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Arrest of Hyperparathyroid Bone Disease with Dihydrotachysterol in Patients Undergoing Chronic Hemodialysis
- MICHAEL KAYE, M.B., F.R.C.P.(C);
- G. CHATTERJEE, M.B.;
- G. F. COHEN, M.B., B.Ch.; and
- S. SAGAR, M.B.
Abstract
Six patients with active bone disease who were on a chronic dialysis program were treated with dihydrotachysterol, 0.25 to 0.375 mg/day. There was marked improvement, probably due in part to increased calcium absorption from the gut and subsequent calcium deposition in bone. An equivalent dose of calciferol elicited no response. Plasma antirachitic bioassay suggested that dihydrotachysterol was not converted to vitamin D or to 25-hydroxy D in man or in rat.
Article and Author Information
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▸From the Division of Nephrology, Department of Medicine, The Montreal General Hospital, Montreal, Quebec, Canada
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Supported in part by grant P. H. 43-66-542, U. S. Public Health Service, Washington, D.C.
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▸Requests for reprints should be addressed to Michael Kaye, M.B., Director, Division of Nephrology, The Montreal General Hospital, Montreal, Quebec, Canada
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- Received January 26, 1970.
- Accepted May 12, 1970.
