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Hypercalcemia and osteoclast proliferation in adult T‐cell leukemia
Author(s) -
Kiyokawa Tetsuyuki,
Yamaguchi Kazunari,
Takeya Motohiro,
Takahashi Kiyoshi,
Watanabe Toshiki,
Matsumoto Toshio,
Lee Sung Yul,
Takatsuki Kiyoshi
Publication year - 1987
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19870315)59:6<1187::aid-cncr2820590626>3.0.co;2-8
Subject(s) - medicine , osteoclast , bone resorption , parathyroid hormone , endocrinology , resorption , autopsy , leukemia , t cell leukemia , calcium , pathology , receptor
Eighteen autopsy cases of adult T‐cell leukemia (ATL) were investigated clinicopathologically. Thirteen of the patients had hypercalcemia during their clinical course. Nine of the thirteen had a high level of serum calcium at the terminal stage, even after extensive chemotherapy. Microscopic examination of the bone revealed proliferation of osteoclasts and bone resorption in eight patients. No osteoclast proliferation or bone resorption was found in the other nine normocalcemic patients. The infiltration of ATL cells was observed in only two patients—one was hypercalcemic and the other, normocalcemic. The factors affecting the serum calcium level were examined in two hypercalcemic patients. Hypercalcemia could not be accounted for by parathyroid hormone or prostaglandins E levels, which were in the normal range, or by 25‐hydroxyvitamin D and 1,25‐dihydroxyvitamin D, which were low. Our findings are consistent with the mechanism proposed by several investigators, that the malignant T‐lymphocytes produced an osteoclastactivating‐factor‐like substance that caused osteoclast proliferation and hypercalcemia. Cancer 59:1187‐1191, 1987.