The Effect of One-Year Cross-Sex Hormonal Treatment on Bone Metabolism and Serum Insulin-Like Growth Factor-l in Transsexuals

The Effect of One-Year Cross-Sex Hormonal Treatment on Bone Metabolism and Serum Insulin-Like Growth Factor-l in Transsexuals

 

P. van Kesteren, P. Lips, W. Deville, C. Popp-Snijders, H. Asscheman, J. Megens, and L. Gooren.
Departments of Endocrinology (P.u.K., P.L., C.P.S., H.A., J.M., L.G.) and Biostatistics (W.D.), Free University Hospital, 1007 MB Amsterdam, The Netherlands.
Abstract [Full Text] PDF

Abstract

The effects of treatment with estrogens and antiandrogens in male to female (M-F) transsexuals and androgens in female to male (F-M) transsexuals on their respective bone metabolism, bone mineral density (BMD), serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) levels were investigated. BMD and variables of bone turnover in serum were measured at baseline and after 3 months (except for BMD) and 1 yr of treatment in 56 M+F and 35 F-M transsexuals. Serum IGF-I, IGFBP-3, and propeptide of type I procollagen (PlCP) were measured at baseline and after 1 yr of treatment in 10 M-F and 10 F-M transsexuals.

In M-F, BMD increased significantly. Bone turnover decreased, as shown by a significant decline in levels of osteocalcin, alkaline phosphatase, PlCP, and fasting urinary calciumlcreatinine and hydroxyproline/creatinine ratios. Serum IGF-I levels decreased significantly without significant changes in IGFBP-3 levels.

In F-M, BMD did not change. Bone formation increased, as suggested by an increase in alkaline phosphatase and a borderline increase in PlCP values. IGF-I levels increased significantly, whereas no significant changes were seen in IGFBP-3 levels.
We conclude that in males, estrogens (in combination with anti-androgens) decrease bone turnover, with a subsequent increase in BMD and a decrease in serum IGF-I. In females, testosterone administration increases bone formation, but this is not reflected in an increased BMD, whereas serum IGF-I increases.

 

Citation: J Clin Endocrinol Metab 81: 2227-2232, 1996.