Pathogenetic Role of lα,25-Dihydroxyvitamin D inarcoidosis and Absorptive Hypercalciuria: DifferentResponse to Prednisolone Therapy*

Abstract

Intestinal hyperabsorption of calcium (Ca) is frequently observed in sarcoidosis and is characteristic of absorptive hypercalciuria (AH). The potential pathogenetic role of la,25-dihydroxyvitamin D [1,25(OH)²D] in these two conditions was sought by a careful assessment of the circulating concentration of this vitamin D metabolite and various measures of Ca metabolism before and after prednisolone therapy. In eight patients with sarcoidosis, prednisolone treatment (50 mg⁄day for 8 days) produced a significant fall in serum 1,25(OH)2D [4.8 ± 1.9 to 3.3 ± 1.0 (SD) ng⁄dl; P < 0.025], concomitant with a significant decrease in the fractional intestinal Ca absorption (a) from 0.58 ± 0.14 to 0.46 ± 0.13 (±SD; P < 0.005). Urinary Ca and serum parathyroid hormone did not change significantly. However, in six patients with AH, prednisolone therapy resulted in a nonsignificant rise in serum 1,25(OH)2D from 3.6 ± 0.7 to 4.4 ± 1.0 ng⁄ dl and no significant fall in a (from 0.73 ± 0.08 to 0.70 ± 0.10). Urinary Ca was significantly increased in AH patients from 230 ± 35 to 343 ± 74 (SD) mg⁄day (P < 0.005), while serum parathyroid hormone rose slightly. Serum 1,25(OH)JD and ex were significantly correlated (r = 0.543; P < 0.05) for patients with sarcoidosis but not in AH patients. These results suggest that the hyperabsorption of calcium in sarcoidosis is dependent on the serum concentration of 1,25(OH)²D, while in AH it may result from additional vitamin D-independent processes.