Journal of Bone and Mineral Research · 1990 · 37 citations · 15 references
MedicineEndocrinologyNutritionBone MetabolismHuman NutritionMineral MetabolismCalcium EndocrinologyCalcium MetabolismEndocrine Regulation Of CalciumMenopause Hormone TherapyParathyroid Hormone PhysiologyParathyroid Hormone RegulationCalcitriol TherapyMenopause NutritionParathyroid Hormone BiologyPhosphorus MetabolismSerum 25-Hydroxyvitamin D StatusSerum Calcium Measurement
Abstract We studied the effects of estrogen on daylong circulating levels of calcium, inorganic phosphorus, parathyroid hormone (PTH), and 1,25-(OH)2D3 (calcitriol) in a group of 10 postmenopausal women (68.5 ± 1.4 years, mean ± SEM). The study was conducted under strict dietary control, with mean calcium and phosphorus intakes of 845 and 970 mg. After treatment with conjugated equine estrogens, 1.25 mg/day, for 1 month, significant decreases in fasting (0800 h) serum levels were observed for calcium (9.09 ± 0.08 versus 9.46 ± 0.10 mg/dl, p < 0.01) and phosphorus (3.38 ± 0.10 versus 3.73 ± 0.08 mg/dl, p < 0.01). On the 0800 h fasting specimen, midmolecule PTH concentrations were higher (44.0 ± 7.9 versus 34 ± 8.2 pg/ml, p < 0.05), but intact PTH was unchanged (28.6 ± 2.7 versus 29.1 ± 1.7 pg/ml) and a rise in circulating calcitriol (39.8 ± 4.3 versus 31.6 ± 2.1 pg/ml) was marginally significant (p = 0.07). When data represented multiple samples averaged over 7 and 15 h, significant estrogen-related reductions in serum calcium and phosphorus concentrations were observed. In addition, estrogen was associated with a significant rise in the daylong (15 h) level of calcitriol (39.4 ± 4 versus 30.5 ± 2.4 pg/ml, p < 0.01). Daylong mid- and intact PTH concentrations were unchanged on estrogen compared to baseline values. No significant correlations were observed between changes in fasting calcitriol level and changes in fasting concentrations of calcium, phosphorus, or PTH. Further, the rise in daylong calcitriol concentration did not correlate significantly with changes in fasting or integrated values of calcium or PTH. However, the rise in calcitriol did correlate significantly with the decrements in 3 and 7 h serum phosphorus levels (Δcalcitriol versus Δ 7 h phosphorus, r = 0.65, p < 0.05; calcitriol fold-increase versus Δ 7 h phosphorus, r = 0.78, p < 0.01). We conclude that the rise in circulating calcitriol on estrogen appears to be related primarily to changes in blood levels of inorganic phosphorus, not to changes in calcium and PTH, the other primary regulators of calcitriol production.
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NOMOGRAM FOR DERIVATION OF RENAL THRESHOLD PHOSPHATE CONCENTRATION
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