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November 1974

1,25-Dihydroxycholecalciferol: Effect on Skeletal Lesions and Plasma Parathyroid Hormone Levels in Uremic Osteodystrophy

Author Affiliations

From the Medical and Research Services, Veterans Administration Wadsworth Hospital Center, Los Angeles (Drs. Brickman, Singer, and Coburn); Seattle Veterans Administration Hospital, Seattle (Drs. Sherrard, Baylink, and Maloney); the Orthopedic Research Unit, Mayo Clinic and Foundation, Rochester, Minn (Dr. Jowsey); the Department of Biochemistry, University of California at Riverside, Riverside (Dr. Norman); the Department of Medicine, Cedars-Sinai Medical Center (Dr. Massry), and UCLA School of; Medicine, Los Angeles (Drs. Brickman, Singer, Coburn, and Massry). Dr. Singer is now at the Los Angeles County-USC Medical Center, Los Angeles.

Arch Intern Med. 1974;134(5):883-888. doi:10.1001/archinte.1974.00320230093020

Skeletal abnormalities and plasma immunoreactive parathyroid hormone (iPTH) levels were evaluated in eight patients with uremic osteodystrophy treated with 1,25-dihydroxycholecalciferol (1,25-(OH)2D3), 0.14μg to 0.68μg/day, for 8 to 17 weeks. Serum calcium levels increased in all but exceeded 10 mg/100 ml in only three; serum phosphorus level changes were small and variable. Plasma iPTH levels decreased noticeably in six patients, reaching normal values in two. Bone biopsies showed reduction in resorptive surface in four patients with skeletal lesions primarily of secondary hyperparathyroidism; in one, marrow fibrosis decreased from 11.5% to 0.3%. In four persons with osteomalacic lesions predominating, osteoid width was reduced slightly in three and calcification front improved in two. Observations indicate that administration of small quantities of 1,25-(OH)2D3to uremic patients can markedly reverse hyperparathyroid manifestations and improve lesions of osteomalacia.

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