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

ObjectiveTo evaluate the effect of FSH levels in the development of human osteoporosis.DesignCase-series study.SettingGynecology department in a teaching hospital.Patient(s)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).Intervention(s)We assessed the pituitary–gonadal axis, bone turnover markers, bone mass, and patient characteristics.Main Outcome Measure(s)Bone mineral density as assessed by dual-energy X-ray absorptiometry, plasma FSH, LH, E2, 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.Result(s)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 E2 or bone marker levels. Bone mineral density correlated positively with FSH levels but not with E2; 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.Conclusion(s)Follicle-stimulating hormone does not appear to have a major role in the development of bone loss in young women with primary amenorrhea.