Abstracts at 33rd Kansai Calcium Conference November 12, 1994 Osaka Obayashi Building, Osaka, Japan

s at 33rd Kansai Calcium Conference November 12, 1994 Osaka Obayashi Building, Osaka, Japan Oncogenic hypophosphatemia: report of a case KATSUHIKO SAKAGUCHI', MAKOTO URUSHITANI', MASAKUNI KAMEYAMA', SHIGETO MORIMOTO 2 , TOSHIO OGIHARAZ , and KOUSEI YOU3 'Department of Medicine, Sumitomo Hospital, 2 Department of Geriatric Medicine, Osaka University Medical School, and 'Department of Orthopedics, Hyogo University Medical School, Hyogo, Japan A 55-year-old man was admitted to our hospital for investigation of muscle pain and bilateral thigh weakness. Laboratory examinations on admission revealed a severely decreased level of serum inorganic phosphate (Pi), elevated levels of serum alkaline phosphatase, and fractional excretion of Pi into the urine. The serum level of 1,25-dihydroxyvitamin D3 was in the lower normal range despite severe hypophosphatemia, and the circulating levels of calcium, parathyroid hormone, parathyroid hormonerelated protein, 25-hydroxyvitamin D, and 24,25dihydroxyvitamin D were all within the respective normal ranges. Oral administration of neutral phosphate and 1,25-dihydroxyvitamin D 3 hardly increased the serum level of Pi . Meanwhile, a chest computed tomographic (CT) examination revealed the presence of a tumor in the lower posterior mediastinum . Surgical resection of this tumor and pathological examination revealed it to be a phosphaturic mesenchymal tumor (mixed connective tissue variant) . Surgery resulted in prompt and complete normalization of the biochemical and hormonal abnormalities as well as disappearance of clinical symptoms . We speculate that the tumor secreted humoral substance(s) which may inhibit renal phosphate reabsorption and renal la hydroxylase activity . Recently, Cai and coworkers demonstrated that the substance(s) elaborated by the tumor cells had a low molecular weight and were heat-sensitive [1] . References 1. Cai Q, Hodgson SF, Kao PC, et al. (1994) Inhibition of renal phosphate transport by tumor production in a patient with oncogenic osteomalacia . N Engl J Med 330 :1645-1649 Hypercalcemia induced by immobilization in asymptomatic Paget's disease of bone K. KOGAWA, Y. NISHIZAWA, A. SHIOI, M. INABA, K. NAKATSUKA, H. KAWAKAMI, T. MIKI, and H . MORII Second Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan Hypercalcemia is quite rare in Paget's disease of bone except for certain conditions such as immobilization . The pathophysiological mechanism of hypercalcemia induced by immobilization is considered to be due to the high calcium efflux from the affected bones . We report here an adolescent with Paget's disease in whom severe hypercalcemia was due to immobilization . A 16year-old male suffered from hypercalcemia which had developed during long-term bed rest due to bilateral tears of the quadriceps muscle of the thigh . His father, grandmother, uncle, and cousin had all been diagnosed as having Paget's disease . The patient's laboratory findings on admission were as follows : serum calcium 13 mg/dl, phosphate 3 .4 mg/dl, alkaline phosphatase 475 (100-280) IU/1, intact-osteocalcin 200 (2.3-9.0) ng/ml, urinary pyridinoline 631 (17 .7-14.9) pmol/μmol Cr, deoxypyridinoline 136 (2 .2-6.1)pmol/ tmol Cr, intactPTH undetectable. Bone scintigraphy demonstrated the accumulation of 99mTc-HMDP in the maxilla and mandible, although radiological examination did not reveal any typical appearance of Paget's disease . Intravenous saline infusion and calcitonin administration were not effective in suppressing serum calcium and markers for bone metabolism. After daily oral administration of 1000 mg of etidronate for 12 consecutive days, serum Journal of Bone and Mineral Metabolism © Springer-Verlag 1996