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From the Clinical Research Centers |
Bone Center and Burns and Allen Research Institute, Cedars-Sinai Medical Center, University of California School of Medicine (J.S.A., V.K., C.W., M.J.), Los Angeles, California 90048; and the Department of Pediatrics, Medical University of South Carolina (B.W.H.), Charleston, South Carolina 29425
Address all correspondence and requests for reprints to: John S. Adams, M.D., B131, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048. E-mail: adamsj{at}cshs.org
Vitamin D insufficiency is characterized biochemically by the presence
of secondary hyperparathyroidism, which can contribute to bone loss in
osteopenic patients. Over a 2-yr period of evaluation of 118
consecutive, free living patients with osteopenia or osteoporosis, we
identified 18 subjects with depressed serum 25-hydroxyvitamin D (25OHD;
14 ng/mL). Twelve of these subjects harbored a low 25OHD level and
consented to undergo replacement with 50,000 IU vitamin D2
twice weekly for 5 weeks. Five hundred thousand units of oral vitamin
D2 resulted in significant increases in 25OHD (+24.3
± 16.9 ng/mL; P < 0.001) and the fasting urinary
calcium/creatinine excretion ratio (+0.06 ± 0.004;
P = 0.01) and significant decreases in the serum
concentration of PTH (-32.9 ± 36.9 pg/mL; P
< 0.001) and osteocalcin (-4.9 ± 2.4 ng/mL;
P < 0.001). Vitamin D repletion was associated
with a significant 45% annualized increase in bone mineral density
at both the lumbar spine (P < 0.001) and the
femoral neck (P = 0.03), indicating that resolution
of vitamin D insufficiency in a population of patients with low bone
mass results in a rapid rebound increase in bone mineral density.
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