title: Reversible bone loss in women treated with GnRH-agonists for endometriosis and uterine leiomyoma.
abstract: Oestrogen deficiency at the menopause is associated with changes in calcium and bone metabolism. Hypo-oestrogenism induced by the use of GnRH-agonists is clinically useful in the treatment of oestrogen-dependent diseases. This study was done to investigate calcium homeostasis and bone metabolism of pre-menopausal women in a GnRH-agonist-induced pseudo-menopause. Eighteen patients with endometriosis or uterine leiomyoma received monthly i.m. injections of 3.2 mg of long-acting D-Trp-6-LHRH over a 6-month period. Plasma oestradiol-17 beta and progesterone levels under treatment were significantly decreased to the levels of the early follicular phase. Plasma total calcium, serum osteocalcin and plasma alkaline phosphatase concentrations increased, while plasma phosphate levels did not change. Levels of 1,25-dihydroxyvitamin D3 decreased significantly, but 25-hydroxyvitamin D3 values remained constant. Trabecular bone mineral density of lumbar spine decreased continuously during the 6-month period. Nine women completed 6-9 months follow-up. In these women bone loss was reversible. Cortical bone measurements at the proximal radius showed no change during oestrogen deficiency. In conclusion, our findings demonstrate that GnRH-agonist-induced bone loss is reversible. Furthermore, they suggest that the state of pseudo-menopause induced by GnRH-agonist may serve as a model for further pathophysiological studies on calcium homeostasis and bone metabolism in the post-menopause.
authors.affiliation: Department of Obstetrics and Gynaecology, Städtische Kliniken, Darmstadt, FRG.
authors.forename: S
authors.initials: S
authors.lastname: Waibel-Treber
authors.forename: H W
authors.initials: HW
authors.lastname: Minne
authors.forename: S H
authors.initials: SH
authors.lastname: Scharla
authors.forename: T
authors.initials: T
authors.lastname: Bremen
authors.forename: R
authors.initials: R
authors.lastname: Ziegler
authors.forename: G
authors.initials: G
authors.lastname: Leyendecker
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D000970:Antineoplastic Agents; D001842:Bone and Bones / Q000378:metabolism; D002112:Calcifediol / Q000097:blood; D002117:Calcitriol / Q000097:blood; D002118:Calcium / Q000097:blood; D002135:Calcium-Binding Proteins / Q000097:blood; D004715:Endometriosis / Q000188:drug therapy*; D004958:Estradiol / Q000097:blood; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D006801:Humans; D007889:Leiomyoma / Q000188:drug therapy*; D008903:Minerals / Q000378:metabolism; D015675:Osteocalcin; D010024:Osteoporosis / Q000097:blood / Q000139:chemically induced* / Q000378:metabolism; D011374:Progesterone / Q000097:blood; D017329:Triptorelin Pamoate; D014594:Uterine Neoplasms / Q000188:drug therapy*
chemical_list: D000970:Antineoplastic Agents; D002135:Calcium-Binding Proteins; D008903:Minerals; D017329:Triptorelin Pamoate; D015675:Osteocalcin; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol; D000469:Alkaline Phosphatase; D002117:Calcitriol; D002112:Calcifediol; D002118:Calcium