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dc.contributor.authorWalls, J
dc.contributor.authorBundred, Nigel J
dc.contributor.authorHowell, Anthony
dc.date.accessioned2010-05-14T10:02:20Z
dc.date.available2010-05-14T10:02:20Z
dc.date.issued1995-03
dc.identifier.citationHypercalcemia and bone resorption in malignancy. 1995 (312):51-63 Clin. Orthop. Relat. Res.en
dc.identifier.issn0009-921X
dc.identifier.pmid7634618
dc.identifier.urihttp://hdl.handle.net/10541/98837
dc.description.abstractHypercalcemia is the most common paraneoplastic syndrome associated with cancer. This paper addresses the etiology and pathogenesis of hypercalcemia of malignancy and discusses the relative contributions of local and humoral effects on bone and renal calcium homeostasis. The roles of parathyroid hormone-related protein and other osteolytic cytokines are outlined. New biochemical markers that enable more specific monitoring of the response of bone metastases to treatment are introduced, including urinary excretion of the collagen crosslinks pyridinoline and deoxypyridinoline. The clinical management and prevention of hypercalcemia is systemically outlined, including indications for bisphosphonate, glucocorticoid, and calcitonin therapy. The results of recent trials of bisphosphonate therapy for the prevention of tumor progression and its subsequent problems such as bone pain, fracture, and hypercalcemia also are discussed.
dc.language.isoenen
dc.subjectBone Canceren
dc.subjectBreast Canceren
dc.subject.meshAnimals
dc.subject.meshBone Neoplasms
dc.subject.meshBreast Neoplasms
dc.subject.meshCytokines
dc.subject.meshDiphosphonates
dc.subject.meshDisease Progression
dc.subject.meshHumans
dc.subject.meshHypercalcemia
dc.subject.meshOsteolysis
dc.subject.meshParaneoplastic Syndromes
dc.titleHypercalcemia and bone resorption in malignancy.en
dc.typeArticleen
dc.contributor.departmentDepartment of Surgery, Northern General Hospital, Sheffield, England.en
dc.identifier.journalClinical Orthopaedics and Related Researchen
html.description.abstractHypercalcemia is the most common paraneoplastic syndrome associated with cancer. This paper addresses the etiology and pathogenesis of hypercalcemia of malignancy and discusses the relative contributions of local and humoral effects on bone and renal calcium homeostasis. The roles of parathyroid hormone-related protein and other osteolytic cytokines are outlined. New biochemical markers that enable more specific monitoring of the response of bone metastases to treatment are introduced, including urinary excretion of the collagen crosslinks pyridinoline and deoxypyridinoline. The clinical management and prevention of hypercalcemia is systemically outlined, including indications for bisphosphonate, glucocorticoid, and calcitonin therapy. The results of recent trials of bisphosphonate therapy for the prevention of tumor progression and its subsequent problems such as bone pain, fracture, and hypercalcemia also are discussed.


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