Calcium bioavailability and parathyroid hormone acute changes after oral intake of dairy and nondairy products in healthy volunteers.

This study was designed to compare calcium bioavailability and serum parathyroid hormone acute changes after oral intake of 500 mg of elemental calcium from liquid milk, yogurt, calcium-citrate-enriched powdered milk or a calcium carbonate pill; or after intake of soybean imitation-milk. After a 12-h fast, blood samples were drawn both at baseline and 1, 2, 3 and 4 h after an oral intake of the above-mentioned products, which were ingested together with a light neutral breakfast. The administration order of the study products was randomly assigned to each of 19 healthy young volunteers (11 females, 8 males). The baseline serum concentrations of ionized calcium, phosphorus and intact parathyroid hormone (iPTH) were normal. Calcium-citrate-enriched powdered milk induced a significant increase in serum ionized calcium (p<0.001) and a significant and continuous decrease in serum iPTH concentration (p<0. 001). Yogurt and the calcium carbonate pill induced a similar but less significant effect, increasing serum ionized calcium (p<0.05) and decreasing serum iPTH (p<0.01). Liquid milk only induced a significant change in serum ionized calcium and iPTH concentration during the first 2 h; this effect was lost during the following 2 h. In conclusion, our study suggests the possibility that the addition of calcium citrate to powered milk may improve calcium bioavailability and enhance the inhibitory effect on serum iPTH in the assayed conditions.

The increase in spinal bone density that occurs in response to fluoride therapy for osteoporosis is not maintained after the therapy is discontinued.

In 44 osteoporotic subjects who had been treated with fluoride for 37 +/- 16 months, the fluoride was discontinued because they had shown fluoride-dependent increases in trabecular spinal bone densities from low initial levels (below the fracture threshold) to values that were equivalent to normal peak bone densities in the spines of young adults. During the subsequent period, after discontinuation of the fluoride therapy (i.e. 19 +/- 9 months), spinal bone density decreased in 73% of the subjects (i.e. 32 of 44, p < 0.03), at a rate that was comparable to the rate of the previous gain that had occurred during the treatment with fluoride (i.e. -3.23 +/- 2.39 mg/cm3 per month, compared with + 3.91 +/- 1.96 mg/cm3 per month in this, subgroup of patients, p < 0.001). Although 9 of the 44 subjects showed continuing increases in spinal bone density after discontinuation of the fluoride therapy, spinal bone density decreased in the entire group of 44 at an average rate of -1.02 +/- 4.72 mg/cm3 per month (p < 0.001, compared with the rate of the previous gain during the treatment with fluoride; i.e. +3.83 +/- 1.82 mg/cm3 per month). Surprisingly, our data showed that the rate of decrease in spinal bone density during the post-fluoride period was not affected by concurrent (undesigned) treatment with calcium, calcium plus estrogen, or calcium plus calcitriol. The cessation of fluoride therapy was also associated with a decrease in serum alkaline phosphatase activity (i.e. a decrease from the elevated levels that were observed during the period of fluoride therapy, back to the original, pre-treatment levels; p < 0.001), and that the rate of spinal bone loss after cessation of fluoride could be correlated with the prior rate of increase in serum alkaline phosphatase activity that had occurred during the treatment with fluoride (n = 44, r = 0.312, p = 0.039). Together, the observations from this retrospective analysis of data obtained from our clinical subjects suggest that fluoride-treated osteoporotic subjects who have exhibited increases in trabecular spinal bone density are at risk for bone loss after discontinuation of the fluoride therapy.

Coexistence of Paget's bone disease and diffuse idiopathic skeletal hyperostosis in males.

The coexistence of Paget's bone disease (PBD) and diffuse idiopathic skeletal hyperostosis (DISH) of the spine is controversial and could have implications for the pathogenic mechanisms involved in these disorders. In order to assess the prevalence of DISH in patients with Paget's disease, a prospective controlled study was carried out in which roentgenograms were obtained from a group of 50 consecutive ambulatory patients previously diagnosed as having PBD (25 males and 25 females; mean age: 66.2 +/- 8.9 years) and these were compared with 50 age- and sex-matched subjects selected randomly from various categories of medical disorders excluding PBD. DISH was found in 12 of 50 Paget's patients, this corresponding to an incidence of 24%; 10 (83%) of these 12 subjects were males. In the control population the incidence of DISH was 6%-2 males and 1 female. This difference between the two groups was statistically significant (chi 2 test; p = 0.02). Apart from the male gender, which was clearly associated with the presence of DISH in the Paget's group (p = 0.019), no other biological variable or characteristic of PBD was linked to the presence of DISH. In conclusion, our data revealed that PBD patients have a significantly greater prevalence of DISH than non-PBD probands. It would seem that the genetic mechanism which is responsible for the susceptibility of PBD to osteoclast viral infection could be related to the pathogenia of DISH in a sex-linked manner.

Spinal fractures during fluoride therapy for osteoporosis: relationship to spinal bone density.

Recent studies report that fluoride therapy for osteoporosis increases spinal bone density without improving vertebral fracture rate, challenging the notion that restoration of bone mass improves bone fragility. To further evaluate this issue, the relationship between spinal bone density and vertebral fracture rate was examined in a large number of fluoride-treated, osteoporotic patients. A retrospective assessment was made of clinical data collected from our observations of 389 osteoporotics treated with fluoride 30 +/- 8 mg/day (mean +/- SD) (equivalent to 66 +/- 17 mg NaF/day) and calcium 1500 mg/day for 28 +/- 18 months. Fracture rate and bone density were assessed in the same region of the spine (i.e., T12 through L4) using quantitative computed tomography (QCT). Spinal bone density increased with time on fluoride, but the relationship was hyperbolic (r = 0.99, p less than 0.0001; asymptote = 167 mg/cc on double-reciprocal plot), suggesting a plateau in the response. The spinal fracture rate decreased as a function of time on therapy (r = -0.83, p less than 0.01), and was inversely related to spinal bone density during fluoride therapy (r = 0.70, p less than 0.001 on arithmetic plot; r = -0.79, p less than 0.001 on semi-log plot). The subgroup of patients who responded to treatment with a significant increase in spinal bone density had a 48% reduction in spinal fracture rate compared with non-responders (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)