Kamphuis Lieke S, Bonte-Mineur Femke, van Laar Jan A, van Hagen P Martin, van Daele Paul L
Department of Immunology, Erasmus MC, University Medical Centre, Rotterdam, The Netherlands; Department of Internal Medicine, Section of Clinical Immunology, Erasmus MC, University Medical Centre, Rotterdam, The Netherlands.
J Bone Miner Res. 2014 Nov;29(11):2498-503. doi: 10.1002/jbmr.2262.
Granulomas in sarcoidosis express high levels of 1α-hydroxylase, an enzyme that catalyzes the hydroxylation of 25-OH vitamin D to its active form, 1,25(OH)2 vitamin D. Overproduction of 1α-hydroxylase is held responsible for the development of hypercalcemia in sarcoidosis patients. Corticosteroids are used as first-line treatment in organ-threatening sarcoidosis. In this light, osteoporosis prevention with calcium and vitamin D (CAD) supplementation is often warranted. However, sarcoidosis patients are at risk for hypercalcemia, and CAD supplementation affects the calcium metabolism. We studied calcium and vitamin D disorders in a large cohort of sarcoidosis patients and investigated if CAD supplementation is safe. Retrospectively, data of 301 sarcoidosis patients from July 1986 to June 2009 were analyzed for serum calcium, 25-hydroxy vitamin D (25-(OH)D), 1,25-dihydroxy vitamin D (1,25(OH)2 D), and use of CAD supplementation. Disease activity of sarcoidosis was compared with serum levels of vitamin D. Hypercalcemia occurred in 8%. A significant negative correlation was found between 25-(OH)D and disease activity of sarcoidosis measured by somatostatin receptor scintigraphy. In our study, 5 of the 104 CAD-supplemented patients developed hypercalcemia, but CAD supplementation was not the cause of hypercalcemia. Patients without CAD supplementation were at higher risk for developing hypercalcemia. During CAD supplementation, no hypercalcemia developed as a result of supplementation. Hypovitaminosis D seems to be related with more disease activity of sarcoidosis and, therefore, could be a potential risk factor for disease activity of sarcoidosis. Thus, vitamin D-deficient sarcoidosis patients should be supplemented.
结节病中的肉芽肿表达高水平的1α-羟化酶，该酶催化25-羟基维生素D羟基化为其活性形式1,25(OH)₂维生素D。1α-羟化酶的过量产生被认为是结节病患者高钙血症发生的原因。皮质类固醇被用作威胁器官的结节病的一线治疗药物。因此，补充钙和维生素D（CAD）以预防骨质疏松症通常是必要的。然而，结节病患者有高钙血症的风险，而补充CAD会影响钙代谢。我们研究了一大群结节病患者的钙和维生素D紊乱情况，并调查了补充CAD是否安全。回顾性分析了1986年7月至2009年6月期间301例结节病患者的血清钙、25-羟基维生素D（25-(OH)D）、1,25-二羟基维生素D（1,25(OH)₂D）以及CAD补充剂的使用情况。将结节病的疾病活动度与维生素D的血清水平进行了比较。8%的患者发生了高钙血症。通过生长抑素受体闪烁显像测量发现，25-(OH)D与结节病的疾病活动度之间存在显著的负相关。在我们的研究中，104例补充CAD的患者中有5例发生了高钙血症，但补充CAD并非高钙血症的原因。未补充CAD的患者发生高钙血症的风险更高。在补充CAD期间，未因补充而发生高钙血症。维生素D缺乏似乎与结节病的更多疾病活动度相关，因此可能是结节病疾病活动度的一个潜在风险因素。因此，维生素D缺乏的结节病患者应该进行补充。
