• L M Sandler, C G Winearls, L J Fraher, T L Clemens, R Smith, and J L O'Riordan.
• Q. J. Med. 1984 Jan 1; 53 (210): 165-80.

AbstractHypercalcaemia in six patients with sarcoidosis was associated with elevated circulating 1,25-dihydroxy vitamin D3 (187-475 pmol/l): the concentration of this metabolite of vitamin D was a function of the concentration of its precursor, 25-hydroxy vitamin D which remained within the normal range. Corticosteroids, in reducing serum calcium, eliminated this abnormal substrate--product relationship by rapidly reducing circulating 1,25-dihydroxy vitamin D3 while having no effect on 25-hydroxy vitamin D. The fall in circulating 1,25-dihydroxy vitamin D3 preceded the fall of calcium. Studies on the clearance of exogenous 1,25-dihydroxy vitamin D3 indicated that during hypercalcaemic episodes, the plasma disappearance time of the sterol was delayed and that this reverted to normal with steroid therapy. Administration of vitamin D3 to these patients with sarcoidosis increased the circulating concentration of 1,25-dihydroxy vitamin D3 and this resulted in hypercalcaemia, thus accounting for their hypersensitivity to vitamin D and sunlight.

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