Hypergonadotropic amenorrhea and bone density: new approach to an old problem

Amenorrhea can cause bone loss, but not all mechanisms in this process are known. The degree of bone loss in amenorrheic women is determined by the cause of the amenorrhea. The aim of this study was to investigate the influence of secondary amenorrhea on bone density and to compare the bone density between hypogonadotropic amenorrheic women and hypergonadotropic amenorrheic women. Twenty-two amenorrheic and 12 eumenorrheic women under the age of 40 were involved in this study. Every woman underwent measurements of lumbar spine and femoral neck bone density, body mass index (BMI), and serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, progesterone, and prolactin. According to FSH levels, we divided the women with amenorrhea into two groups: hypergonadotropic (n = 7; FSH, >40 IU/l) and hypogonadotropic (n = 15; FSH, less than or equal to40 IU/l) amenorrheic women. Amenorrheic women had a lower lumbar spine bone density than eumenorrheic controls (P = 0.002). Hypergonadotropic amenorrheic women had lower lumbar spine bone density (P = 0.026) than hypogonadotropic ameneorrheic women. In the hypergonadotropic group, only FSH level had a correlation (negative) with lumbar spine bone density (P = 0.05), but in the hypogonadotropic group, there was no correlation between hormonal levels, BMI, age, or duration of amenorrhea. BMI was positively correlated with lumbar spine bone density in amenorrheic women (P < 0.025). Amenorrheic women had lower bone density than eumenorrheic women, but hypergonadotropic amenorrheic women had lower bone density than hypogonadotropic women. The greater bone loss in the hypergonadotropic amenorrheic group could have been caused by a potential direct effect of FSH on bone metabolism.