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代谢综合征增加骨关节炎风险:来自英国生物库前瞻性队列研究的结果。

Metabolic syndrome increases osteoarthritis risk: findings from the UK Biobank prospective cohort study.

机构信息

Department of Joint Surgery, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong, China.

Department of Epidemiology and Biostatistics, Clinical Big Data Research Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518000, Guangdong, China.

出版信息

BMC Public Health. 2024 Jan 19;24(1):233. doi: 10.1186/s12889-024-17682-z.

DOI:10.1186/s12889-024-17682-z
PMID:38243159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10799367/
Abstract

OBJECTIVE

The association between Metabolic Syndrome (MetS), its components, and the risk of osteoarthritis (OA) has been a topic of conflicting evidence in different studies. The aim of this present study is to investigate the association between MetS, its components, and the risk of OA using data from the UK Biobank.

METHODS

A prospective cohort study was conducted in the UK Biobank to assess the risk of osteoarthritis (OA) related to MetS. MetS was defined according to the criteria set by the International Diabetes Federation (IDF). Additionally, lifestyle factors, medications, and the inflammatory marker C-reactive protein (CRP) were included in the model. Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI). The cumulative risk of OA was analyzed using Kaplan-Meier curves and log-rank tests. To explore potential nonlinear associations between MetS components and OA risk, a restricted cubic splines (RCS) model was employed. In addition, the polygenic risk score (PRS) of OA was calculated to characterize individual genetic risk.

RESULTS

A total of 45,581 cases of OA were identified among 370,311 participants, with a median follow-up time of 12.48 years. The study found that individuals with MetS had a 15% higher risk of developing OA (HR = 1.15, 95%CI:1.12-1.19). Additionally, central obesity was associated with a 58% increased risk of OA (HR = 1.58, 95%CI:1.5-1.66), while hyperglycemia was linked to a 13% higher risk (HR = 1.13, 95%CI:1.1-1.15). Dyslipidemia, specifically in triglycerides (HR = 1.07, 95%CI:1.05-1.09) and high-density lipoprotein (HR = 1.05, 95%CI:1.02-1.07), was also found to be slightly associated with OA risk. When stratified by PRS, those in the high PRS group had a significantly higher risk of OA compared to those with a low PRS, whereas no interaction was found between MetS and PRS on OA risks. Furthermore, the presence of MetS significantly increased the risk of OA by up to 35% in individuals with elevated CRP levels (HR = 1.35, 95% CI:1.3-1.4).

CONCLUSION

MetS and its components have been found to be associated with an increased risk of OA, particularly in individuals with elevated levels of CRP. These findings highlight the significance of managing MetS as a preventive and intervention measure for OA.

摘要

目的

代谢综合征(MetS)及其各组分与骨关节炎(OA)风险之间的关联在不同研究中存在相互矛盾的证据。本研究旨在使用英国生物库的数据来探讨 MetS、其组分与 OA 风险之间的关联。

方法

在英国生物库中进行了一项前瞻性队列研究,以评估与 MetS 相关的 OA 风险。MetS 根据国际糖尿病联合会(IDF)制定的标准进行定义。此外,还将生活方式因素、药物和炎症标志物 C 反应蛋白(CRP)纳入模型中。使用 Cox 比例风险回归计算风险比(HR)和 95%置信区间(CI)。使用 Kaplan-Meier 曲线和对数秩检验分析 OA 的累积风险。为了探索 MetS 组分与 OA 风险之间潜在的非线性关联,使用了限制性立方样条(RCS)模型。此外,还计算了 OA 的多基因风险评分(PRS)以表征个体遗传风险。

结果

在 370311 名参与者中,共确定了 45581 例 OA 病例,中位随访时间为 12.48 年。研究发现,患有 MetS 的个体发生 OA 的风险增加了 15%(HR=1.15,95%CI:1.12-1.19)。此外,中心性肥胖与 OA 风险增加 58%相关(HR=1.58,95%CI:1.5-1.66),而高血糖与 OA 风险增加 13%相关(HR=1.13,95%CI:1.1-1.15)。血脂异常,特别是甘油三酯(HR=1.07,95%CI:1.05-1.09)和高密度脂蛋白(HR=1.05,95%CI:1.02-1.07),也与 OA 风险略有相关。按 PRS 分层,高 PRS 组发生 OA 的风险明显高于低 PRS 组,而 MetS 与 PRS 之间在 OA 风险上没有交互作用。此外,在 CRP 水平升高的个体中,MetS 的存在使 OA 的风险增加了高达 35%(HR=1.35,95%CI:1.3-1.4)。

结论

MetS 及其各组分与 OA 风险增加相关,尤其是在 CRP 水平升高的个体中。这些发现强调了将 MetS 作为 OA 的预防和干预措施进行管理的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/61ebf7d5751f/12889_2024_17682_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/e7d2ddb8ac8c/12889_2024_17682_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/7a0a292fc485/12889_2024_17682_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/12a0ffef2b84/12889_2024_17682_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/61ebf7d5751f/12889_2024_17682_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/e7d2ddb8ac8c/12889_2024_17682_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/7a0a292fc485/12889_2024_17682_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/12a0ffef2b84/12889_2024_17682_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8de/10799367/61ebf7d5751f/12889_2024_17682_Fig4_HTML.jpg

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