Follicle-stimulating hormone does not directly regulate bone mass in human beings: evidence from nature

Abstract

To evaluate the effect of FSH levels in the development of human osteoporosis. Case-series study. Gynecology department in a teaching hospital. A total of 8 women diagnosed with Kallman syndrome (KS) were compared with 11 with Turner syndrome and 11 with pure gonadal dysgenesia (GD, karyotype 46,XX). We assessed the pituitary-gonadal axis, bone turnover markers, bone mass, and patient characteristics. Bone mineral density as assessed by dual-energy X-ray absorptiometry, plasma FSH, LH, E(2), osteocalcin (BGP), and urinary type I collagen cross-linked N-telopeptide. Other biochemical markers included 25-hydroxyvitamin D, as well as parathyroid hormone and urine concentration of calcium and creatinine. In girls with Turner syndrome and GD, FSH (64.03 +/- 29.2 and 90.08 +/- 22.41 mIU/mL, respectively) and LH (45.29 +/- 11.90 and 48.83 +/- 12.44 mIU/mL, respectively) levels were significantly higher compared with those observed in girls with KS (FSH: 1.87 +/- 0.64 and LH: 1.02 +/- 0.57), whereas no differences were detected in E(2) or bone marker levels. Bone mineral density correlated positively with FSH levels but not with E(2); however, after adjusting for previous growth-hormone therapy, these differences were not found. In addition, bone mineral density in spine and total hip was significantly lower in patients with KS. Follicle-stimulating hormone does not appear to have a major role in the development of bone loss in young women with primary amenorrhea.