Tophi and carotid atherosclerosis in gout patients: Role of insulin resistance.

Carotid atherosclerosis Gout Insulin resistance Tophi

Journal

Nutrition, metabolism, and cardiovascular diseases : NMCD
ISSN: 1590-3729
Titre abrégé: Nutr Metab Cardiovasc Dis
Pays: Netherlands
ID NLM: 9111474

Informations de publication

Date de publication:
15 Dec 2023
Historique:
received: 26 06 2023
revised: 25 11 2023
accepted: 30 11 2023
medline: 15 1 2024
pubmed: 15 1 2024
entrez: 14 1 2024
Statut: aheadofprint

Résumé

Gout and cardiovascular disease are closely related, but the mechanism linking them is still unknown. Gout may affect the insulin signaling pathway inducing insulin resistance (IR). The study aims to evaluate the association between tophi and carotid atherosclerosis, considering the potential role of IR. A total of 595 patients with gout aged 18 to 80 were enrolled in this study. Carotid intima-media thickness, plaques and tophi were evaluated by B-mode ultrasonography. IR was assessed by the HOMA index (hepatic IR) and Gutt index (peripheral IR). Multivariable logistic regression and interaction analysis were used to examine the association between tophi and IR and its impact on carotid atherosclerosis. Among these participants, the average age was 55.4 (±12.54) years, and 94.6 % were male. Tophi were associated with increased odds of carotid atherosclerosis and burden after adjustment for confounders (P < 0.05). Tophi and IR synergically interacted for inducing carotid atherosclerosis. The interaction between peripheral IR with tophi was more pronounced than hepatic IR with tophi. Tophi were independently associated with carotid atherosclerosis risk. IR mediated a significant amount of the effect of tophi on the development of carotid atherosclerosis. Peripheral IR probably plays a more important role than hepatic IR does.

Sections du résumé

BACKGROUND AND AIM OBJECTIVE
Gout and cardiovascular disease are closely related, but the mechanism linking them is still unknown. Gout may affect the insulin signaling pathway inducing insulin resistance (IR). The study aims to evaluate the association between tophi and carotid atherosclerosis, considering the potential role of IR.
METHODS AND RESULTS RESULTS
A total of 595 patients with gout aged 18 to 80 were enrolled in this study. Carotid intima-media thickness, plaques and tophi were evaluated by B-mode ultrasonography. IR was assessed by the HOMA index (hepatic IR) and Gutt index (peripheral IR). Multivariable logistic regression and interaction analysis were used to examine the association between tophi and IR and its impact on carotid atherosclerosis. Among these participants, the average age was 55.4 (±12.54) years, and 94.6 % were male. Tophi were associated with increased odds of carotid atherosclerosis and burden after adjustment for confounders (P < 0.05). Tophi and IR synergically interacted for inducing carotid atherosclerosis. The interaction between peripheral IR with tophi was more pronounced than hepatic IR with tophi.
CONCLUSIONS CONCLUSIONS
Tophi were independently associated with carotid atherosclerosis risk. IR mediated a significant amount of the effect of tophi on the development of carotid atherosclerosis. Peripheral IR probably plays a more important role than hepatic IR does.

Identifiants

pubmed: 38220503
pii: S0939-4753(23)00481-7
doi: 10.1016/j.numecd.2023.11.019
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no competing interests.

Auteurs

Ke Si (K)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Jingwei Chi (J)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Lili Xu (L)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Bingzi Dong (B)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Yajing Huang (Y)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Haowen Zhang (H)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Ying Chen (Y)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Yangang Wang (Y)

Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao 266003, China. Electronic address: wangyg1966@126.com.

Classifications MeSH