Seifert-Klauss, V.; Mueller, J. E.; Probst, R.; Wilker, J.; Höß, C.; Treumann, T.; Kastner, C.; Ulm, Kurt; Luppa, P. (2000): Bone Metabolism During the Perimenopausal Transition: a Prospective Study. Sonderforschungsbereich 386, Discussion Paper 194
Volltext auf 'Open Access LMU' nicht verfügbar.


Objective: A study characterizing changes in biochemical markers of bone formation and resorption over the course of one year in premenopausal, perimenopausal and early postmenopausal women is presented. Methods: 64 subjects were included in the analysis, grouped according to their menstrual pattern, menopausal complaints and endocrinological parameters to be premenopausal (n=20), perimenopausal (n=24) or early postmenopausal (n=20). The parameters studied at four visits during the 12 month-study period were the urinary pyridinium crosslinks pyridinolin (PYD) and desoxypyridinolin (DPD), and N-terminal telopeptides (NTX) as bone resorption markers, as well as osteocalcin (OC) and bone-specific alkaline phophatase (BAP) in serum, representing bone formation. The longitudinal changes over time as well as intergroup differences were analyzed using generalised estimating equations (GEE) in connection with Wald statistics. Results: Over the course of one year BAP levels decreased in the late premenopausal group. The perimenopausal group exhibited a rise of PYD, DPD and OC, NTX levels were higher than in premenopause. Postmenopausal subjects had elevated NTX values, while PYD and DPD levels remained close to the perimenopausal range. A time effect was seen for OC during postmenopause. Conclusions: Changes in bone turnover already begin in the late premenopause. The rise of NTX from late premenopause through perimenopause into early postmenopause indicates diagnostic sensitivity of this parameter to changes in bone metabolism induced by estrogen withdrawal. Since PYD and DPD do not follow this pattern, but change significantly with time during perimenopause but then remain largely unchanged in early postmenopause may reflect the sensitivity of pyridinium crosslinks to progesterone-deficiency.