Association between female sex hormones and biochemical markers of bone turnover in peri- and postmenopausal women.

In an epidemiological study, markers of bone formation (serum osteocalcin and C-terminal propeptide of type I collagen) and bone resorption [urinary type I collagen peptides (Crosslaps), urinary total pyridinoline (TPYRI), urinary deoxypyridinoline (DPYRI) as well as female sex hormones (serum estradiol)], follicle-stimulating hormone (FSH) and luteinizing hormone were measured in 237 women. This cohort aged 44-66 years, came for their first medical examination since menopause to the outpatient menopause clinic at the Kaiser-Franz-Josef-Hospital, Vienna. The women were all 0.5-5.0 years since cessation of menses and were not taking medications other than hormone replacement therapy [52 cases, 21.9%)] and had no diseases known to affect bone and mineral metabolism. The best correlation was found between urinary DPYRI and urinary TPYRI (r = 0. 63, P = 0.0001), followed by urinary Crosslaps and urinary DPYRI (r = 0.47, p = 0.0001). Only weak but significant correlations between E2 and urinary Crosslaps (r = -0.21, P < 0.0001) as well as serum E2 and serum osteocalcin (r = -0.16, P = 0.0007), were observed. Of the 237 women 53% suffered from a severe E2 deficiency (E2 < 10.0 ng/liter). In these patients, urinary Crosslaps (+48%) and serum osteocalcin (+22%) were significantly higher (P < 0.0001) compared with those patients with E2 levels > 10 ng/liter. Women with E2 levels >10 ng/liter were further subdivided into those with and without sex hormone replacement therapy, whereby no statistical differences in any of the biochemical markers could be observed between these groups. We could clearly demonstrate that in postmenopausal women suffering from severe E2 deficiency (E2 < 10 ng/liter), urinary Crosslaps and serum osteocalcin are significantly increased, indicating in principle a clear correlation between E2 deficiency and these markers of bone turnover.

Biochemical markers in menopausal women.

Markers of bone formation (osteocalcin and C-Terminal Propeptide of Type I Collagen [CICP]) and of resorption (Crosslaps, total pyridinoline [Pyd] and deoxypyridinoline [Dpd]) as well as female sex hormones (estradiol [E2], follicle stimulating hormone [FSH] and luteinizing hormone [LH]) were measured in 237 women aged 44-66 years coming for the first medical examination to the outpatient clinic of menopause at the Kaiser-Franz-Josef-Hospital, Vienna. All women (0.5-5.0 years since cessation of menses) selected were not taking medications other than hormone replacement therapy in 52 cases (21.9%) and did not have diseases known to affect bone and mineral metabolism. The best correlation was found between Dpd and Pyd (r = 0.63, p = 0.0001), followed by Crosslaps and Dpd (r = 0.47, p = 0.0001). Only weak but significant correlations between E2 and Crosslaps (r = 0.21, p < 0.0001) as well as E2 and osteocalcin (r = 0.16, p = 0.0007) were observed, 53% of the 237 women suffered from a severe E2 deficiency (E2 < 10.0 ng/L). In these patients Crosslaps (approx. +48%) and osteocalcin (+22%) were significantly higher (p < 0.0001) compared to those with E2 concentrations > 10 ng/L. Women with E2 concentrations > 10 ng/L were further subdivided into women with and without sex hormone replacement therapy, whereby no statistical differences in any of the biochemical markers could be observed between these both groups. In conclusion, we could clearly demonstrate that in postmenopausal women suffering from severe E2 deficiency (E2 < 10 ng/L) Crosslaps and osteocalcin are significantly increased, indicating in principle a clear correlation between E2 deficiency and these markers of bone turnover.