Department of Internal Medicine, Endocrine-Metabolic Sciences and Biochemistry, University of Siena, Viale Braccci, 53100 Siena, Italy.
J Endocrinol Invest. 2011 Jul;34(7 Suppl):45-9.
Vitamin D via its receptor has essential actions on parathyroid cells, inhibiting PTH secretion, and parathyroid cell proliferation. While the effects of vitamin D depletion in the pathogenesis of secondary hyperparathyroidism in elderly individuals or in the occurrence of parathyroid hyperplasia in patients with renal insufficiency are well established, the association between hypovitaminosis D and primary hyperparathyroidism (P-HPT) has only recently become appreciated. In different cohorts of patients with P-HPT, vitamin D deficiency has been recently associated with higher PTH levels, larger adenomas, and a more severe phenotype (including osteitis fibrosa cystica) as well as negative post-operative outcomes following parathyroidectomy. Despite current guidelines recommend measurement of serum 25OHD (25-hydroxy-cholecalciferol) in P-HPT and their repletion if the levels are <20 ng/ml, future well-designed trials of vitamin D supplementation in P-HPT patients with coexisting vitamin D deficiency are needed to evaluate the risk/benefit profile of this treatment.
维生素 D 通过其受体对甲状旁腺细胞发挥重要作用，抑制 PTH 分泌和甲状旁腺细胞增殖。虽然维生素 D 缺乏在老年个体继发性甲状旁腺功能亢进症的发病机制或肾功能不全患者甲状旁腺增生的发生中的作用已得到充分证实，但低维生素 D 血症与原发性甲状旁腺功能亢进症（P-HPT）之间的关联最近才受到关注。在不同队列的 P-HPT 患者中，最近发现维生素 D 缺乏与更高的 PTH 水平、更大的腺瘤以及更严重的表型（包括纤维性骨炎囊性变）以及甲状旁腺切除术后的不良结局相关。尽管目前的指南建议在 P-HPT 中测量血清 25OHD（25-羟胆钙化醇），如果水平<20ng/ml，则进行补充，但仍需要设计良好的维生素 D 补充试验来评估这种治疗的风险/获益情况。
