BACKGROUND　　Imatinib mesylate inhibits several tyrosine kinases，including BCR-ABL，the C-KIT receptor，and the platelet-derived growth factor receptors αand β,all of which are associated with disease．We observed that hypophos-phatemia developed in some patients witheither chronic myelogenous leukemia or gastroiotestinal stromal tumors who were receiving imatinib.

METHODS　　We identified 16 natients who had low serum phosphate levels and(18 patients who had normal serum phosphate levels，all of whom were receiving imatinib．We performed the following biochemical measurements：whole-blood levels of ionized calcium,plasma levels of intact parathyroid hormone,and serum levels of total calcium，phosphate，25-hydroxyvitamin D,1.25-dihydroxyvi-tamin D,magnesium,and markers of bone formation(bone alkaline phosphatase and osteocalcin) and bone resorption (N-telopeptide of collagen cross-links); urinalysis；and phosphate，caleium，and creatinine levels in“spot”urine specimens.

RESULTS　　Patients in the low-phosphate group(median serum phosphatelevel，2.0 mg per deciliter [O.6 mmol perliter]；normal level，<2.5 mg per deciliter [O.8 mmol per liter]) had elevated parathyroid hormone levels and low-to-normal serum calcium levels，were younger，and were receiving a higher dose of imatinib than patients in the normal-phosphate group(median level，3.2 mg perdeciliter[1.O mmol per liter])．Both groups had high levels of phosphate excreted in the urine and markedly decreased serum levels of osteocalcin and N-telopeptide of collagen cross-links．

CONCLUSIONS　　Hypophos-phatemia，with associated changes in bone and mineral metabolism develops in a proportion of patients taking imatinib for either chronic myelogenous leukemia or gastrointestinal stromal tumors．The drug may inhibit bone remodeling (formation and resorption)，even in patients with normal serum phosphate levels．

(N Engl J Med 2006；354：2006-13．May 11，2006