Hyponatremia Is Linked to Bone Loss, Osteoporosis, Fragility and Bone Fractures.

2区 医学 Q2 Medicine Frontiers of Hormone Research Pub Date : 2019-01-01 Epub Date: 2019-01-15 DOI:10.1159/000493237
Julianna Barsony, Lauren Kleess, Joseph G Verbalis
{"title":"Hyponatremia Is Linked to Bone Loss, Osteoporosis, Fragility and Bone Fractures.","authors":"Julianna Barsony,&nbsp;Lauren Kleess,&nbsp;Joseph G Verbalis","doi":"10.1159/000493237","DOIUrl":null,"url":null,"abstract":"<p><p>Chronic hyponatremia may not cause overt symptoms, and therefore frequently remains untreated. More recently, growing evidence indicate that this condition is not benign, and can lead to unsteady gait, deterioration of bone mass and strength, increased fragility, and increased all-cause mortality. We provided the first evidence for hyponatremia-induced osteoporosis based on markedly reduced bone mineral density and bone structural changes in hyponatremic rats, which is an experimental model of the syndrome of inappropriate antidiuresis (SIAD). These animal data were supported by results of the analysis of the National Health and Nutrition Examination Survey III dataset showing a 2.5-fold increased OR of osteoporosis in participants with serum sodium concentration [Na+] below 135 mmol/L. A subsequent cross-sectional study from Michigan analyzed data from 25,000 patients and found a strong association between the odds of osteoporosis by bone density and hyponatremia. This study pointed out that age-dependent decline in bone density may mask hyponatremia-induced bone loss. Multiple independent retrospective studies, epidemiological studies, and prospective clinical studies have since confirmed and extended our findings, reporting evidence for increased bone fractures and increased mortality in patients with hyponatremia. Cell culture studies have elucidated some of the adaptive mechanisms by which low extracellular fluid [Na+] increases osteoclast formation and bone resorbing activity, thereby liberating stored sodium from the bone matrix. Studies on older SIAD rats indicated that the damage may not be restricted to bone alone, but may involve other organs, including the heart, testis, kidney, and the brain. Finally, compelling open questions and future research directions about the effect of hyponatremia on bone are outlined.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"52 ","pages":"49-60"},"PeriodicalIF":0.0000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000493237","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers of Hormone Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000493237","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2019/1/15 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 10

Abstract

Chronic hyponatremia may not cause overt symptoms, and therefore frequently remains untreated. More recently, growing evidence indicate that this condition is not benign, and can lead to unsteady gait, deterioration of bone mass and strength, increased fragility, and increased all-cause mortality. We provided the first evidence for hyponatremia-induced osteoporosis based on markedly reduced bone mineral density and bone structural changes in hyponatremic rats, which is an experimental model of the syndrome of inappropriate antidiuresis (SIAD). These animal data were supported by results of the analysis of the National Health and Nutrition Examination Survey III dataset showing a 2.5-fold increased OR of osteoporosis in participants with serum sodium concentration [Na+] below 135 mmol/L. A subsequent cross-sectional study from Michigan analyzed data from 25,000 patients and found a strong association between the odds of osteoporosis by bone density and hyponatremia. This study pointed out that age-dependent decline in bone density may mask hyponatremia-induced bone loss. Multiple independent retrospective studies, epidemiological studies, and prospective clinical studies have since confirmed and extended our findings, reporting evidence for increased bone fractures and increased mortality in patients with hyponatremia. Cell culture studies have elucidated some of the adaptive mechanisms by which low extracellular fluid [Na+] increases osteoclast formation and bone resorbing activity, thereby liberating stored sodium from the bone matrix. Studies on older SIAD rats indicated that the damage may not be restricted to bone alone, but may involve other organs, including the heart, testis, kidney, and the brain. Finally, compelling open questions and future research directions about the effect of hyponatremia on bone are outlined.

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
低钠血症与骨质流失、骨质疏松、脆弱和骨折有关。
慢性低钠血症可能不会引起明显的症状,因此经常得不到治疗。最近,越来越多的证据表明,这种情况不是良性的,并可能导致步态不稳,骨量和强度的恶化,脆弱性增加,以及全因死亡率增加。我们基于低钠血症大鼠的骨矿物质密度显著降低和骨结构改变提供了低钠血症诱导骨质疏松症的第一个证据,这是不适当抗利尿综合征(SIAD)的实验模型。这些动物数据得到了国家健康和营养检查调查III数据集分析结果的支持,结果显示,血清钠浓度[Na+]低于135 mmol/L的参与者骨质疏松症的OR增加了2.5倍。密歇根大学随后进行的一项横断面研究分析了25000名患者的数据,发现骨密度导致骨质疏松症的几率与低钠血症之间存在很强的关联。该研究指出,年龄依赖性骨密度下降可能掩盖低钠血症引起的骨质流失。多个独立的回顾性研究、流行病学研究和前瞻性临床研究已经证实并扩展了我们的发现,报告了低钠血症患者骨折增加和死亡率增加的证据。细胞培养研究已经阐明了一些适应性机制,通过低细胞外液[Na+]增加破骨细胞的形成和骨吸收活性,从而从骨基质中释放储存的钠。对老年SIAD大鼠的研究表明,损伤可能不仅限于骨骼,还可能涉及其他器官,包括心脏、睾丸、肾脏和大脑。最后,对低钠血症对骨影响的开放性问题和未来的研究方向进行了概述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Frontiers of Hormone Research
Frontiers of Hormone Research 医学-内分泌学与代谢
自引率
0.00%
发文量
0
期刊介绍: A series of integrated overviews on cutting-edge topics New sophisticated technologies and methodological approaches in diagnostics and therapeutics have led to significant improvements in identifying and characterizing an increasing number of medical conditions, which is particularly true for all aspects of endocrine and metabolic dysfunctions. Novel insights in endocrine physiology and pathophysiology allow for new perspectives in clinical management and thus lead to the development of molecular, personalized treatments. In view of this, the active interplay between basic scientists and clinicians has become fundamental, both to provide patients with the most appropriate care and to advance future research.
期刊最新文献
Endocrine and Metabolic Late Effects in Cancer Survivors Cardiometabolic Risk, Part 1: Chemotherapy and Radiotherapy - Old Foes Still Threatening Cancer Survivors? Hypothalamic-Pituitary Dysfunctions Other Than Growth Hormone Deficiency in Cancer Survivors. Diabetes in Cancer Patients: Risks, Goals and Management. Thyroid Dysfunction and Thyroid Cancer in Childhood Cancer Survivors: Prevalence, Surveillance and Management.
×
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