Beckerman P, Silver J
Minerva Center for Calcium and Bone Metabolism, Nephrology Services, Hadassah University Hospital, Jerusalem, Israel.
Am J Med Sci. 1999 Jun;317(6):363-9. doi: 10.1097/00000441-199906000-00003.
Vitamin D's biologically active metabolite, 1,25(OH)2D3, has important effects upon the parathyroid cell that are relevant to both the physiology of mineral metabolism and the regulation of the secondary hyperparathyroidism of chronic renal failure. 1,25(OH)2D3 markedly decreases parathyroid hormone (PTH) gene transcription and thus PTH synthesis and secretion. It also acts to decrease parathyroid cell proliferation. Nonhypercalemic analogs of 1,25(OH)2D3 are being developed that may have a wider therapeutic window than 1,25(OH)2D3 itself. In the situations of chronic hypocalcemia and hypophosphatemia, there are interesting interrelationships between 1,25(OH)2D3 and the post-transcriptional regulation of the PTH gene. In nodular secondary hyperparathyroidism, there is down-regulation of the vitamin D receptor in the parathyroid. Different vitamin D receptor genotypes may be associated with higher levels of serum PTH and a predisposition to autonomous hyperplasia.
维生素D的生物活性代谢产物1,25(OH)₂D₃对甲状旁腺细胞具有重要作用，这与矿物质代谢的生理学以及慢性肾衰竭继发性甲状旁腺功能亢进的调节均相关。1,25(OH)₂D₃显著降低甲状旁腺激素（PTH）基因转录，从而减少PTH的合成与分泌。它还能减少甲状旁腺细胞增殖。正在研发1,25(OH)₂D₃的非高钙血症类似物，其治疗窗可能比1,25(OH)₂D₃本身更宽。在慢性低钙血症和低磷血症情况下，1,25(OH)₂D₃与PTH基因的转录后调节之间存在有趣的相互关系。在结节性继发性甲状旁腺功能亢进中，甲状旁腺中的维生素D受体下调。不同的维生素D受体基因型可能与更高水平的血清PTH以及自主性增生易感性相关。
