Long-term follow-up of bone mineral density and bone metabolism in transsexuals treated with cross-sex hormones
Paul van Kesteren, Paul Lips, Louis J. G. Gooren,
Henk Asscheman and Jos Megens
Department of Endocrinology, Academic Hospital Vrje
Universiteit, Amsterdam, The Netherlands
(Received 5 June 1997; returned for revision 25 July 1997;
finally revised 5 September 1997; accepted 14 October 1997)
Summary
OBJECTIVE lt is unknown whether long term cross sex hormone treatment affects the human skeleton. We monitored bone mineral density and biochemical markers of bone turnover for 28—63 months in 20 male-to-female transsexuals (M-F) treated with anti-androgens and oestrogens, and 19 female-to-male transsexuals (F-M) treated with androgens. They underwent gonadectomy 13—35 months after the start of cross-sex hormone administration.
DESIGN Bone mineral density (BMD) and the markers of bone turnover osteocalcin, alkaline phosphatase, fasting urinary calcium/creatinine and hydroxyproline/creatinine, were measured at baseline, after 1 year and after 28—63 months of cross-sex hormone administration.
RESULTS In oestrogen-treated M—F, variables of bone turnover decreased significantly with consecutive measurements. BMD had increased significantly after 1 year, but decreased again to baseline levels after 28—63 months of cross-sex hormones.
In F—M, alkaline phosphatase levels increased during the first year. BMD did not change during the first year but had decreased significantly after 28—63 months following ovariectomy. In both M — F and F—M, the change of BMD correlated inversely with serum LH and FSH levels. Of all biochemical variables LH levels appeared to be the best predictor of loss of BMD; in the long-term LH levels were more elevated in testosterone-treated F— M than in oestrogen-treated M —. F transsexuals.
CONCLUSION In M-F, oestrogen treatment prevented bone loss after testosterone deprivation. In F — M the testosterone dosage used, associated with a decline in serum oestradiol levels, was unable to maintain bone mass fully in all subjects in the Longer term. The inverse relationship between BMD and serum LH levels suggests that the dose of hormone replacement has been too 10w in subjects with a decline in their BMD. Its cause might be under dosing or non-compliance in some patients. We propose that serum LH levels may be used as a measure of the adequacy of replacement with sex steroids.
I did read another survey on the subject specifically for post menopause women.
There they claimed that HRT(hormone replacement therapy) did stop or significantly reduce osteoporosis.
Noticed and very interesting was the fact that every time HRT was ceased that the patients showed a significant loss of bone density.
This result of bone density loss would occur every time the patient stopped taking HRT.
Multiplies the risk of osteoporosis and bone density loss!
The suggestion therefor was that patients with high risk or signs of osteoporosis should take HRT in small doses for the rest of their lives.
If the patient is less dangered of being osteoporous then it would be better looking for other methods of treatment(calcium supplementation).
I think what IEunich is experiencing is just what I have described.
His HRT is not regular and he seems to stop for several months and then continues.
This would result in a high % of bone mineral loss every time he does this.
When he recontinues HRT his bone mineral density does not increase...because HRT does not support bone mineral increase...just prevents the loss!!!
your antonia
:withstupi
:withstupi
A-1 
