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This study was performed to investigate the effect of monthly oral administration of 500 μg of calcidiol (25-hydroxyvitamin D(3)) for 4 months on both serum vitamin D levels and sequential changes of parameters of calcium metabolism; 18 normal women aged 24-72 years were investigated. There was a significant increase of serum 25(OH)D after the first administration; thereafter all values persisted significantly higher compared to the basal value (P < 0.001). Mean 1,25(OH)(2)D serum levels peaked at day 3 and then tended to stabilize following day 30. During the first month, all mean values observed following the initial administration were significantly higher than basal values. The first calcidiol dose produced a significant reduction of serum PTH levels (P < 0.001), which then remained constant over time. Concerning serum calcium and phosphorus, we were not able to demonstrate any significant change during the entire observation period. Considering the single values for both serum ionized and total calcium, the values of Ca(2+) exceeded upper limits of normal on only two occasions. Regarding biochemical markers of bone remodeling, mean changes of serum bone isoenzyme of alkaline phosphatase activity showed a significant trend to decrease, starting at day 30. No significant changes of serum CTX values were noted. Overall, 24-h urinary excretion of calcium did not change, seven values exceeding the threshold of 4 mg/kg body weight. Monthly administration of 500 μg of 25-hydroxyvitamin D(3) may be considered an alternative for vitamin D repletion, without any detrimental effect.

We investigated the frequency of hypercalcemia and/or hypercalciuria following parathyroid hormone (PTH) 1-34 and 1-84 administration in a crossover trial. Ten postmenopausal osteoporotic women previously treated with bisphosphonates were subdivided into two groups of five patients each. A 24-h urine collection to determine baseline calcium (Ca) and creatinine (Cr) the day before administration of PTH was followed by determination of serum ionized Ca (Ca(2+)), Cr, 25(OH)D, and 1,25(OH)(2)D at baseline. Thereafter, 100 mcg of PTH(1-84) or 20 mcg of PTH(1-34) was administered. A 24-h urinary collection and blood samples 2, 4, and 24-h after each PTH administration were again taken. One week after the first PTH administration patients were rechallenged with the second PTH. The PTH peptides did not differ with respect to changes in Ca(2+) at 2, 4, and 24 h postinjection; at the last time point the values were virtually identical to the initial values. There was no difference in urinary Ca on the day following PTH injection compared to baseline, in terms both of Ca/Cr and of Ca excretion. The two PTH peptides did not differ with respect to changes in 1,25(OH)(2)D at 2, 4, and 24 h considering both the absolute values and the percent changes with respect to baseline (24-h 1-84 = 125.6 + or - 58.6 pg/ml, 153% increase; 1-34 = 124.1 + or - 64.7, 130%). Our results indicate no difference in postinjection serum Ca(2+), 1,25(OH)(2)D, or urinary Ca excretion after a single dose of either PTH(1-84) or PTH(1-34) in patients previously treated with bisphosphonates.

In patients with monoclonal gammopathy of undetermined significance (MGUS) the increase of bone turnover rate can increase the risk of fracture. Thus, a treatment normalizing this negative balance could be of benefit in these patients. We studied 100 patients affected by MGUS, grouped according to the presence (group A, 50 patients) or absence (group B) of vertebral fractures and/or osteoporosis. Group A was treated with alendronate (70 mg/weekly) plus calcium and cholecalciferol for 18 months, and group B was treated with calcium and cholecalciferol. After 18 months, the mean bone mineral density (BMD) of the lumbar spine and total femur had increased by 6.1% and 1.5%, respectively, in group A. In the nine patients of this group not taking alendronate, BMD values of the lumbar spine and total femur decreased by 1.6% (P < or = 0.001 ) and 1.3% (P < or = 0.01), respectively. In patients of group B, BMD increased by 1.2% at the lumbar spine and decreased by 1.2% at the total femur. Corresponding figures of those patients in the same group not taking calcium and vitamin D supplementation were -0.1% and -1.2%, respectively. At 18 months we observed significant decreases of serum bone markers: the difference between the groups was -23.2 (P < or = 0.01) for bone alkaline phosphatase, -23.6 for osteocalcin (P < or = 0.01), -35.1 for C-terminal telopeptides of collagen type I (P < or = 0.001), and -0.47 for bone sialoprotein (P = nonsignificant). Treatment with alendronate could lead to a significant reduction in fracture risk in MGUS patients with skeletal fragility.