help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Journal of Clinical Endocrinology & Metabolism Vol. 56, No. 6 1319-1322
doi:10.1210/jcem-56-6-1319
Copyright © 1983 by the Endocrine Society.
This Article
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
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
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 Lufkin, E. G.
Right arrow Articles by Heath, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lufkin, E. G.
Right arrow Articles by Heath, H., III

Hyperphosphatemic Tumoral Calcinosis: Effects of Phosphate Depletion on Vitamin D Metabolism, and of Acute Hypocalcemia on Parathyroid Hormone Secretion and Action*

Edward G. Lufkin, Rajiv Kumar and Hunter Heath, III

Division of Endocrinology and Metabolism, Endocrine Research Unit, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905

Address requests for reprints to: Edward G. Lufkin, M.D., Department of Internal Medicine, Mayo Clinic, 200 First Street Southwest, Rochester, Minnesota 55905.

In hyperphosphatemic tumoral calcinosis, plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels are inappropriately elevated, suggesting an abnormality in vitamin D metabolism. To define this abnormality further, we measured vitamin D metabolites in two patients and four controls before and after phosphate depletion. The patients showed elevated plasma levels of 1,25(OH)2D in the basal state. Phosphate depletion reduced serum phosphate in patients from a mean of 6.1 to 2.6 mg/dl; this was accompanied by a rise in plasma 25-hydroxyvitamin D from 33.6 to 41.9 ng/dl, and in 1,25(OH)2D from 67.7 to 93.2 pg/ml. The absolute rise in 1,25(OH)2D was similar to that of controls. EDTA infusion produced a normal increase of serum immunoreactive PTH levels and urinary cAMP excretion. In this form of tumoral calcinosis, 1,25(OH)2D levels are elevated despite hyperphosphatemia, normal immunoreactive PTH, and normal serum calcium concentrations, suggesting an abnormality in the regulation of 1,25(OH)2D synthesis or metabolism, or alternatively, another undefined stimulus for 1,25(OH)2D synthesis. These patients appear to have concurrent abnormalities of renal tubular phosphate transport and vitamin D metabolism. (J Clin Endocrinol Metab 56:1319, 1983)

* This work was supported in part by Grants AM-19607, AM-27440, AM-25409, and AM-26808 from the USPHS, NIH.

Received August 24, 1982.




This article has been cited by other articles:


Home page
Hum Mol GenetHome page
A. Benet-Pages, P. Orlik, T. M. Strom, and B. Lorenz-Depiereux
An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia
Hum. Mol. Genet., February 1, 2005; 14(3): 385 - 390.
[Abstract] [Full Text] [PDF]


Home page
Arch Pediatr Adolesc MedHome page
R. Steinherz, R. W. Chesney, B. Eisenstein, A. Metzker, H. F. DeLuca, and M. Phelps
Elevated Serum Calcitriol Concentrations Do Not Fall in Response to Hyperphosphatemia in Familial Tumoral Calcinosis
Arch Pediatr Adolesc Med, August 1, 1985; 139(8): 816 - 819.
[Abstract] [PDF]




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 © 1983 by The Endocrine Society