儿童急性淋巴细胞白血病骨坏死与骨密度下降关系的最新研究进展。

Faculty reviews Pub Date : 2021-06-23 eCollection Date: 2021-01-01 DOI:10.12703/r/10-57
Jenneke E van Atteveld, Demi Tc de Winter, Rob Pieters, Sebastian Jcmm Neggers, Marry M van den Heuvel-Eibrink
{"title":"儿童急性淋巴细胞白血病骨坏死与骨密度下降关系的最新研究进展。","authors":"Jenneke E van Atteveld,&nbsp;Demi Tc de Winter,&nbsp;Rob Pieters,&nbsp;Sebastian Jcmm Neggers,&nbsp;Marry M van den Heuvel-Eibrink","doi":"10.12703/r/10-57","DOIUrl":null,"url":null,"abstract":"<p><p>The attention to treatment-related toxicity has increased since the survival of children with acute lymphoblastic leukemia (ALL) has improved significantly over the past few decades. Intensive ALL treatment schedules including corticosteroids and asparaginase have been shown to give rise to skeletal abnormalities such as osteonecrosis and low bone mineral density (BMD), which may lead to debilitating sequelae in survivors. Although osteonecrosis and low BMD are different entities with suggested separate pathophysiological mechanisms, recent studies indicate that osteonecrosis is associated with accelerated BMD decline. Common underlying mechanisms for osteonecrosis and BMD decline are considered, such as an enhanced sensitivity to corticosteroids in children who suffer from both osteonecrosis and low BMD. In addition, restriction of weight-bearing activities, which is generally advised in patients with osteonecrosis, could aggravate BMD decline. This induces a clinical dilemma, since bone stimulation is important to maintain BMD but alternative interventions for osteonecrosis are limited. Furthermore, this recent finding of accelerated BMD decline in children with osteonecrosis emphasizes the need to develop effective preventive measures for osteonecrosis, which may include targeting BMD decline.</p>","PeriodicalId":73016,"journal":{"name":"Faculty reviews","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265561/pdf/","citationCount":"1","resultStr":"{\"title\":\"Recent perspectives on the association between osteonecrosis and bone mineral density decline in childhood acute lymphoblastic leukemia.\",\"authors\":\"Jenneke E van Atteveld,&nbsp;Demi Tc de Winter,&nbsp;Rob Pieters,&nbsp;Sebastian Jcmm Neggers,&nbsp;Marry M van den Heuvel-Eibrink\",\"doi\":\"10.12703/r/10-57\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The attention to treatment-related toxicity has increased since the survival of children with acute lymphoblastic leukemia (ALL) has improved significantly over the past few decades. Intensive ALL treatment schedules including corticosteroids and asparaginase have been shown to give rise to skeletal abnormalities such as osteonecrosis and low bone mineral density (BMD), which may lead to debilitating sequelae in survivors. Although osteonecrosis and low BMD are different entities with suggested separate pathophysiological mechanisms, recent studies indicate that osteonecrosis is associated with accelerated BMD decline. Common underlying mechanisms for osteonecrosis and BMD decline are considered, such as an enhanced sensitivity to corticosteroids in children who suffer from both osteonecrosis and low BMD. In addition, restriction of weight-bearing activities, which is generally advised in patients with osteonecrosis, could aggravate BMD decline. This induces a clinical dilemma, since bone stimulation is important to maintain BMD but alternative interventions for osteonecrosis are limited. Furthermore, this recent finding of accelerated BMD decline in children with osteonecrosis emphasizes the need to develop effective preventive measures for osteonecrosis, which may include targeting BMD decline.</p>\",\"PeriodicalId\":73016,\"journal\":{\"name\":\"Faculty reviews\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265561/pdf/\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Faculty reviews\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.12703/r/10-57\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Faculty reviews","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12703/r/10-57","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

摘要

在过去的几十年里,急性淋巴细胞白血病(ALL)儿童的生存率显著提高,因此对治疗相关毒性的关注也随之增加。包括皮质类固醇和天冬酰胺酶在内的强化ALL治疗方案已被证明会引起骨骼异常,如骨坏死和低骨密度(BMD),这可能导致幸存者的衰弱后遗症。虽然骨坏死和低骨密度是不同的实体,有不同的病理生理机制,但最近的研究表明骨坏死与骨密度加速下降有关。骨坏死和骨密度下降的共同潜在机制被考虑,例如骨密度低和骨坏死的儿童对皮质类固醇的敏感性增强。此外,骨坏死患者通常建议限制负重活动,这可能会加剧骨密度下降。这引起了临床困境,因为骨刺激对维持骨密度很重要,但骨坏死的替代干预措施有限。此外,最近发现骨密度在骨坏死儿童中加速下降,这强调了制定有效的骨密度预防措施的必要性,其中可能包括针对骨密度下降。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Recent perspectives on the association between osteonecrosis and bone mineral density decline in childhood acute lymphoblastic leukemia.

The attention to treatment-related toxicity has increased since the survival of children with acute lymphoblastic leukemia (ALL) has improved significantly over the past few decades. Intensive ALL treatment schedules including corticosteroids and asparaginase have been shown to give rise to skeletal abnormalities such as osteonecrosis and low bone mineral density (BMD), which may lead to debilitating sequelae in survivors. Although osteonecrosis and low BMD are different entities with suggested separate pathophysiological mechanisms, recent studies indicate that osteonecrosis is associated with accelerated BMD decline. Common underlying mechanisms for osteonecrosis and BMD decline are considered, such as an enhanced sensitivity to corticosteroids in children who suffer from both osteonecrosis and low BMD. In addition, restriction of weight-bearing activities, which is generally advised in patients with osteonecrosis, could aggravate BMD decline. This induces a clinical dilemma, since bone stimulation is important to maintain BMD but alternative interventions for osteonecrosis are limited. Furthermore, this recent finding of accelerated BMD decline in children with osteonecrosis emphasizes the need to develop effective preventive measures for osteonecrosis, which may include targeting BMD decline.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
What’s New in The Diagnosis and Treatment of Premature Ovarian Insufficiency (POI)? ‘All About’ Extremophiles Recent advances in the understanding of tubal ectopic pregnancy. Recent advances in understanding TCR signaling: a synaptic perspective. Recent advances in understanding Alzheimer's Disease: diagnosis and management strategies.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1