1. The response of circulating 1,25-dihydroxyvitamin D [l,25-(OH)2D] to challenge with vitamin D treatment both before and after 7–10 days of prednisone therapy (25 mg/day) was investigated in five anephric subjects, six patients with chronic renal failure (CRF), two patients with vitamin D intoxication and four patients with hypoparathyroidism.

2. In anephric subjects serum 25-hydroxyvitamin D [25-(OH)D] rose from 58 ± 48 (sd) to 377±221 (sd) nmol/l after administration of 150 μg of 25-(OH)D3 for 1 month. Serum l,25-(OH)2D, which was barely detectable in only two out of five patients under basal conditions, rose to 30 ± 21 pmol/l after 2 weeks of therapy with 25-(OH)D3, but fell to 10 ± 5 pmol/l during prednisone treatment.

3. In CRF patients circulating l,25-(OH)2D rose from 37 ± 24 to 58 ± 24 pmol/l during 25-(OH)D3 therapy, but fell to 41 ± 31 pmol/l during prednisone treatment. In two patients with rheumatoid arthritis, hypercalcaemia due to vitamin D intoxication was associated with raised levels of 1,25-(OH)2D (288 and 317 pmol/l). Administration of prednisore resulted in suppression of l,25-(OH)2D levels (132 and 96 pmol/l respectively) and reduction of serum calcium to within the normal range.

4. In the hypoparathyroid patients prednisone therapy did not affect circulating 25-(OH)D levels but serum l,25-(OH)2D fell from 192 ± 42 to 117 ± 23 pmol/l and serum calcium from 2.41 ± 0.21 to 2.20 ± 0.05 mmol/l.

5. These findings indicate that a steroid sensitive extrarenal production of l,25-(OH)2D may occur in all subjects with a threshold serum concentration of the precursor 25-(OH)D.

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