Decreased serum endoglin level in patients with amyotrophic lateral sclerosis: a preliminary report.

J Iłzecka
{"title":"Decreased serum endoglin level in patients with amyotrophic lateral sclerosis: a preliminary report.","authors":"J Iłzecka","doi":"10.1080/00365510701604628","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Angiogenic mechanisms may have a role to play in the neurodegeneration observed in amyotrophic lateral sclerosis (ALS). The aim of the present study was to measure serum angiogenic factor endoglin (ENG) levels in patients with ALS.</p><p><strong>Material and methods: </strong>The study involved 25 ALS patients and 25 controls. Concentrations of ENG in serum samples were measured using a human Endoglin/CD105 ELISA kit (R&D Systems, Minneapolis, Minn., USA).</p><p><strong>Results: </strong>Serum ENG concentrations were 14 % lower in the patients with ALS compared to controls (4.57 versus 3.97 ng/mL; p<0.05). There was no significant difference in serum ENG levels between subgroups of patients with ALS subdivided depending on clinical state, type of ALS onset and duration of the disease (p>0.05). The correlation between serum ENG levels and clinical parameters of ALS was not significant either (p>0.05).</p><p><strong>Conclusions: </strong>Results indicate that ENG may be implicated in the pathomechanism of ALS. A decrease in ENG levels, as observed in this study, may accelerate neurodegeneration of motor neurons in ALS through chronic ischaemia caused by impaired perfusion.</p>","PeriodicalId":501634,"journal":{"name":"Scandinavian Journal of Clinical and Laboratory Investigation","volume":" ","pages":"348-51"},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00365510701604628","citationCount":"11","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Scandinavian Journal of Clinical and Laboratory Investigation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/00365510701604628","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 11

Abstract

Objectives: Angiogenic mechanisms may have a role to play in the neurodegeneration observed in amyotrophic lateral sclerosis (ALS). The aim of the present study was to measure serum angiogenic factor endoglin (ENG) levels in patients with ALS.

Material and methods: The study involved 25 ALS patients and 25 controls. Concentrations of ENG in serum samples were measured using a human Endoglin/CD105 ELISA kit (R&D Systems, Minneapolis, Minn., USA).

Results: Serum ENG concentrations were 14 % lower in the patients with ALS compared to controls (4.57 versus 3.97 ng/mL; p<0.05). There was no significant difference in serum ENG levels between subgroups of patients with ALS subdivided depending on clinical state, type of ALS onset and duration of the disease (p>0.05). The correlation between serum ENG levels and clinical parameters of ALS was not significant either (p>0.05).

Conclusions: Results indicate that ENG may be implicated in the pathomechanism of ALS. A decrease in ENG levels, as observed in this study, may accelerate neurodegeneration of motor neurons in ALS through chronic ischaemia caused by impaired perfusion.

肌萎缩性侧索硬化症患者血清内啡肽水平降低:初步报告。
目的:血管生成机制可能在肌萎缩侧索硬化症(ALS)中观察到的神经变性中发挥作用。本研究的目的是测量肌萎缩侧索硬化症患者血清血管生成因子内啡肽(ENG)水平。材料和方法:研究纳入25例ALS患者和25例对照。使用人内啡肽/CD105酶联免疫吸附测定试剂盒(R&D Systems, Minneapolis, minnesota)检测血清样品中ENG的浓度。美国)。结果:ALS患者血清ENG浓度比对照组低14% (4.57 ng/mL vs 3.97 ng/mL;p0.05)。血清ENG水平与ALS临床参数的相关性也无统计学意义(p>0.05)。结论:结果提示ENG可能参与ALS的病理机制。本研究观察到,ENG水平的降低可能通过灌注受损引起的慢性缺血加速ALS运动神经元的神经退行性变。
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 求助全文
来源期刊
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信