It is well known that some patients with renal lithiasis due to idiopathic hypercalciuria (IH) may exhibit decreased bone mineral density (BMD). We have studied a large group of children with IH and related their BMD values to several renal function parameters and calcium and bone metabolism markers. Children with IH had higher osteocalcin and calcitriol levels and higher urinary excretion of magnesium and prostaglandin E2, as well as lower tubular reabsorption of phosphate, urinary excretion of ammonium, maximum urinary PCO2, and BMD compared with control group of children. In children with IH we observed a negative correlation between BMD and age. We found osteopenia in 22 of 73 children with IH (30.1%); these children showed lower citraturia levels and higher fractional excretion of uric acid than children with normal BMD. In osteopenic children there was a negative correlation between BMD and calcitriol levels. Several possible pathogenetic factors have been proposed for the bone mass loss. Our results demonstrate that, at least in some cases, it may be related to high levels of calcitriol, which has a wellknown resorption ability. Whether a certain degree of intracellular acidosis or a higher production of prostaglandin E2 could play a role in some cases is still an open question. In children with normal BMD we observed a direct correlation between osteocalcin and tartrate-resistant acid phosphatase levels; this correlation did not hold for children with osteopenia.
We studied whether biochemical markers of bone turnover (urinary CrossLaps corrected for creatinine (uCL) and serum osteocalcin (sN-Mid)) can predict the response in bone mass to Tibolone treatment. Data from a 2-year double-blind, randomized trial with 57 completing Tibolone-treated women and 13 placebotreated women were studied. BMD of the spine (QDR-1000) and uCL and sN-Mid were determined every three months throughout the study. The res~nee in bone mass correlated to prestudy values of uCl (R=0.27 ; ~><0.05) but not to baseline values of sN-MID. At I year: (uCL: R=0.54 ; ~><0.001 , SN-MID: R=D.49 ; ~0.0Ol). The change in uCL from baseline correlated significantly with the overall change in BMD from the 6 months" timepoint and throughout the rest of the study. The same pattern, although
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