Thyroid function and PCSK9 in euthyroid subjects with coronary artery disease

Q Medicine

Clinical Lipidology Pub Date : 2015-06-01 DOI:10.2217/clp.15.13

Sha Li, R. Xu, Yuan-Lin Guo, Yan Zhang, Cheng-gang Zhu, Jing Sun, Jian‐Jun Li

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引用次数: 2

Abstract

Abstract Thyroid function and PCSK9 in euthyroid subjects with coronary artery disease Background: Both thyroid hormone and PCSK9 are key regulators of lipid metabolism. Their respective impacts on dylipidemia and the development of associated coronary artery disease (CAD) have received continued interest. Aim: To examine whether plasma PCSK9 levels were correlated with thyroid hormones in euthyroid subjects with stable CAD. Materials & methods: A total of 447 euthyroid subjects with stable CAD were prospectively enrolled. Angiography and lipid-lowering therapy were parts of the screening process. Baseline clinical characteristics were collected. Fasting free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH), glucose and lipid profiles were measured. Plasma PCSK9 levels were determined by ELISA. Results: Plasma PCSK9 levels exhibited an inverse correlation with FT3 (r = -0.182, p < 0.001) and a positive correlation with TSH (r = -0.100, p = 0.035). After adjustment for cardiometabolic risk factors, patients with higher levels of PCSK9 differed from those with lower levels of PCSK9 in FT3, FT4 and TSH levels (p < 0.05, all). When Logistic analysis was performed with PCSK9 tertiles as the dependent variable, FT3 (OR = 0.430, 95% CI: 0.206–0.897), FT4 (OR = 0.863, 95% CI: 0.708–0.995) and TSH (OR = 2.114, 95% CI: 1.003–4.457) exhibited independent associations with an elevated PCSK9 level (tertile 3). Finally, multiple linear analysis revealed that PCSK9 levels were related significantly and independently to FT3 (β = -0.110, p = 0.019) but not FT4 (β = -0.073, p = 0.110) or TSH (β = -0.087, p = 0.060). Conclusion: The study demonstrates a negative association between thyroid function and PCSK9 levels in euthyroid subjects with stable CAD, suggesting a potential interaction between PCSK9 and lower levels of thyroid hormones in patients with CAD.

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冠状动脉疾病伴甲状腺功能正常者的甲状腺功能和PCSK9

背景:甲状腺激素和PCSK9都是脂质代谢的关键调节因子。它们各自对血脂和相关冠状动脉疾病(CAD)发展的影响一直受到关注。目的:探讨稳定型冠心病患者血浆PCSK9水平与甲状腺激素水平的相关性。材料与方法:前瞻性纳入447例甲状腺功能正常且病情稳定的冠心病患者。血管造影和降脂治疗是筛查过程的一部分。收集基线临床特征。测定空腹游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、促甲状腺素(TSH)、血糖和血脂水平。ELISA法检测血浆PCSK9水平。结果:血浆PCSK9水平与FT3呈负相关(r = -0.182, p < 0.001)，与TSH呈正相关(r = -0.100, p = 0.035)。在调整心脏代谢危险因素后，PCSK9水平高的患者与PCSK9水平低的患者在FT3、FT4和TSH水平上存在差异(p < 0.05)。当物流分析与PCSK9 tertiles作为因变量,发生(或= 0.430,95% CI: 0.206—-0.897),FT4(或= 0.863,95% CI: 0.708—-0.995)和TSH(或= 2.114,95% CI: 1.003—-4.457)表现出独立的协会PCSK9水平升高(tertile 3)。最后,多元线性分析表明PCSK9水平显著相关,独立发生(β= -0.110,p = 0.019),但不是FT4(β= -0.073,p = 0.110)或TSH(β= -0.087,p = 0.060)。结论:本研究表明，在稳定型CAD患者中，甲状腺功能与PCSK9水平呈负相关，提示PCSK9与CAD患者甲状腺激素水平较低可能存在相互作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinical Lipidology 生物-生化与分子生物学

CiteScore

0.44

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The Journal of Clinical Lipidology is published to support the diverse array of medical professionals who work to reduce the incidence of morbidity and mortality from dyslipidemia and associated disorders of lipid metabolism. The Journal''s readership encompasses a broad cross-section of the medical community, including cardiologists, endocrinologists, and primary care physicians, as well as those involved in the treatment of such disorders as diabetes, hypertension, and obesity. The Journal also addresses allied health professionals who treat the patient base described above, such as pharmacists, nurse practitioners and dietitians. Because the scope of clinical lipidology is broad, the topics addressed by the Journal are equally diverse. Typical articles explore lipidology as it is practiced in the treatment setting, recent developments in pharmacological research, reports of treatment and trials, case studies, the impact of lifestyle modification, and similar academic material of interest to the practitioner. While preference is given to material of immediate practical concern, the science that underpins lipidology is forwarded by expert contributors so that evidence-based approaches to reducing cardiovascular and coronary heart disease can be made immediately available to our readers. Sections of the Journal will address pioneering studies and the clinicians who conduct them, case studies, ethical standards and conduct, professional guidance such as ATP and NCEP, editorial commentary, letters from readers, National Lipid Association (NLA) news and upcoming event information, as well as abstracts from the NLA annual scientific sessions and the scientific forums held by its chapters, when appropriate.