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The pathogenesis of age-related osteoporotic fracture: effects of dietary calcium deprivation.

Abstract
The pathogenesis of osteoporotic fracture after the menopause is uncertain. We studied the effects of a 4-day low calcium diet on 17 subjects with vertebral osteoporotic fracture and 17 age-matched controls with a bone density within the young normal range and without fracture. At baseline, the osteoporotic patients were well matched to normal subjects in terms of calcium intake and absorption and renal function, but had higher bone turnover and relative secondary hyperparathyroidism. After the low calcium diet, the rise in calcitriol was deficient in the osteoporotic subjects. These data are consistent with the suggested pathogenesis of type II or age-related osteoporosis and show that in these subjects with osteoporotic fracture there was a primary defect in calcitriol production that resulted in secondary hyperparathyroidism. This defect may be the cause of the high bone turnover and may play an important role in the development of bone loss in these subjects.
AuthorsR L Prince, I M Dick, J Lemmon, D Randell
JournalThe Journal of clinical endocrinology and metabolism (J Clin Endocrinol Metab) Vol. 82 Issue 1 Pg. 260-4 (Jan 1997) ISSN: 0021-972X [Print] United States
PMID8989271 (Publication Type: Journal Article)
Chemical References
  • Parathyroid Hormone
  • Calcitriol
  • Calcifediol
  • Calcium
Topics
  • Aged
  • Aging
  • Calcifediol (blood)
  • Calcitriol (blood, metabolism)
  • Calcium (administration & dosage, blood, urine)
  • Diet
  • Female
  • Fractures, Bone (etiology)
  • Humans
  • Hyperparathyroidism (etiology)
  • Middle Aged
  • Osteoporosis, Postmenopausal (etiology)
  • Parathyroid Hormone (blood)

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