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Saltzman Institute for Clinical Investigation, The Mt. Sinai Hospital of Cleveland, and Case Western Reserve University School of Medicine Cleveland, Ohio
Washington University School of Medicine St. Louis, Missouri
Reprint requests to: Saul M. Genuth, M.D., The Mt. Sinai Hospital of Cleveland, 1800 East 105th Street, Cleveland, Ohio 44106.
A patient with concurrent idiopathic hypoparathyroidism and dietary vitamin D deficiency was studied. Acute renal responsiveness to PTH was demonstrated by immediate increases in urinary cyclic AMP and phosphorus excretion. An impaired bone response to sustained PTH administration was demonstrated by absence of significant increases in serum calcium or urine hydroxyproline during 3 days of PTH administration. Skeletal responsiveness was restored either by raising the initial serum calcium with constant calcium infusion or by raising serum 25-OH-D levels to normal by administration of 1, 000 units vitamin D daily. These results extend to the human, animal observations which suggest that vitamin D is required for the skeletal but not for the renal actions of parathyroid hormone.
Received March 19, 1976.
This article has been cited by other articles:
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H. I. HOCHMAN Idiopathic (Pseudoidiopathic?) Hypoparathyroidism Arch Pediatr Adolesc Med, April 1, 1979; 133(4): 435 - 436. [Abstract] [PDF] |
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