BONE TURNOVER MARKERS AND BONE-DENSITY ACROSS THE MENOPAUSAL TRANSITION

Citation
Pr. Ebeling et al., BONE TURNOVER MARKERS AND BONE-DENSITY ACROSS THE MENOPAUSAL TRANSITION, The Journal of clinical endocrinology and metabolism, 81(9), 1996, pp. 3366-3371
Citations number
29
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
81
Issue
9
Year of publication
1996
Pages
3366 - 3371
Database
ISI
SICI code
0021-972X(1996)81:9<3366:BTMABA>2.0.ZU;2-M
Abstract
We measured lunbar spine and femoral neck bone mineral density (BMD); urine markers of bone resorption; serum markers of bone formation; and serum gonadotrophin, estradiol and inhibin concentrations in a popula tion-based cohort of 281 women aged 45-57 yr. Women were classified in to pre-, peri-, and postmenopausal groups, depending on menstrual blee ding patterns. Compared with premenopausal women, BMD was lower only i n postmenopausal women but not in women currently using hormone replac ement therapy (HRT). BMD decreased with age in the perimenopausal grou p. Compared with premenopausal women, perimenopausal women had 20% gre ater urine N-telopeptide excretion (P < 0.05) and a doubling of gonado trophin levels (P < 0.01), whereas serum estradiol and bone formation marker concentrations were no different, Postmenopausal women had grea ter levels of bone turnover markers (P < 0.0001), except free deoxypyr idinoline and type I procollagen propeptide. Among postmenopausal wome n, bone resorption markers were lower in those using HRT. Levels of ne arly all bone turnover markers were positively related to serum FSH co ncentrations (P < 0.0001). Overall, the major independent predictors o f BMD were age, urine N-telopeptide, serum bone alkaline phosphatase, and serum FSH, whereas urine free deoxypyridinoline was positively rel ated to BMD in pre- and perimenopausal women. In conclusion, the perim enopause is associated. with elevated bone resorption rates and declin ing BMD, and factors in addition to estrogen deficiency may also contr ibute to the pathogenesis of postmenopausal osteoporosis.