Excretion of urinary N-telopeptides reflects changes in bone turnover during ovarian suppression and indicates individually variable estradiol threshold for bone loss.
OBJECTIVE
To evaluate the effectiveness of N-telopeptides and E2 in monitoring bone turnover during GnRH agonist- (GnRH-a) or danazol-induced hypoestrogenism.


METHODS
Comparative, nonrandomized prospective study.


METHODS
Institute for the Study and Treatment of Endometriosis.


METHODS
Premenopausal women undergoing ovarian suppression with GnRH-a (n = 16) or danazol (n = 9).


METHODS
Serum and urine samples were collected and bone mineral density was measured before, during, and after treatment.


METHODS
N-telopeptide excretion, serum E2, and bone mineral density at L1 to L4 and femoral neck.


RESULTS
During treatment in the GnRH-a group, mean E2 levels were 53% below and N-telopeptides were 38% above the mean baseline. At 1 month post-treatment, L1 to L4 bone mineral density decreased by 3.85%. In the danazol group, E2, N-telopeptides and L1 to L4 bone mineral density changed nonsignificantly in the opposite direction with the mean 1.25% increase in L1 to L4 at 1 month post-treatment. In combined groups, L1 to L4 bone mineral density better correlated with other measures than femoral neck bone mineral density. N-telopeptide excretion was more predictive of L1 to L4 change, with correlation the highest between N-telopeptides at month 4 and bone mineral density at month 1 afterward, while E2 appeared more predictive of the less reliable femoral neck bone mineral density. Individual exceptions to the model of an E2 threshold for bone loss were observed. Also noted were high correlation between on-therapy levels of E2 and N-telopeptides, as well as the presence of a 1-month time lag between E2 and N-telopeptide changes.


CONCLUSIONS
Bone density decreases during GnRH-a and may slightly increase during danazol treatment. However, E2 threshold for bone loss varies individually. N-telopeptides predict changes in bone mineral density at L1 to L4 better than E2.
Dmowski
W P
WP
Institute for the Study and Treatment of Endometriosis, Columbia Grant Hospital, Chicago, Illinois, USA.
Rana
N
N
Pepping
P
P
Cain
D F
DF
Clay
T H
TH
D000328:Adult; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000378:metabolism*; D003094:Collagen / Q000652:urine*; D024042:Collagen Type I; D003613:Danazol / Q000627:therapeutic use*; D004958:Estradiol / Q000097:blood*; D004965:Estrogen Antagonists / Q000627:therapeutic use*; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006801:Humans; D010024:Osteoporosis / Q000097:blood*; D010053:Ovary / Q000187:drug effects* / Q000503:physiopathology; D010455:Peptides / Q000652:urine*; D011446:Prospective Studies
D024042:Collagen Type I; D004965:Estrogen Antagonists; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D007987:Gonadotropin-Releasing Hormone; D004958:Estradiol; D003094:Collagen; D003613:Danazol