Add-back medrogestone does not prevent bone loss in premenopausal women treated with goserelin

Citation
M. Sillem et al., Add-back medrogestone does not prevent bone loss in premenopausal women treated with goserelin, EXP CL E D, 107(6), 1999, pp. 379-385
Citations number
37
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
ISSN journal
09477349 → ACNP
Volume
107
Issue
6
Year of publication
1999
Pages
379 - 385
Database
ISI
SICI code
0947-7349(1999)107:6<379:AMDNPB>2.0.ZU;2-E
Abstract
To investigate the effect of medrogestone on bone mineral density (BMD) and bone turnover under conditions of estrogen withdrawal, premenopausal women with endometriosis were treated with goserelin (Zoladex(R)), combined with either placebo (group A, n = 12) or 10 mg medrogestone (Prothil(R), group B, n = 11) for six months, and followed for an additional six months. Lumba r spine BMD was measured at 0 and 6 month. Markers of bone turnover were se rum bone alkaline phosphatase (sBAP) and osteocalcin (sOC) by ELISA, and ur inary total pyridinoline (uPYD) and deoxypyridinoline crosslinks (uDPD) by HPLC. Patients in both groups had a similar and significant decrease BMD after 6 months (4%, p < 0.01). The time course of changes in bone turnover, in cont rast, was different in both groups. In group A, crosslink excretion increas ed from one month onwards, while no changes were seen in group B. In group A, sBAP levels rose during treatment, while in group B, this rise was delay ed until treatment was terminated. Additionally, group B showed an initial suppression of sBAP and sOC. In both groups, sOC increased after treatment was discontinued. Medrogestone at 10 mg/d does not prevent lumbar bone loss in premenopausal women under estrogen deprivation. In the medrogestone add back group, the c hanges in bone turnover are compatible with low turnover bone loss,as oppos ed to a state of high turnover seen in the unopposed goserelin group. This effect may be due to glucocorticoid receptor mediated actions of medrogesto ne on bone.