Arrest of Hyperparathyroid Bone Disease with Dihydrotachysterol in Patients Undergoing Chronic Hemodialysis

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.