Lockefeer J H
Ned Tijdschr Geneeskd. 1990 Oct 6;134(40):1931-4.
Vitamin D in large doses is a proper therapy in hypoparathyroidism, osteomalacia, vitamin D-resistant rickets and also in chronic renal failure although in those cases the active metabolite of vitamin D is preferred because of the much shorter biologic halflife. Apart from these disorders there are no good reasons for using megadoses of vitamin D. Pseudo-vitamin D intoxication is caused by granulomatous diseases as a so-called inappropriate calcitriol secretion. In cases of vitamin D intoxication the 25-OHD3 content in the serum is much too high, the parathyroid hormone concentration is suppressed and the I,25-(OH)2D3 level is low, whereas in pseudo-vitamin D intoxication the 25-OHD3 content in the serum is normal and the I,25-(OH)2D3 is seriously elevated. Cultured alveolar macrophages of patients with sarcoidosis can produce I,25-(OH)2D3 as can sarcoid lymph node homogenate. I,25-(OH)2D3 proved to promote the fusion of alveolar macrophages to form polykaryons. Local concentrations of I,25-(OH)2D3 may be higher at sites of granulomatous tissue and can act in a paracrine or autocrine fashion to enhance granuloma formation. The action of glucocorticoids and chloroquine in patients with sarcoidosis and hypercalcaemia is presumably an interruption of the described vicious circle.
大剂量维生素D是甲状旁腺功能减退、骨软化症、维生素D抵抗性佝偻病以及慢性肾衰竭的合适治疗方法，不过在这些情况下，由于维生素D活性代谢物的生物半衰期短得多，所以更倾向于使用它。除了这些病症外，没有充分理由使用大剂量维生素D。伪维生素D中毒是由肉芽肿性疾病引起的，表现为所谓的不适当的骨化三醇分泌。在维生素D中毒的情况下，血清中25-OHD3含量过高，甲状旁腺激素浓度受到抑制，而1,25-(OH)2D3水平较低，而在伪维生素D中毒时，血清中25-OHD3含量正常，而1,25-(OH)2D3严重升高。结节病患者的培养肺泡巨噬细胞以及结节病淋巴结匀浆都能产生1,25-(OH)2D3。事实证明，1,25-(OH)2D3可促进肺泡巨噬细胞融合形成多核细胞。在肉芽肿组织部位，1,25-(OH)2D3的局部浓度可能更高，并可通过旁分泌或自分泌方式发挥作用，增强肉芽肿形成。糖皮质激素和氯喹对结节病和高钙血症患者的作用可能是打断了上述恶性循环。
