Hypophosphatemic Osteomalacia: Association with Prostatic Carcinoma

  1. KENNETH W. LYLES, M.D.;
  2. WILLIAM R. BERRY, M.D.;
  3. MARK HAUSSLER, Ph.D.;
  4. JOHN M. HARRELSON, M.D.; and
  5. MARC K. DREZNER, M.D.
  1. Durham, North Carolina; and Tucson, Arizona

    Abstract

    Hypophosphatemic osteomalacia that remits after resection of a coexisting tumor has been described in 35 patients. Because the associated neoplasms have been of mesenchymal origin, it has been inferred that this tumorinduced osteomalacia syndrome is uniquely related to tumors of this derivation. However, in the present investigation we studied subjects with coincident hypophosphatemia and prostatic carcinoma to ascertain whether this endodermal malignancy causes the tumor-induced osteomalacia syndrome. The hypophosphatemic patients had renal phosphate wasting, gastrointestinal malabsorption of calcium and phosphate, and negative phosphate balance. Moreover, bone biopsies showed histomorphologic changes indicative of osteomalacia. Although widespread metastases precluded establishing the diagnosis of tumor-induced osteomalacia by resection of the tumor, a series of studies excluded alternate causes for the osteomalacia. Further, affected subjects had a normal serum concentration of 2 5-hydroxy vitamin D, 28.0 ± 8.3 ng/mL, and serum 1,25-dihydroxyvitamin D levels were low, 15.0 ± 1.0 pg/mL, characteristic of the tumor-induced osteomalacia syndrome. Thus, prostatic carcinoma, although an endodermal malignancy, may cause the tumor-induced osteomalacia syndrome.

    Article and Author Information

    • ▸From the Departments of Medicine, Pathology, and Orthopedics, Duke University Medical Center and Durham Veterans Administration Hospital, Durham, North Carolina; and the Department of Biochemistry, University of Arizona Medical College; Tucson, Arizona.

    • Grant support: by grant MO1 FR 30 from the Clinical Research Center Branch Division of Research Facilities and Resources, U. S. Public Health Service; grants AM 15781 and AM07012 from the National Institute of Arthritis, Metabolism, and Digestive Diseases; grant CA 11265 from the National Cancer Institute; and a grant from Hoffman-LaRoche Inc. At the time of this study Dr. Drezner was a recipient of a Research and Education Award from the Veterans Administration and Research Career Development Award 1 KO AM 00643 from the National Institute of Arthritis, Metabolism, and Digestive Diseases. Dr. Lyles is a Geriatric Fellow of the Veterans Administration.

    • ▸Requests for reprints should be addressed to Marc K. Drezner, M.D.; Duke University Medical Center, Box 3285M; Durham, NC 27710.

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