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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Evaluation of Bone Turnover / Quality Markers and Bone Mineral Density in Prostate Cancer Patients Receiving Androgen Deprivation Therapy with or without Denosumab
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Evaluation of Bone Turnover / Quality Markers and Bone Mineral Density in Prostate Cancer Patients Receiving Androgen Deprivation Therapy with or without Denosumab

机译:骨质周转/质量标志物和骨矿物密度的评估前列腺癌患者接受雄激素剥夺治疗或没有Denosumab

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Background/Aim: Androgen deprivation therapy (ADT) is a mainstay therapy for prostate cancer (PCa). ADT induces bone loss and increases the risk of osteoporosis and fractures. Recently, loss of bone quality has received attention as a factor that causes loss of bone strength independent of bone mineral density (BMD). Pentosidine has been identified as a surrogate marker of bone quality. Therefore, bone quality markers were evaluated retrospectively in PCa patients receiving ADT with or without denosumab. Patients and Methods: This study included 46 PCa patients. Twenty patients received denosumab. We measured pentosidine as bone quality marker and TRACP-5b as bone turnover marker. Pre- and 12month BMD was measured in the lumbar spine and femoral neck. Results: In the denosumab group (D+), BMD at the lumbar spine was increased by 6.7% compared with the group that did not receive denosumab (D-) at 12 months (p=0.0015). BMD at the femoral neck was increased by 3.1% at 12 months (p=0.0076). The mean value of TRAP-5b was lower in the D+ group than the D-group at 12 months (p<0.001). The mean serum levels of pentosidine in the D+ group were decreased by -39.6% compared with the D-group at 12 months (p=0.0036). Conclusion: Denosumab increased BMD during ADT for PCa and inhibited the increasing levels of serum pentosidine in PCa patients undergoing ADT.
机译:背景/目的:雄激素剥夺治疗(ADT)是前列腺癌(PCA)的主要疗法。 ADT诱导骨质损失并增加骨质疏松症和骨折的风险。最近,骨质质量的丧失受到关注,作为导致骨骼强度丧失的因素,与骨矿物密度(BMD)无关。戊胺已被鉴定为骨质质量的替代标志物。因此,回顾性地在接受ADT的PCA患者中进行骨质标记物,接受或不具有Denosumab。患者和方法:本研究包括46名PCA患者。二十名患者接受了Denosumab。我们用骨质质量标记和TRACP-5B测量戊胺,作为骨质周转标记。在腰椎和股骨颈中测量前12个月BMD。结果:在Denosumab组(D +)中,与在12个月内没有接受Denosumab(D-)的基团相比,腰椎的BMD增加了6.7%(p = 0.0015)。股骨颈的BMD在12个月内增加了3.1%(p = 0.0076)。在12个月的D +组中,D +组的陷波-5b的平均值低(P <0.001)。与12个月的D-基团相比,D +基团中戊胺的平均血清水平降低-39.6%(p = 0.0036)。结论:Denosumab在PCA的ADT期间增加BMD,抑制了患者PCA患者血清嘌呤胺的增加。

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