The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelterʹs syndrome: the influence of vitamin D deficiency and hormonal status

The aim of this study was to evaluate the effects of a 2-year treatment with intravenous ibandronate (2 mg every 3 months) and calcium (1000 mg daily) on bone mineral density (BMD) and bone markers in 14 patients with Klinefelterʹs syndrome who served as their own controls. During the follow-up of 5.9 years before the treatment was started, the mean rates of bone loss per year were 1.3, 0.9, and 0.6% in the lumbar spine, femoral neck, and total body, respectively. The rate of bone loss from the spine was significantly inversely related to both serum estradiol and testosterone. At the onset of treatment, the average age of the patients was 55.2 years (48–64 years), and T score, mean ± SD, at the lumbar spine was −2.6 ± 1.0. After 6 months, the mean serum CTX and PINP decreased by 39 and 55% below the pretreatment concentrations, respectively (P< 0.05). After 12 months of treatment, the patients gained mean ± SD, 7.8 ± 2.3% of BMD in the lumbar spine, 3.8 ± 4.0% in the femoral neck, and 4.7 ± 2.2% in the total body (P< 0.05). During the second year of treatment, all patients also received 700 IU of vitamin D daily. After 24 months of treatment, the patients gained 10.1 ± 4.3% of BMD in the lumbar spine, 6.7 ± 5.5% in the femoral neck, and 5.5 ± 2.5% in the total body. The increase in BMD in the second year of ibandronate treatment was not significant. The rate of gain of BMD in the femoral neck was positively related to serum concentrations of testosterone and inversely related to 25-hydroxyvitamin D (P< 0.005). After the discontinuation of treatment, serum CTX and PINP increased to the pretreatment levels, and the lumbar spine and femur neck BMD decreased (P< 0.05). In conclusion, ibandronate was effective in increasing BMD at all sites, but the effects were adversely influenced by vitamin D insufficiency or deficiency. The overall changes in biochemical markers of bone remodeling were consistent with the antiresorptive effect of the drug.