Sandler L M, Winearls C G, Fraher L J, Clemens T L, Smith R, O'Riordan J L
Q J Med. 1984 Spring;53(210):165-80.
Hypercalcaemia 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.
6例结节病患者出现高钙血症,同时循环中的1,25-二羟维生素D3水平升高(187 - 475 pmol/L):维生素D的这种代谢产物的浓度是其前体25-羟维生素D浓度的函数,而25-羟维生素D浓度仍在正常范围内。皮质类固醇在降低血清钙时,通过迅速降低循环中的1,25-二羟维生素D3,消除了这种异常的底物-产物关系,而对25-羟维生素D没有影响。循环中1,25-二羟维生素D3的下降先于钙的下降。对外源性1,25-二羟维生素D3清除率的研究表明,在高钙血症发作期间,该固醇的血浆消失时间延迟,而类固醇治疗后恢复正常。给这些结节病患者服用维生素D3会增加循环中1,25-二羟维生素D3的浓度,进而导致高钙血症,这就解释了他们对维生素D和阳光的超敏反应。