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Impact of denosumab on cardiovascular calcification in patients with secondary hyperparathyroidism undergoing dialysis: a pilot study.
Breast Cancer Research and Treatment ( IF 3.8 ) Pub Date : 2020-04-03 , DOI: 10.1007/s00198-020-05391-3
C-L Chen,N-C Chen,F-Z Wu,M-T Wu

Summary

The receptor activator of nuclear factor-kappa B ligand (RANKL)/RANK/osteoprotegerin system is dysregulated in hyperparathyroid bone diseases. The introduction of denosumab preceding elective surgery as an alternative option when surgery is not possible immediately.

Introduction

The effects of denosumab on vascular calcification in patients with chronic renal failure and low bone mass have been a subject of interest. Therefore, this investigation aimed to determine the short-term changes in vascular calcification after denosumab treatment using a serial electrocardiography-gated computed tomography (CT) to measure coronary artery calcification (CAC) in patients with secondary hyperparathyroidism (SHPT) and low bone mass.

Methods

This 6-month study enrolled patients with SHPT and low bone mass (T-score < − 2.5) owing to dialysis. The 2 groups administered denosumab at a dose of 60 mg (denosumab group), and conventional treatment (control group) had 21 patients each. All patients underwent CT scans at baseline and at the follow-up examination at 6 months to determine the bone mineral density and CAC.

Results

The control group demonstrated a significant increase in Agatston scores (187.79 ± 72.27) (P = 0.004). However, no significant change was noted in the denosumab group (P = 0.41). In the denosumab group, only the baseline serum alkaline phosphatase levels correlated negatively with changes in the CAC score (P = 0.01); the baseline alkaline phosphatase levels were the deciding biomarkers for non-responsive CAC scores by Berry Criteria after denosumab treatment (P = 0.02). The denosumab group demonstrated significantly increased bone mineral density in the femoral neck and lumbar spine (P < 0.01).

Conclusion

The findings provide evidence that denosumab may suppress the progression of CAC and also regress osseous calcification in severe cases of high bone turnover.



中文翻译:

地诺单抗对接受透析的继发性甲状旁腺功能亢进患者心血管钙化的影响:一项初步研究。

概要

在甲状旁腺功能亢进的骨疾病中,核因子-κB配体(RANKL)/ RANK /骨保护素系统的受体激活剂失调。当无法立即进行手术时,在择期手术前引入denosumab作为替代选择。

介绍

地诺单抗对慢性肾功能衰竭和低骨量患者血管钙化的影响已成为关注的主题。因此,本研究旨在确定在地诺单抗治疗后,使用系列心电图门控计算机断层扫描(CT)来测量继发性甲状旁腺功能亢进症(SHPT)和低骨量患者的冠状动脉钙化(CAC)的短期钙化变化。

方法

这项为期6个月的研究招募了因透析而患有SHPT和低骨量(T评分<-2.5)的患者。两组分别以60 mg的剂量补充denosumab(denosumab组),常规治疗(对照组)各21例。所有患者均在基线和6个月的随访检查中均进行了CT扫描,以确定骨矿物质密度和CAC。

结果

对照组的Agatston评分明显提高(187.79±72.27)(P  = 0.004)。然而,地诺单抗组未见明显变化(P  = 0.41)。在地诺单抗组中,仅基线血清碱性磷酸酶水平与CAC评分的变化呈负相关(P =  0.01);denosumab治疗后,根据Berry Criteria,基线碱性磷酸酶水平是无反应的CAC评分的决定性生物标志物(P  = 0.02)。denosumab组在股骨颈和腰椎中的骨矿物质密度显着增加(P  <0.01)。

结论

这些发现提供了证据,表明狄诺塞麦可能抑制严重骨代谢高的病例中CAC的进展,并使骨钙化退化。

更新日期:2020-04-03
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