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pubmed-article:2734758pubmed:issue12lld:pubmed
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pubmed-article:2734758pubmed:abstractTextAbout 10% of cancer patients develop hypercalcemia. The mechanisms behind the development of hypercalcemia are complex, but the most important facts seems to be increased osteoclastic bone resorption. Several cellular mediators play a part in creating and sustaining hypercalcemia. The article discusses these mechanisms, and reviews the principles of treatment. Emphasis is placed on rehydration and on inhibition of bone resorption. The use of diphosphonates (bisphosphonates), a group of potent osteoclast inhibitors, is discussed in some detail.lld:pubmed
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pubmed-article:2734758pubmed:issn0029-2001lld:pubmed
pubmed-article:2734758pubmed:authorpubmed-author:LamvikJJlld:pubmed
pubmed-article:2734758pubmed:authorpubmed-author:AasarødKKlld:pubmed
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pubmed-article:2734758pubmed:day30lld:pubmed
pubmed-article:2734758pubmed:volume109lld:pubmed
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pubmed-article:2734758pubmed:pagination1293-6lld:pubmed
pubmed-article:2734758pubmed:dateRevised2008-7-16lld:pubmed
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pubmed-article:2734758pubmed:year1989lld:pubmed
pubmed-article:2734758pubmed:articleTitle[Hypercalcemia in malignant diseases. Physiopathology and treatment].lld:pubmed
pubmed-article:2734758pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2734758pubmed:publicationTypeEnglish Abstractlld:pubmed