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Tumor‐induced hypercalcemia in a patient with extensive soft tissue sarcoma: Effects of bisphosphonate therapy and surgery
Author(s) -
Oleffe Véronique,
Dumon JeanClaude,
Body JeanJacques
Publication year - 1996
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/(sici)1096-9098(199610)63:2<125::aid-jso10>3.0.co;2-5
Subject(s) - medicine , reabsorption , bisphosphonate , sarcoma , soft tissue , parathyroid hormone , complication , cancer , urology , calcium , endocrinology , surgery , gastroenterology , pathology , kidney , osteoporosis
Tumor‐induced hypercalcemia (TIH) is a frequent complication of advanced cancer, but it has been rarely reported in patients with sarcoma. We describe the case of a young female patient with TIH and with an extensive synoviosarcoma of the left lower limb destroying the bony structures. Hypercalcemia was severe (18.3 mg/dl) and accompanied by low serum P i and suppressed parathyroid hormone (PTH) and 1,25(OH) 2 vit D 3 serum concentrations. Hypercalcemia was successfully treated with ibandronate, a new third‐generation bisphosphonate, and radical surgery was performed when the patient was normocalcemic. Circulating levels of PTH‐related protein (PTHrP) were elevated at 22.5 pmol/L (NI <9) PTHrP levels did not change after successful therapy of TIH, in contrast with PTH, which increased sharply. PTHrP levels were normalized after radical surgery. Moreover, low serum Pi with reduced threshold for phosphate excretion and increased tubular calcium reabsorption supported the notion that PTHrP was indeed the essential mediator of paraneoplastic hypercalcemia in this case despite the extensive bone destruction. © 1996 Wiley‐Liss, Inc.

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