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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 10 3541-3543
Copyright © 2000 by The Endocrine Society


From the Clinical Research Centers

Bone Mineral Density Increases with Vitamin D Repletion in Patients with Coexistent Vitamin D Insufficiency and Primary Hyperparathyroidism1

Vitaly Kantorovich, Mercedes A. Gacad, Leanne L. Seeger and John S. Adams

Burns and Allen Research Institute and Division of Endocrinology, Diabetes, and Metabolism, Cedars-Sinai Medical Center, University of California School of Medicine (V.K., M.A.G., J.S.A.), Los Angeles, California 90048; and Department of Radiological Sciences, Center for the Health Sciences, University of California School of Medicine (L.L.S.), Los Angeles, California 90095

Address all correspondence and requests for reprints to: Dr. John S. Adams, Burns and Allen Research Institute, Division of Endocrinology, Diabetes, and Metabolism, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room B131, Los Angeles, California 90048. E-mail: adamsj{at}cshs.org

Two hundred and twenty-nine consecutive subjects, 202 women and 27 men, referred for evaluation of osteoporosis or low bone mineral density (BMD) had serum measurements of immunoreactive PTH (iPTH) and 25-hydroxyvitamin D (25OHD) performed. Fifteen individuals (mean age ± SE, 75 ± 2.4 yr) had depressed serum 25OHD (<15 pg/mL) and concomitantly elevated (>65 pg/mL) iPTH levels. After successful treatment of vitamin D insufficiency in all subjects, iPTH remained inappropriately high or frankly elevated in 5, describing a 2.2% prevalence rate of coexistent primary hyperparathyroidism and vitamin D insufficiency in our population. Despite persistent primary hyperparathyroidism, normalization of serum 25OHD levels in these 5 subjects increased their BMD at an annual rate of 6.3% and 8.2% in spine and hip, respectively. Our results suggest that coexistent vitamin D insufficiency can obscure the diagnosis of primary hyperparathyroidism and, when treated effectively, can result in substantial short-terms gains in BMD despite persistence of the inappropriate production of PTH.




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