The cause for the intestinal hyperabsorption of calcium (Ca) in various forms of hypercalciurias was explored by a careful measurement of plasma 1α,25-dihydroxycholecalciferol [1α,25(OH)2D] and by an assessment of intestinal Ca absorption and of parathyroid function. In 18 cases of primary hyperparathyroidism (PHPT), the mean plasma concentration of 1α,25-(OH)2D was significantly increased (4.9±2.2 SD ng/dl vs. 3.4±0.9 ng/dl for the control group), and was significantly correlated from fractional Ca absorption (α) (r=0.80, P<0.001). Plasma 1α,25(OH)2D was also correlated with urinary Ca (P<0.05), but not with serum Ca or phosphorus (P), P clearance, urinary cyclic AMP, or serum immunoreactive parathyroid hormone. In 21 cases of absorptive hypercalciuria (AH), plasma 1α,25-(OH)2D was elevated in one-third of cases, and the mean value of 4.5±1.1 ng/dl was significantly higher than that of the control group (P<0.01). Since relative hypoparathyroidism may be present, the normal absolute value of plasma 1α,25-(OH)2D, found in two-thirds of cases of AH, may be considered to be inappropriately high. Moreover, in the majority of cases of AH, the data points relating plasma 1α,25-(OH)2D and α fell within 95% confidence limits of values found in non-AH groups (including PHPT). The results suggest that the intestinal hyperabsorption of Ca in PHPT and AH may be vitamin D dependent. However, the disturbance in vitamin D metabolism may not be the sole cause for the high Ca absorption in AH, since in some patients with AH, the intestinal Ca absorption appears to inappropriately high for the level of plasma 1α,25-(OH)2D.
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