Different vitamin D substrate-product relationship after oral vitamin D supplementation in familial benign hypercalcemia, primary hyperparathyroidism, and healthy controls.

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State: Public
Version: Final published version
License: Not specified
Serval ID
serval:BIB_5B2CE3DA8126
Type
Article: article from journal or magazin.
Collection
Publications
Title
Different vitamin D substrate-product relationship after oral vitamin D supplementation in familial benign hypercalcemia, primary hyperparathyroidism, and healthy controls.
Journal
European Journal of Endocrinology / European Federation of Endocrine Societies
Author(s)
Bevilacqua M., Invernizzi M., Righini V., Carda S., Cisari C.
ISSN
1479-683X (Electronic)
ISSN-L
0804-4643
Publication state
Published
Issued date
2011
Peer-reviewed
Oui
Volume
164
Number
5
Pages
833-838
Language
english
Notes
Publication types: Comparative Study ; Journal Article Publication Status: ppublish
Abstract
CONTEXT: In healthy subjects and in patients with primary hyperparathyroidism (PH), the administration of a low dose of 25(OH)D (25 μg/day) increases the serum levels of both 25(OH)D and 1,25(OH)(2)D. It is unknown whether this relationship is present in patients affected by familial benign hypocalciuric hypercalcemia (FBH).
OBJECTIVE: To evaluate the different vitamin D substrate-product relationship after oral vitamin D supplementation in familial benign hypercalcemia, PH, and healthy controls.
DESIGN: We evaluated the main physiological regulators of 1α-hydroxylase and the substrate-product relationship of 25(OH)D and 1,25(OH)(2)D in 20 patients with PH, 25 with FBH, and 122 healthy sex- and age-matched controls before and after administration of 25(OH)D for 2 weeks.
RESULTS: 25(OH)D increased significantly in all subjects, whereas 1,25(OH)(2)D serum levels increased significantly in PH patients and healthy controls but not in patients with FBH. Therefore, a significant positive substrate-product relationship of 25(OH)D-1,25(OH)(2)D was found in PH and healthy controls, but not in FBH. Monomeric calcitonin (hCT-M) was significantly lower at baseline and after 25(OH)D supplementation in the FBH group compared with the other two groups.
CONCLUSIONS: The lack of 1,25(OH)(2)D increase in FBH may be due to a direct inhibitory effect on 1α-hydroxylase of hypercalcemia per se, increased metabolic clearance of 1,25(OH)(2)D, or a decreased stimulus of 1α-hydroxylase related to persistently low levels of hCT.
Keywords
Administration, Oral, Aged, Dietary Supplements, Female, Humans, Hypercalcemia/blood, Hypercalcemia/congenital, Hyperparathyroidism, Primary/blood, Hyperparathyroidism, Primary/drug therapy, Male, Middle Aged, Substrate Specificity, Vitamin D/administration & dosage, Vitamin D/blood
Pubmed
Open Access
Yes
Create date
25/03/2013 18:18
Last modification date
15/07/2020 6:26
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