Maesaka J K, Batuman V, Pablo N C, Shakamuri S
Arch Intern Med. 1982 Jun;142(6):1206-7. doi: 10.1001/archinte.142.6.1206.
It is generally agreed that the kidneys are the only site of 1-hydroxylation of vitamin D and that the abnormal calcium metabolism in sarcoidosis is caused by increased production of 1,25-dihydroxyvitamin D (1,25-[OH]2D). We describe a patient with sarcoidosis with hypercalcemic nephropathy and end-stage renal disease undergoing long-term maintenance hemodialysis who was initially seen with hypercalcemia and elevated serum levels of 1,25-(OH)2D. Prednisone administration resulted in decreased serum calcium and 1,25-(OH)2D levels. These results confirm the recent evidence for extrarenal production of 1,25-(OH)2D in sarcoidosis and illustrate the importance of altered vitamin D metabolism in the development of hypercalcemia in sarcoidosis.
人们普遍认为,肾脏是维生素D 1α-羟化的唯一部位,结节病中异常的钙代谢是由1,25-二羟基维生素D(1,25-[OH]2D)生成增加所致。我们描述了一名患有高钙血症肾病和终末期肾病且正在接受长期维持性血液透析的结节病患者,该患者最初表现为高钙血症和血清1,25-(OH)2D水平升高。给予泼尼松后,血清钙和1,25-(OH)2D水平降低。这些结果证实了近期关于结节病中1,25-(OH)2D肾外生成的证据,并说明了维生素D代谢改变在结节病高钙血症发生中的重要性。