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Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial

Background: The most leading cause of death in end-stage renal disease (ESRD) patients are cardiovascular disease and inflammatory markers are related to coronary events. CO-Q10 (coenzyme Q10) is a protective supplement from free radical oxidative damage. In addition, hyperhomocysteinemia is an inde...

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Autores principales: Zahed, Narges-Sadat, Ghassami, Maryam, Nikbakht, Hajar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society of Diabetic Nephropathy Prevention 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790186/
https://www.ncbi.nlm.nih.gov/pubmed/27047809
http://dx.doi.org/10.15171/jnp.2016.07
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author Zahed, Narges-Sadat
Ghassami, Maryam
Nikbakht, Hajar
author_facet Zahed, Narges-Sadat
Ghassami, Maryam
Nikbakht, Hajar
author_sort Zahed, Narges-Sadat
collection PubMed
description Background: The most leading cause of death in end-stage renal disease (ESRD) patients are cardiovascular disease and inflammatory markers are related to coronary events. CO-Q10 (coenzyme Q10) is a protective supplement from free radical oxidative damage. In addition, hyperhomocysteinemia is an independent coronary artery disease (CAD) risk factor. Objectives: Due to increasing oxidative stress in dialysis patients, and the effect of CO-Q10 in decrease oxidative stress, in this work, we assessed the effect of CO-Q10 on C-reactive protein (CRP) level as an inflammatory marker and homocysteine in dialysis patients. Patients and Methods: This was a single-blind, randomized cross over clinical trial. Patients with ESRD were randomly allotted to two groups. All patients received placebo and C0- Q10 100mg/d during the three months in each stage, with two week washout period. Plasma level of CRP and homocysteine from the start of the work and at the conclusion of each menses, are evaluated. Results: Thirty-four patients randomized, but 26 patients complete study protocol. The treatment effect of CO-Q10 on CRP level is significant (P < 0.001) (95% CI = -20.1 to -10.5) and it was also significant for the increasing albumin level. (P = 0.044) (95% CI = 0. 0-0.6), But there was not any substantial effect on serum homocysteine level (P = 0.630). Conclusions: CO-Q10 could significantly decrease CRP level as an inflammatory marker and can protect cardiovascular events.
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spelling pubmed-47901862016-04-04 Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial Zahed, Narges-Sadat Ghassami, Maryam Nikbakht, Hajar J Nephropathol Original Article Background: The most leading cause of death in end-stage renal disease (ESRD) patients are cardiovascular disease and inflammatory markers are related to coronary events. CO-Q10 (coenzyme Q10) is a protective supplement from free radical oxidative damage. In addition, hyperhomocysteinemia is an independent coronary artery disease (CAD) risk factor. Objectives: Due to increasing oxidative stress in dialysis patients, and the effect of CO-Q10 in decrease oxidative stress, in this work, we assessed the effect of CO-Q10 on C-reactive protein (CRP) level as an inflammatory marker and homocysteine in dialysis patients. Patients and Methods: This was a single-blind, randomized cross over clinical trial. Patients with ESRD were randomly allotted to two groups. All patients received placebo and C0- Q10 100mg/d during the three months in each stage, with two week washout period. Plasma level of CRP and homocysteine from the start of the work and at the conclusion of each menses, are evaluated. Results: Thirty-four patients randomized, but 26 patients complete study protocol. The treatment effect of CO-Q10 on CRP level is significant (P < 0.001) (95% CI = -20.1 to -10.5) and it was also significant for the increasing albumin level. (P = 0.044) (95% CI = 0. 0-0.6), But there was not any substantial effect on serum homocysteine level (P = 0.630). Conclusions: CO-Q10 could significantly decrease CRP level as an inflammatory marker and can protect cardiovascular events. Society of Diabetic Nephropathy Prevention 2016-01 2015-11-07 /pmc/articles/PMC4790186/ /pubmed/27047809 http://dx.doi.org/10.15171/jnp.2016.07 Text en © 2016 The Author(s) Published by Society of Diabetic Nephropathy Prevention. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Zahed, Narges-Sadat
Ghassami, Maryam
Nikbakht, Hajar
Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
title Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
title_full Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
title_fullStr Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
title_full_unstemmed Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
title_short Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
title_sort effects of coenzyme q10 supplementation on c-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790186/
https://www.ncbi.nlm.nih.gov/pubmed/27047809
http://dx.doi.org/10.15171/jnp.2016.07
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