoma. in vitro methods used to study the cell line included karyotype analysis, reverse-transcriptase polymerase chain reaction, ribonuclease protection assay and Western blot analysis. An intratibial injection model in the nude mouse resulted in bone lesions similar to those in human patients. RESULTS: Chromosomal analysis of this cell line revealed characteristic cytogenetic abnormalities common in renal cell carcinoma. RBM1 cells expressed parathyroid hormone parathyroid hormone related peptide, interleukin-6 and macrophage colony-stimulating factor, which are cytokines involved in osteoclast activation and subsequent bone resorption. Western blot analysis revealed the presence of high levels of epidermal growth factor receptor and c-MET. Reproducible osteolytic lesions developed in the nude mouse after injecting 1 x 106 cells into the tibia. CONCLUSIONS: This cell line and animal model may allow further study of the biology and mechanism of renal cell carcinoma bone metastasis.
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3/5. The role of 1,25-dihydroxyvitamin D in the maintenance of hypercalcemia in a patient with an ovarian carcinoma producing parathyroid hormone-related protein.

    The syndrome of humoral hypercalcemia of malignancy (HHM) is thought to be mainly a result of the production of parathyroid hormone-related protein (PTHRP) by malignant tumors. serum 1,25-dihydroxyvitamin D (1,25-DHD) concentrations are generally low in such patients, which contrasts with the findings in animal studies. A patient is reported with HHM from a clear cell ovarian carcinoma and elevated serum immunoreactive PTHRP (about five times the upper limit of normal) in whom serum 1,25-DHD concentrations were abnormally high (200 pmol/l) and associated with increased intestinal calcium absorption. Treatment with two different nitrogen-containing bisphosphonates (pamidronate and [3-dimethyl-amino-1-hydroxypropylidene]-1,1-bisphosphonate) did not normalize serum and urinary calcium despite effective inhibition of bone resorption. These observations suggested an additional intestinal contribution to the maintenance of hypercalcemia. Tumor removal was followed by decreases in serum immunoreactive PTHRP and 1,25-DHD concentrations to their respective normal ranges and normocalcemia. Separating HHM into Types I and II, according to the prevailing serum 1,25-DHD concentrations, can provide a basis for a better understanding of the pathogenesis of hypercalcemia, and it also may have practical use in the successful management of these patients.
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4/5. A case of idiopathic hypoparathyroidism and dietary vitamin d deficiency: the requirement for calcium and vitamin D for bone, but not renal responsiveness to PTH.

    A patient with concurrent idiopathic hypoparathyroidism and dietary vitamin d deficiency was studied. Acute renal responsiveness to PTH was demonstrated by immediate increases in urinary cyclic amp and phosphorus excretion. An impaired bone response to sustained PTH administration was demonstrated by absence of significant increases in serum calcium or urine hydroxyproline during 3 days of PTH administration. Skeletal responsiveness was restored either by raising the initial serum calcium with constant calcium infusion or by raising serum 25-OH-D levels to normal by administration of 1,000 units vitamin D daily. These results extend to the human, animal observations which suggest that vitamin D is required for the skeletal but not for the renal actions of parathyroid hormone.
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5/5. Effects of bisphosphonate (pamidronate) on bone resorption resulting from metastasis of a squamous cell carcinoma: report of an autopsy case and evaluation of bone resorbing activity in an experimental animal model.

    PURPOSE: This study evaluated the ability of bisphosphonate to prevent bone resorption induced by metastatic tumor cells. MATERIALS AND methods: autopsy specimens of a bone metastasis from a woman with a primary squamous cell carcinoma of the tongue who developed multiple osteolytic lesions and hypercalcemia and was treated with pamidronate were studied histologically, histochemically, and ultrastructurally. In an animal experiment, cultured tumor cells (1 x 10(5)) obtained from a metastatic submandibular lymph node in the same patient were injected in the left ventricle of nude mice, and a resulting metastatic bone lesion was studied histologically and histochemically. RESULTS: In the autopsy specimens, despite the presence of many resorption lacunae on bone surface, only a few small tartrate-resistant acid phosphatase (TRAPase)-positive cells were observed, and most of them were stained weakly and detached from the bone surface. In the animal experiment, 1 of 10 animals (10%) formed osteolytic bone metastasis, and many TRAPase-positive cells were observed histochemically. CONCLUSIONS: Biphosphonate inhibits bone resorption induced by tumor, possibly by decreasing the number of osteoclasts and inhibiting their function.
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