help button home button Endocrine Society JCEM JCEM Call for Nominations for EIC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Davies, M.
Right arrow Articles by Mawer, E. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Davies, M.
Right arrow Articles by Mawer, E. B.
The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 1 209-212
Copyright © 1997 by The Endocrine Society

Clinical Studies

Increased Catabolism of 25-Hydroxyvitamin D in Patients with Partial Gastrectomy and Elevated 1,25-Dihydroxyvitamin D Levels. Implications for Metabolic Bone Disease1

Michael Davies, Sara E. Heys, Peter L. Selby, Jacqueline L. Berry and E. Barbara Mawer

Bone Disease Research Centre, University Department of Medicine, Manchester Royal Infirmary, Manchester, M13 9WL, United Kingdom

Address all correspondence and requests for reprints to: Dr. M. Davies, University Department of Medicine, Manchester Royal Infirmary, Manchester, M13 9WL, United Kingdom.

Serum vitamin D metabolites and PTH were measured in seven subjects with a history of previous partial gastrectomy (PGX) and metabolic bone disease. The elimination t1/2 of [3H]25-hydroxyvitamin D3 ([3H]25OHD3) in serum was assessed after an iv pulse dose of 5 µCi [26,27-3H]25OHD3. Median serum 25OHD3 was 37.5 (27.5–101.3) nmol/L, [normal range (NR) 10.8–58.5 nmol/L], mean serum 1,25-dihydroxyvitamin D [1, 25-(OH)2D3] was raised at 175 ± 72 pmol/L, (NR 48–120 pmol/L) and mean PTH was also high, 67 ± 27 ng/L, (NR 10–60 ng/L). Serum t1/2 [3H]25OHD3 ranged from 10.9–21.2 days. A strong negative correlation existed between t1/2 [3H]25OHD3 and serum 1,25-(OH)2D3 [Spearman’s rank correlation coefficient (r = -0.82, P = 0.002)] and PTH [Spearman’s rank correlation coefficient (r = -0.81, P = 0.001)]. Four subjects who had high initial PTH concentrations (60–115 ng/L) and elevated 1,25-(OH)2D levels (162–300 pmol/L) were reassessed after calcium supplementation to suppress secondary hyperparathyroidism (2°HPT). In this subgroup, after-treatment PTH fell from 82 ± 24 to 52 ± 24 ng/L (mean ± SD), not significant; 1,25-(OH)2D fell from 210 ± 61 to 116 ± 28 pmol/L, P = 0.015; and t1/2 [3H]25OHD3 increased from 13.2 ± 1.9 to 18.9 ± 3.1 days, P = 0.012.

Patients with PGX and evidence of 2°HPT with elevated 1,25-(OH)2D have a reduced t1/2 [3H]25OHD3, and this may explain the increased susceptibility of the subjects to osteomalacia. Calcium supplementation suppresses 2°HPT, increases t1/2 [3H]25OHD3 and may protect against PGX osteoporosis and osteomalacia.




This article has been cited by other articles:


Home page
 Eur J EndocrinolHome page
L. Rejnmark, P. Vestergaard, L. Heickendorff, and L. Mosekilde
Plasma 1,25(OH)2D levels decrease in postmenopausal women with hypovitaminosis D.
Eur. J. Endocrinol., April 1, 2008; 158(4): 571 - 576.
[Abstract] [Full Text] [PDF]

Home page
 CJASNHome page
A. J. Felsenfeld, M. Rodriguez, and E. Aguilera-Tejero
Dynamics of Parathyroid Hormone Secretion in Health and Secondary Hyperparathyroidism
Clin. J. Am. Soc. Nephrol., November 1, 2007; 2(6): 1283 - 1305.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
A. Grey, J. Lucas, A. Horne, G. Gamble, J. S. Davidson, and I. R. Reid
Vitamin D Repletion in Patients with Primary Hyperparathyroidism and Coexistent Vitamin D Insufficiency
J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 2122 - 2126.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
J. M Pettifor
Nutritional rickets: deficiency of vitamin D, calcium, or both?
Am. J. Clinical Nutrition, December 1, 2004; 80(6): 1725S - 1729S.
[Abstract] [Full Text] [PDF]

Home page
 JNMHome page
M. Piert, T. T. Zittel, M. Jahn, A. Stahlschmidt, G. A. Becker, and H.-J. Machulla
Increased Sensitivity in Detection of a Porcine High-Turnover Osteopenia After Total Gastrectomy by Dynamic 18F-Fluoride Ion PET and Quantitative CT
J. Nucl. Med., January 1, 2003; 44(1): 117 - 124.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
P. Lips
Vitamin D Deficiency and Secondary Hyperparathyroidism in the Elderly: Consequences for Bone Loss and Fractures and Therapeutic Implications
Endocr. Rev., August 1, 2001; 22(4): 477 - 501.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
D. Fatayerji, E. B. Mawer, and R. Eastell
The Role of Insulin-Like Growth Factor I in Age-Related Changes in Calcium Homeostasis in Men
J. Clin. Endocrinol. Metab., December 1, 2000; 85(12): 4657 - 4662.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1997 by The Endocrine Society