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口服骨化三醇补充维生素D期间,继发性甲状旁腺功能亢进血液透析患者的人血清白蛋白氧化还原状态及炎症生物标志物

Redox State of Human Serum Albumin and Inflammatory Biomarkers in Hemodialysis Patients with Secondary Hyperparathyroidism During Oral Calcitriol Supplementation for Vitamin D.

作者信息

Nasif Wesam A, Mukhtar Mohammed H, El-Emshaty Hoda M, Alwazna Ahmed H

机构信息

Department of Biochemistry, Faculty of Medicine, Umm Al-Qura University, Makkah, Kingdom of Saudi Arabia.

Molecular Biology Department, Genetic Engineering and Biotechnology Research Institute, Sadat City University, Sadat City, Egypt.

出版信息

Open Med Chem J. 2018 Oct 18;12:98-110. doi: 10.2174/1874104501812010098. eCollection 2018.

DOI:10.2174/1874104501812010098
PMID:30450134
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6198414/
Abstract

BACKGROUND

Hemodialysis (HD) patients with secondary Hyperparathyroidism (s-HPT) are exposed to increased inflammation and oxidative stress. In HD patients, oxidized albumin is a reliable marker of oxidative stress and its clinical significance has been rarely studied.

OBJECTIVE

The objective of this study was to evaluate Cys34 Human Serum Albumin (HSA) as oxidative stress biomarker in HD patients with s-HPT and its relationship with inflammation on bone turnover markers during oral calcitriol supplementation for vitamin D.

PATIENTS AND METHODS

Fifteen stable hemodialysis patients with s-HPT (mean age 48.67±8.15, 11 males and 4 females) were used in the experiment to receive calcitriol treatment for 16 weeks (0.25mcg or 0.5 mcg once a day according to serum level of Ca and P for each). The changes in the serum biochemical parameters (Ca, P, ALP, and iPTH), inflammatory markers (CRP and IL-6 levels) and serum oxidative stress condition (SOD, IS and albumin ratio HNA/HMA) were evaluated before and at 8 and 16 weeks of calcitriol treatment. The correlations between those factors were studied.

RESULTS

All patients responded to oral calcitriol therapy, with a significant decrease in the serum iPTH. The results showed that calcitriol could effectively suppress iPTH secretion with a significant elevation of serum Ca and P but ALP remained unchanged during the study. It can also effectively reduce the inflammatory markers (CRP and IL-6), while increasing the oxidative markers (SOD and IS). Oxidative albumin ratio HNA/HMA showed a significant (=0.001) reduction after 16 weeks of calcitriol treatment and the redox state of HSA showed a positive prediction for hyperparathyroidism and for inflammation.

CONCLUSION

The redox state of HSA could be used as a predictor for monitoring hyperparathyroidism and inflammation during calcitriol treatment by retarding albumin oxidation in HD patients with secondary hyperparathyroidism.

摘要

背景

继发性甲状旁腺功能亢进(s-HPT)的血液透析(HD)患者面临炎症和氧化应激增加的情况。在HD患者中,氧化型白蛋白是氧化应激的可靠标志物,但其临床意义鲜有研究。

目的

本研究旨在评估Cys34人血清白蛋白(HSA)作为s-HPT的HD患者氧化应激生物标志物,以及在口服骨化三醇补充维生素D期间其与骨转换标志物炎症的关系。

患者和方法

15例稳定的s-HPT血液透析患者(平均年龄48.67±8.15岁,男性11例,女性4例)用于实验,接受骨化三醇治疗16周(根据每位患者的血清钙和磷水平,每天一次0.25μg或0.5μg)。在骨化三醇治疗前、治疗8周和16周时评估血清生化参数(钙、磷、碱性磷酸酶和iPTH)、炎症标志物(CRP和IL-6水平)和血清氧化应激状况(超氧化物歧化酶、IS和白蛋白比率HNA/HMA)的变化。研究这些因素之间的相关性。

结果

所有患者对口服骨化三醇治疗均有反应,血清iPTH显著降低。结果表明,骨化三醇可有效抑制iPTH分泌,血清钙和磷显著升高,但研究期间碱性磷酸酶保持不变。它还可有效降低炎症标志物(CRP和IL-6),同时增加氧化标志物(超氧化物歧化酶和IS)。骨化三醇治疗16周后,氧化型白蛋白比率HNA/HMA显著降低(=0.001),HSA的氧化还原状态对甲状旁腺功能亢进和炎症有正向预测作用。

结论

HSA的氧化还原状态可作为继发性甲状旁腺功能亢进的HD患者在骨化三醇治疗期间监测甲状旁腺功能亢进和炎症的预测指标,通过延缓白蛋白氧化来实现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/d98794886ab6/TOMCJ-12-98_F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/202051eeb8e8/TOMCJ-12-98_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/4347d2f57887/TOMCJ-12-98_F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/6d7ee407fac2/TOMCJ-12-98_F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/df4dd363d5e5/TOMCJ-12-98_F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/d98794886ab6/TOMCJ-12-98_F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/202051eeb8e8/TOMCJ-12-98_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/4347d2f57887/TOMCJ-12-98_F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/6d7ee407fac2/TOMCJ-12-98_F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/df4dd363d5e5/TOMCJ-12-98_F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec44/6198414/d98794886ab6/TOMCJ-12-98_F5.jpg

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