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本文引用的文献

1
Incidence of hypocalcemia and hypercalcemia in hospitalized patients: Is it changing?住院患者低钙血症和高钙血症的发病率:它正在发生变化吗?
J Clin Transl Endocrinol. 2018 May 29;13:9-13. doi: 10.1016/j.jcte.2018.05.004. eCollection 2018 Sep.
2
A RANKL Wrinkle: Denosumab-Induced Hypocalcemia.RANKL的一个问题:地诺单抗诱导的低钙血症。
J Med Toxicol. 2016 Sep;12(3):305-8. doi: 10.1007/s13181-016-0543-y. Epub 2016 Mar 17.
3
Using denosumab to treat immobilization hypercalcemia in a post-acute care patient.使用地舒单抗治疗急性后期护理患者的制动性高钙血症。
J Clin Endocrinol Metab. 2014 Oct;99(10):3531-5. doi: 10.1210/jc.2013-4205. Epub 2014 Jul 17.
4
A practical approach to hypercalcemia.高钙血症的实用处理方法。
Am Fam Physician. 2003 May 1;67(9):1959-66.
5
Immobilization hypercalcemia treatment with pamidronate disodium after spinal cord injury.脊髓损伤后用帕米膦酸二钠治疗制动后高钙血症
Arch Phys Med Rehabil. 1999 Sep;80(9):998-1000. doi: 10.1016/s0003-9993(99)90050-3.
6
Successful treatment of immobilization hypercalcemia using calcitonin and etidronate.使用降钙素和依替膦酸盐成功治疗制动性高钙血症。
Arch Phys Med Rehabil. 1993 Mar;74(3):316-9.
7
Immobilization hypercalcemia.制动后高钙血症
Am J Dis Child. 1972 Nov;124(5):723-7. doi: 10.1001/archpedi.1972.02110170101017.
8
Calcitonin therapy in prolonged immobilization hypercalcemia.降钙素治疗长期制动所致高钙血症
Arch Phys Med Rehabil. 1985 Sep;66(9):640-4.
9
Immobilization-induced hypercalcemia and regional osteoporosis.
Clin Orthop Relat Res. 1987 Mar(216):247-52.
10
Immobilization hypercalcemia in spinal cord injury.脊髓损伤中的制动性高钙血症
Arch Phys Med Rehabil. 1977 Jan;58(1):16-24.

一名肾衰竭患者的制动诱导性高钙血症。

Immobilization-induced hypercalcemia in a patient with renal failure.

作者信息

Gandhi Anand, Mortensen Mike, Sunny Sonie, Techathaveewat Pawarid, Targovnik Jerome, Alsayed Mahmoud

机构信息

Division of Internal Medicine, University of Arizona, College of Medicine - Phoenix, Phoenix, Arizona, USA.

Banner University Medical Center - Phoenix, Phoenix, Arizona, USA.

出版信息

Endocrinol Diabetes Metab Case Rep. 2021 Oct 1;2021. doi: 10.1530/EDM-21-0086.

DOI:10.1530/EDM-21-0086
PMID:34612208
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8558878/
Abstract

SUMMARY

Immobilization-induced hypercalcemia is an uncommon cause of elevated calcium which is usually diagnosed following extensive systemic workup and exclusion of more common etiologies. Previously reported cases have largely described this phenomenon in adolescents and young adults a few weeks to months after the initial onset of immobilization. Metabolic workup tends to demonstrate hypercalcemia, hypercalciuria, and eventual osteoporosis. While the exact mechanism remains largely unclear, a dysregulation between bone resorption and formation is central to the pathogenesis of this disease. Decreased mechanical loading from prolonged bedrest tends to increase osteoclast induced bone resorption while promoting osteocytes to secrete proteins such as sclerostin to reduce osteoblast mediated bone formation. We describe the case of an 18-year-old male who was admitted following intraabdominal trauma. He underwent extensive abdominal surgery including nephrectomy resulting in initiation of dialysis. After 6 months of hospitalization, the patient gradually began developing uptrending calcium levels. Imaging and laboratory workup were unremarkable for any PTH-mediated process, malignancy, thyroid disorder, adrenal disorder, or infection. Workup did reveal significant elevated bone turnover markers which in combination with the clinical history led the physicians to arrive at the diagnosis of immobilization induced hypercalcemia. In order to prevent decreased rates of bone loss, the patient was administered denosumab for treatment. Hypocalcemia followed treatment expectedly and was repleted with supplementation via the patient's total parenteral nutrition.

LEARNING POINTS

Immobilization-induced hypercalcemia should remain as a differential diagnosis of patients with prolonged hospitalizations with hypercalcemia. Extensive workup of common etiologies of hypercalcemia should be considered prior to arriving at this diagnosis. Denosumab, while off-label for this usage, offers an effective treatment option for immobilization-induced hypercalcemia though it carries a risk of hypocalcemia especially among patients with renal disease.

摘要

摘要

制动引起的高钙血症是导致血钙升高的一种罕见原因,通常在进行广泛的全身检查并排除更常见的病因后才能确诊。先前报道的病例大多描述了青少年和年轻人在制动开始后的几周至几个月出现这种现象。代谢检查往往显示高钙血症、高钙尿症以及最终的骨质疏松症。虽然确切机制仍不清楚,但骨吸收与形成之间的失调是该疾病发病机制的核心。长期卧床导致的机械负荷减少往往会增加破骨细胞诱导的骨吸收,同时促使骨细胞分泌如硬化蛋白等蛋白质,从而减少成骨细胞介导的骨形成。我们描述了一名18岁男性因腹部外伤入院的病例。他接受了包括肾切除术在内的广泛腹部手术,随后开始透析。住院6个月后,患者的血钙水平逐渐开始上升。影像学和实验室检查未发现任何由甲状旁腺激素介导的过程、恶性肿瘤、甲状腺疾病、肾上腺疾病或感染的迹象。检查确实发现骨转换标志物显著升高,结合临床病史,医生诊断为制动引起的高钙血症。为了防止骨丢失率下降,给患者使用地诺单抗进行治疗。治疗后出现了预期的低钙血症,并通过患者的全胃肠外营养补充进行了纠正。

学习要点

制动引起的高钙血症应作为长期住院且血钙升高患者的鉴别诊断之一。在做出此诊断之前,应考虑对高钙血症的常见病因进行广泛检查。地诺单抗虽然在此用法上属于超说明书用药,但为制动引起的高钙血症提供了一种有效的治疗选择,不过它有导致低钙血症的风险,尤其是在肾病患者中。