A case of idiopathic hypoparathyroidism and dietary vitamin D deficiency: the requirement for calcium and vitamin D for bone, but not renal responsiveness to PTH.
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.
D001862:Bone Resorption / Q000187:drug effects; D001842:Bone and Bones / Q000187:drug effects*; D002118:Calcium / Q000378:metabolism*; D004357:Drug Synergism; D005260:Female; D006801:Humans; D006887:Hydroxycholecalciferols / Q000097:blood; D007011:Hypoparathyroidism / Q000150:complications*; D007668:Kidney / Q000187:drug effects*; D008875:Middle Aged; D009751:Nutritional Requirements; D010281:Parathyroid Hormone / Q000494:pharmacology*; D014807:Vitamin D / Q000378:metabolism* / Q000494:pharmacology; D014808:Vitamin D Deficiency / Q000150:complications*
D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D014807:Vitamin D; D002118:Calcium