Serum levels of 25-hydroxyvitamin D in postmenopausal osteoporosis

Abstract

Serum concentrations of 25-hydroxy-vitamin D were measured in a group of women with symptomatic postmenopausal osteoporosis, assessed by bone biopsy. A competitive protein binding assay was used, which included a chromatographic step. Accurate surveys of dietary or therapeutic vitamin D intake and light environment were obtained in each patient. Women with severe postmenopausal osteoporosis were found to have significantly (P less than 0.001) higher serum levels of 25-hydroxyvitamin D than age-matched normal women, the mean values being 27.5 ng/ml (+/- 13.6 SD) and 9.2 ng/ml (+/-5.7), respectively. The authors hypothesize that the reduction in 1,25-dihydroxyvitamin D, recently reported in postmenopausal osteoporotic women, might be responsible for the increased serum levels of 25-hydroxyvitamin D through an inadequate product inhibition of liver vitamin D 25-hydroxylase.

Effect of the administration of 1,25-dihydroxyvitamin D3 on serum levels of 25-hydroxyvitamin D in postmenopausal osteoporosis

“…In a previous paper, we reported our observations on the concentrations of 25-hydroxyvitamin D (25-OHD) in a group of postmenopausal osteoporotic women [1]. In that study, only patients with severe symptomatic osteoporosis, characterized by two or more vertebral fractures, were considered and the diagnosis was confirmed in each case by bone biopsy, in order to exclude with certainty women with osteomalacic features.…”

“…The treatment resulted in a significant decrease in serum 25-hydroxyvitamin D levels that were higher than normal in basal conditions, the mean values before and after therapy being 27.7 ng/ml (_+ 17.1 SD) and 19.7 ng/ml (-+12.7), respectively. These findings seem to confirm the hypothesis that an inadequate product-inhibition of liver 25-hydroxylase is responsible for the increased basal levels of 25-hydroxyvitamin D found in postmenopausal osteoporosis.Key words: 25-hydroxyvitamin D --1,25-dihydroxyvitamin Da --Postmenopausal osteoporosis teoporosis had higher serum levels of 25-OHD (27.5 ng/ml _+ 13.6 SD) than normal peers (8.2 ng/ml + 5.7) [1]. Additional cases were studied with similar…”

Osteoporosis: Is 1,25-(OH)₂D₃ of Value in Treatment?

“…Zerwekh et al [13] also have presented data suggesting that, at least in some osteo porotic patients, renal 25-(OH)vitamin D 1-alphahydroxylase may be impaired. Lore et al [14] have found signifi cantly elevated levels of serum 25-(OH)vitamin D in pa tients with postmenopausal osteoporosis, suggesting also the possibility of decreased conversion to l,25-(OH)2D3. Reduced sensitivity to l,25-(OH)2D3 might also be a factor in osteoporosis as suggested by Lund et al [7], On the other hand, work by Sorensen et al [15] also evaluated the response to intravenous injections of PTH ; significant increases in l,25-(OH)2D3 were seen in both normal and osteopenic patients.…”

Metabolic Bone Disease and the Elderly: Current Approach to Diagnosis and Therapy

“…Some data support a decreased calcitonin response to calcium infu sion in osteoporosis [60] and implication of calcitonin deficiency with increasing age in the development of osteoporosis [31,34,39,61]. 25(OH)D levels have been reported to be normal [35,58] or elevated [62] in osteopo rosis. Several studies report that serum 1,25-dihydroxyvitamin D levels are significantly lowered in postmeno pausal osteoporosis [35,63,64]; this has been hypothe sized to account for the decreased calcium absorption seen in osteoporosis [35,39].…”

“…Estrogen therapy increases 1,25-dihydroxyvitamin D le vels and calcium absorption [75] and retention [76]. Com bination therapy of estrogens and gestagen has been reported to produce an average 3%/year increase in min eral content [77], Dosages and therapy regimes have been reviewed elsewhere [62,68,[78][79][80]. Marshall et al [81] found that estrogens tended to inhibit bone formation.…”