Bone mineral density and bone markers in hypogonadotropic and hypergonadotropic hypogonadal men after prolonged testosterone treatment

After prolonged treatment (76.4 +/- 10 and 70.1 +/- 12.3 months, respective ly) (mean +/- SE) with testosterone enanthate (250 mg im every 3 weeks), bo ne mineral density (BMD) and bone metabolism were evaluated in 12 patients (aged 29.3 +/-1.4 yr) affected by idiopathic hypogonadotropic hypogonadism (IHH), in 8 patients (29.6 +/-2.6 yr) affected by Klinefelter's syndrome (K S), and in 10 healthy men (30.6 +/-1.7 yr) matched according to age and BMI . Spinal BMD in IHH was significantly lower than in controls (0.804 +/-0.04 vs 1.080 +/-0.01 g/cm(2); p <0.001), while there was no difference in neck BMD (0.850 +/-0.01 vs 0.948 +/-0.02 g/cm(2)). Neither spinal (0.978 +/-0.0 5 g/cm(2)) nor neck (0.892 +/-0.03 g/cm(2)) BMD in KS were significantly di fferent from controls. Six IHH and one KS subjects were osteoporotic, while 6 IHH and 2 KS subjects were osteopenic. A significant inverse correlation was found between spinal BMD and age at the treatment onset in IHH (r=-0.7 26, p=0.007). In IHH there were significant increases in bone formation (al kaline phosphatase=318.3 +/- 33.9 vs 205.4 +/- 20.0 IU/l; osteocalcin=13.44 +/-1.44 vs 8.57 +/-0.94 ng/ml; p <0.05) and in bone resorption (urinary cr oss-linked N-telopeptides of type I collagen=149.1 +/- 32.3 vs 47.07 +/-8.4 nmol bone collagen equivalents/mmol creatinine; p <0.05) compared to contr ols, while such differences were not present in KS. Our results outline the importance of BMD evaluation in all hypogonadal males. Nevertheless, bone loss is a minor characteristic of KS, while it is a distinctive feature of IHH. Therefore, early diagnosis and age-related replacement therapy coupled with a specific treatment for osteoporosis could be useful in preventing f uture severe bone loss and associated skeletal morbidity. ((C))2001, Editri ce Kurtis.