title: Skeletal responsiveness to endogenous parathyroid hormone in postmenopausal osteoporosis.
abstract: To test the hypothesis that increased sensitivity of bone to PTH may be a major cause of bone loss in postmenopausal osteoporosis, we induced acute calcium deprivation and measured bone responsiveness to endogenous PTH under physiological conditions. Eighteen osteoporotic and 17 normal postmenopausal women with similar dietary calcium intakes were studied before and after 4 days of calcium deprivation (dietary calcium 230 mg/day and treatment with a calcium-binding agent). Despite decreased serum PTH values, the baseline indices of bone turnover (serum osteocalcin level and 24-h urinary excretions of total deoxypyridinoline/creatinine and pyridinoline/creatinine corrected for total body bone mineral content), were higher in the osteoporotic women. During calcium deprivation, the changes in bone markers from baseline were similar in both groups, except for serum osteocalcin and serum type I procollagen carboxy-terminal propeptide. Changes in the normal and the osteoporotic women were, respectively: serum ionized calcium concentration decreased 3.3% and 2.1%; serum intact PTH increased 65% and 56%; plasma 1,25-dihydroxyvitamin D3 increased 29% and 39%; pyridinoline/creatinine increased 12% and 11%; and deoxypyridinoline/creatinine increased 27% and 12%. Serum osteocalcin increased 2.3% and serum procollagen carboxy-terminal propeptide decreased 9.4% in the normal women but did not change in the osteoporotic women. We conclude that women with postmenopausal osteoporosis do not have increased skeletal responsiveness to PTH compared with age-comparable normal postmenopausal women. Therefore, the higher bone turnover in postmenopausal osteoporosis, despite lower serum intact PTH concentration, must be due to other factors. Assessment of acute changes in bone turnover during physiological alterations in endogenous PTH secretion is a useful test in metabolic bone diseases.
authors.affiliation: Division of Endocrinology and Metabolism, Mayo Clinic, Rochester, Minnesota 55905.
authors.forename: P R
authors.initials: PR
authors.lastname: Ebeling
authors.forename: J D
authors.initials: JD
authors.lastname: Jones
authors.forename: M F
authors.initials: MF
authors.lastname: Burritt
authors.forename: C R
authors.initials: CR
authors.lastname: Duerson
authors.forename: A W
authors.initials: AW
authors.lastname: Lane
authors.forename: C
authors.initials: C
authors.lastname: Hassager
authors.forename: R
authors.initials: R
authors.lastname: Kumar
authors.forename: B L
authors.initials: BL
authors.lastname: Riggs
mesh_terms: D015519:Bone Density / Q000502:physiology*; D001862:Bone Resorption / Q000097:blood / Q000503:physiopathology*; D002118:Calcium / Q000097:blood; D002136:Calcium, Dietary / Q000008:administration & dosage; D002940:Circadian Rhythm; D005260:Female; D006801:Humans; D015999:Multivariate Analysis; D015675:Osteocalcin / Q000097:blood; D015663:Osteoporosis, Postmenopausal / Q000097:blood / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000097:blood / Q000502:physiology*; D011726:Pyridinium Compounds / Q000652:urine
chemical_list: D002136:Calcium, Dietary; D010281:Parathyroid Hormone; D011726:Pyridinium Compounds; D015675:Osteocalcin; D002118:Calcium