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40 healthy early postmenopausal women participated in a controlled therapeutic trial with the aim of examining whether treatment with 24,25 vitamin D3 changed the serum concentration of either 1,25 (OH)2D and/or the 24-hour urinary calcium excretion rate. The 40 women were randomized to treatment with either 24R,25 (OH)2D3 (10 micrograms daily) or placebo. Serum concentrations of calcium, 25 (OH) D, 1,25 (OH)2D, 24,25 (OH)2D3 and 24-hour urinary calcium excretion rate were measured before (t0) and after (t1) 6 months of treatment. In the 24,25 (OH)2D3 treated group there was a highly significant increase in the mean serum 24,25 (OH)2D3 concentration, whereas serum 25 (OH) D and 1,25 (OH)2D and serum and urinary calcium were unchanged during the trial. In the placebo group all values were similar before and after the trial. We conclude that treatment with 24,25 (OH)2D3 is not an alternative to conventional treatment of renal hypercalciuria.

To examine the effect of endogenous oestrogens on calcium metabolism during the menstrual cycle, fasting blood and urinary samples were obtained every day throughout the menstrual cycle in 5 young women. Bone turnover was estimated by serum alkaline phosphatase and fasting urinary excretions of hydroxyproline and calcium. Serum levels of oestradiol (E2), oestrone (E1), and androstenedione (A) showed the well known cyclic fluctuations, the serum 1,25-dihydroxyvitamin D (1,25(OH)2D) nearly doubled from the early follicular phase to the time of ovulation, although 25-hydroxyvitamin D (25OHD) and 24,25-dihydroxyvitamin D (24,25(OH)2D) were almost unchanged. No correlation between the rise in the serum 1,25(OH)2D level and the measured parameters of calcium metabolism was observed. In view of these findings, the 1,25(OH)2D3 serum concentration measured in women with functioning ovaries can only be interpreted in the context of the menstrual cycle. The published normal range in women for the metabolite may also require reinterpretation.

Reliable assays to determine the vitamin D metabolites are useful aids in the study of disorders involving vitamin D metabolism, and in the evaluation of the response in patients receiving vitamin D treatment. We report here the establishment in our laboratory of a method capable of measuring 25(OH)D, (including 25(OH)D2 and 25(OH)D3), 1,25(OH)2D and 24,25(OH)2D in a single blood sample. The method involves methanol/dichloromethane extraction and Sephadex LH-20 chromatography. The monhydroxylated fraction was purified on Lipidex 5000 and separated in 25(OH)D2 and 25(OH)D3 on high pressure liquid chromatography (HPLC), followed by ultra violet absorbance (UV) detection. The dihydroxylated fraction was separated by HPLC and quantified by protein-binding assays. The method is precise and accurate. The vitamin D metabolites were measured in different groups of patients and in normal subjects.

A radioimmunoassay for determination of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) in serum, was compared with the radioreceptor assay using cytosol receptor from rachitic chick intestine in order to clarify whether differences in specificity can explain discrepancies in the clinical application of the two techniques. In the literature, seasonal fluctuations in serum 1,25(OH)2D3 are only observed when using radioimmunoassay. Treatment of anticonvulsant osteomalacia with vitamin D3 results in a marked increase in radioimmunologically measured 1,25(OH)2D3, but no effect on the serum 1,25(OH)2D level, measured by the radioreceptor assay, could be observed. The present study demonstrates that another unknown compound is coeluted on high pressure liquid chromatography with 1,25(OH)2D3, and recognised only by the antiserum. It can be concluded that the present radioimmunoassay cannot replace the cytosol receptor assay or either supplement by measuring the 1,25(OH)2D3 metabolite only.

Twenty boys were followed during their puberty for about 2 years with examinations every third month. At each examination we determined serum concentrations of 25OHD3, 1,25(OH)2D3, 24,25(OH)2D3, 25.26(OH)2D3, alkaline phosphatase (AP) and testosterone together with bone mineral content (BMC) at the distal forearm. Highly significant increases in both BMC (P less than 0.001), serum AP (P less than 0.001), and peak height velocity (PHV) followed the increase in serum testosterone. The boys were grouped according to time of maximal increase in BMC, AP, and PHV. The serum levels of the vitamin D metabolites were related to these points. No significant changes in any of the serum vitamin D metabolites were found. Thus vitamin D metabolism does not seem to be significantly influenced during the period of life when both the linear growth and bone mineralization is maximal. [ABSTRACT FROM AUTHOR]