Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Endocr Pract. 2022 Oct;28(10):1069-1071. doi: 10.1016/j.eprac.2022.07.009. Epub 2022 Jul 21.
Secondary hyperparathyroidism commonly occurs in the setting of mid-to low-normal serum calcium levels, often in the setting of chronic kidney disease, phosphate loading, vitamin D deficiency, or insufficient calcium intake or absorption. In this article, we report 9 patients who had adequate kidney function (estimated glomerular filtration rate >60 mL/min/1.73 m) and normal 25-hydroxy vitamin D level (≥30 ng/dL) and whose secondary hyperparathyroidism resolved after starting adequate oral calcium intake.
Our retrospective case series included 8 women and 1 man; the mean age was 69.0 ± 12.2 years (mean ± standard deviation). The initial intact parathyroid hormone (iPTH) level was 80.6 ± 13.4 pg/mL (reference range [ref], 10-65 pg/mL), corrected serum calcium level was 9.2 ± 0.2 mg/dL (ref, 8.5-10.5 mg/dL), serum phosphate level was 3.6 ± 0.4 mg/dL (ref, 2.5-4.9 mg/dL), 25-hydroxy vitamin D level was 42.2 ± 10.5 mg/dL (ref, 20-50 ng/mL), and estimated glomerular filtration rate was 72.6 ± 14.4 mL/min/1.73 m. Patients were treated clinically with oral calcium 600 mg twice a day.
iPTH was retested after a mean duration of 17.6 ± 12.7 days of calcium supplementation; the iPTH level decreased to 51.0 ± 10.6 pg/mL, with all patients achieving iPTH in the normal range with normocalcemia, consistent with hyperparathyroidism being because of insufficient calcium intake or absorption. All patients were normocalcemic after supplementation.
Secondary hyperparathyroidism can result from insufficient oral calcium intake. Calcium challenge is an efficacious and cost-effective tool for confirming and treating secondary hyperparathyroidism in the setting of normal vitamin D levels and kidney function.
在中低水平血清钙的情况下，通常在慢性肾脏病、磷酸盐负荷、维生素 D 缺乏或钙摄入或吸收不足的情况下，常发生继发性甲状旁腺功能亢进症。在本文中，我们报告了 9 例肾功能良好（估计肾小球滤过率＞60ml/min/1.73m）和 25-羟维生素 D 水平正常（≥30ng/dL）的患者，他们在开始摄入足够的口服钙后，继发性甲状旁腺功能亢进症得到缓解。
我们的回顾性病例系列包括 8 名女性和 1 名男性；平均年龄为 69.0±12.2 岁（平均值±标准差）。初始完整甲状旁腺激素（iPTH）水平为 80.6±13.4pg/mL（参考范围[ref]，10-65pg/mL），校正血清钙水平为 9.2±0.2mg/dL（ref，8.5-10.5mg/dL），血清磷酸盐水平为 3.6±0.4mg/dL（ref，2.5-4.9mg/dL），25-羟维生素 D 水平为 42.2±10.5mg/dL（ref，20-50ng/mL），估计肾小球滤过率为 72.6±14.4ml/min/1.73m。患者接受口服钙 600mg，每日 2 次的临床治疗。
在补钙 17.6±12.7 天后，iPTH 进行了复测；iPTH 水平下降至 51.0±10.6pg/mL，所有患者的 iPTH 均恢复正常，血钙正常，符合因钙摄入或吸收不足导致的甲状旁腺功能亢进症。所有患者补钙后血钙均正常。
继发性甲状旁腺功能亢进症可由口服钙摄入不足引起。在维生素 D 水平和肾功能正常的情况下，钙负荷试验是一种有效的、具有成本效益的方法，可用于确认和治疗继发性甲状旁腺功能亢进症。
