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The relationship between fetuin-A and coronary atherosclerotic heart disease (CHD) and CHD-related risk factors : A retrospective study

research-article

Author(s): Jianping Zheng , MM, Maozhi Huang , MM, Qilei Huang , MM, Qiaoxing Chen , MM, Ziguo Chen , BA ^∗

Editor(s): Flavio Palmieri.

Publication date (Electronic): 29 October 2021

Journal: Medicine

Publisher: Lippincott Williams & Wilkins

Keywords: coronary atherosclerotic heart disease, fetuin-A, risk factors

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Abstract

Fetuin-A plays an important role in antivascular calcification and inflammatory response, it is necessary to explore the relationship between fetuin-A and coronary atherosclerotic heart disease (CHD) and CHD-related risk factors.

A total of 92 patients with CHD as the research group, and 60 healthy persons as the control group were enrolled from May 2019 to May 2020. Fetuin-A levels were determined by enzyme-linked immunosorbent assay, and the characteristics and clinical data were collected and compared. Logistic regression was used to analyze the factors influencing CHD.

The age, proportion of males, patients with hypertension and diabetes, as well as fetuin-A level in the research group were significantly higher than those in the control group, but the high-density lipoprotein cholesterol level was significantly lower than that in the control group ( P < .05). Logistic regression analysis and correction showed that gender, age, blood pressure, and diabetes were related to the onset of CHD, and there was a significant correlation between the level of fetuin-A and age ( P < .05).

Serum fetuin-A was related to the onset risk of CHD, and showed a significant correlation with age.

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Most cited references 22

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The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification.

Cora Schäfer, Alexander Heiss, Anke Schwarz … (2003)

Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein alpha2-Heremans-Schmid glycoprotein (Ahsg, also known as fetuin-A) as an important inhibitor of ectopic calcification acting on the systemic level. Ahsg-deficient mice are phenotypically normal, but develop severe calcification of various organs on a mineral and vitamin D-rich diet and on a normal diet when the deficiency is combined with a DBA/2 genetic background. This phenotype is not associated with apparent changes in calcium and phosphate homeostasis, but with a decreased inhibitory activity of the Ahsg-deficient extracellular fluid on mineral formation. The same underlying principle may contribute to many calcifying disorders including calciphylaxis, a syndrome of severe systemic calcification in patients with chronic renal failure. Taken together, our data demonstrate a critical role of Ahsg as an inhibitor of unwanted mineralization and provide a novel therapeutic concept to prevent ectopic calcification accompanying various diseases.

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Plasma fetuin-a levels and the risk of myocardial infarction and ischemic stroke.

Cornelia Weikert, Norbert Stefan, Matthias B. Schulze … (2008)

Fetuin-A, a protein almost exclusively secreted by the liver, induces insulin resistance and subclinical inflammation in rodents. Circulating fetuin-A levels are elevated in humans with metabolic syndrome and insulin resistance, conditions that are associated with increased risk of cardiovascular disease. We investigated the association between fetuin-A levels and the risk of future myocardial infarction (MI) and ischemic stroke (IS) in a case-cohort study based on the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study comprising 27 548 middle-aged subjects of the general population. Fetuin-A levels were measured in plasma of 227 individuals who developed MI, in 168 who developed IS, and in 2198 individuals who remained free of cardiovascular events during a mean follow-up of 8.2+/-2.2 years. Individuals in the highest compared with the lowest quintile of plasma fetuin-A had significantly increased risks of MI (relative risk, 3.80; 95% confidence interval, 2.37 to 6.10; P for trend <0.0001) and IS (relative risk, 3.93; 95% confidence interval, 2.17 to 7.12; P for trend <0.0001) after adjustment for sex and age. Additional adjustment for smoking status, body mass index, waist circumference, alcohol consumption, educational attainment, physical activity, hypertension, diabetes mellitus, total and high-density lipoprotein cholesterol, and C-reactive protein only moderately attenuated these risks (MI: relative risk, 3.25; 95% confidence interval, 2.01 to 5.28; P for trend <0.0001; IS: relative risk, 3.78; 95% confidence interval, 2.06 to 6.94; P for trend <0.0001). Our data provide evidence for a link between high plasma fetuin-A levels and an increased risk of MI and IS. Therefore, more research is warranted to determine the role of fetuin-A in the pathophysiology of cardiovascular disease.

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Low fetuin-A levels are associated with cardiovascular death: Impact of variations in the gene encoding fetuin.

Abdul Rashid Qureshi, Clifford Holmes, Peter Stenvinkel … (2005)

Vascular calcification is common among end-stage renal disease (ESRD) patients and a central characteristic of the atherosclerotic cardiovascular disease observed in dialysis patients. Fetuin-A, a circulating calcium-regulatory glycoprotein that inhibits vascular calcification, is associated with inflammation and outcome in dialysis patients. In the present study, we evaluated the association between fetuin-A, clinical phenotype, and outcome, as well as the impact of fetuin gene (AHSG) polymorphisms on the protein product and outcome. In a cohort of 258 (161 males) ESRD patients starting renal replacement therapy [glomerular filtration rate (GFR) 6.8 +/- 0.2 mL/min] aged 52 +/- 1 years the following parameters were studied: presence of malnutrition (subjective global assessment), comorbidity [diabetes mellitus and clinical manifest cardiovascular disease (CVD)], carotid plaques (N= 101), hs-CRP, fetuin-A, S-albumin, interleukin (IL)-6, and single nucleotide polymorphisms (SNPs) in the AHSG gene (N= 215) at amino acid positions Thr248Met (C-->T), Thr256Ser (C-->G), Asp276Asn (G-->A), and Arg317Cys (C-->T). Both all-cause (P or =10 mg/L). Inflamed (0.199 vs. 0.247 g/L; P < 0.01) and malnourished (0.207 vs. 0.262 g/L; P < 0.05) patients had significantly lower median fetuin-A than noninflamed and well-nourished ESRD patients, respectively. In a logistic regression model (N= 101), fetuin-A was significantly (P < 0.05) associated with the presence of carotid plaques independently of age, CVD, diabetes, S-albumin, gender, and inflammation. Significant correlations were observed between fetuin-A and both S-albumin (Rho = 0.30; P < 0.0001) and IL-6 (Rho =-0.21; P < 0.01). Patients with the AHSG 256Ser allele had lower serum fetuin-A levels, and higher all-cause and cardiovascular mortality rate if they were inflamed. The present study shows that a low fetuin-A level is associated with malnutrition, inflammation, and atherosclerosis (carotid plaques), as well as with increased cardiovascular and all-cause mortality. Because the present study demonstrates an effect of variations in the AHSG gene on both circulating fetuin-A levels and outcome, this indicates that ESRD patients with the AHSG 256Ser allele are at risk of accelerated vascular calcification.

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Author and article information

Journal

Journal ID (nlm-ta): Medicine (Baltimore)

Journal ID (iso-abbrev): Medicine (Baltimore)

Journal ID (publisher-id): MEDI

Title: Medicine

Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )

ISSN (Print): 0025-7974

ISSN (Electronic): 1536-5964

Publication date Collection: 29 October 2021

Publication date (Electronic): 29 October 2021

Volume: 100

Issue: 43

Electronic Location Identifier: e27481

Affiliations

The First Hospital of Nanping City, No. 317 Zhongshan Road, Nanping City, Fujian Province, PR China.

Author notes

[∗ ]Correspondence: Ziguo Chen, Nanping First Hospital Affiliated to Fujian Medical University, No. 317 Zhongshan Road, Yanping District, Nanping City, Fujian Province 353000, China (e-mail: chenziguo21@ 123456163.com ).

Article

Publisher ID: MD-D-21-01601 Accession ID: 27481

DOI: 10.1097/MD.0000000000027481

PMC ID: 8556024

PubMed ID: 34713826

SO-VID: 2ab6de81-ce1c-429a-bcc3-baf6aeb82054

Copyright © Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc/4.0

History

Date received : 25 February 2021

Date revision received : 2 August 2021

Date accepted : 14 September 2021

Categories

Subject: 3400

Subject: Research Article

Subject: Observational Study

Custom metadata

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Keywords: coronary atherosclerotic heart disease,fetuin-a,risk factors

Data availability:

Keywords: coronary atherosclerotic heart disease, fetuin-a, risk factors

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