Liver fibrosis increases the risk of subclinical atherosclerosis in patients with MASLD: a cross-sectional and longitudinal study.

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS

Nutrition & Metabolism Pub Date : 2025-07-01 DOI:10.1186/s12986-025-00951-y

Haoyu Zhang, Fei Lin, Mengyuan Miao, Chengxiao Yu, Wen Guo

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引用次数: 0

Abstract

Background: This study investigated the associations between both the progression and regression of liver fibrosis and subclinical atherosclerosis in patients withmetabolic dysfunction-associated steatotic liver disease (MASLD).

Methods: We conducted a cross-sectional analysis of 5,633MASLD participants who underwent transient elastography and carotid ultrasonography (Stage I). Additionally, a longitudinal study followed 2,670MASLD individuals without carotid atherosclerosis (CAS) at baseline, who underwent at least two health check-up examinations (Stage II). We used CAS and brachial ankle pulse wave velocity (baPWV) as markers of subclinical atherosclerosis and calculated the noninvasive fibrosis index FIB-4 to evaluate the probability of fibrosis.

Results: In Stage I study, liver fibrosis was associated with increased CAS risk (OR = 1.17, 95%CI1.01-1.37, P = 0.045) and elevated baPWV (OR = 1.49, 95%CI 1.06-2.09, P = 0.022). In Stage II study, during a median of 24 months of follow-up, 466 (17.45%)MASLD patients developed CAS. Compared to patients with stable low probability, those who progressed to a high-intermediate probability of advanced fibrosis had a higher risk of incident CAS (HR = 1.89, 95%CI1.42-2.51, P < 0.001). In addition, persistent high-intermediate probability and regression to low probability of advanced fibrosis were associated with 2.32-fold (95%CI 1.86-2.89, P < 0.001) and 1.82-fold (95% 1.22-2.71, P = 0.004) increased risk of incident CAS, respectively. Moreover, persistent high-intermediate probability was independently correlated with elevated baPWV risk (HR = 3.17, 95%CI 1.76-5.71, P < 0.001).

Conclusions: Persistent or progression to high-intermediate probability of fibrosis was associated with an increased risk of subclinical atherosclerosis, while regression to low probability of fibrosis does not significantly reduce this risk.

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肝纤维化增加MASLD患者亚临床动脉粥样硬化的风险：一项横断面和纵向研究

背景：本研究探讨了代谢功能障碍相关脂肪变性肝病（MASLD）患者肝纤维化和亚临床动脉粥样硬化的进展和消退之间的关系。方法：我们对5,633名masld患者进行了横断面分析，他们接受了瞬态弹性成像和颈动脉超声检查（I期）。此外，一项纵向研究随访了2670名基线时无颈动脉粥样硬化（CAS）的masld患者，这些患者接受了至少两次健康检查（II期）。我们采用CAS和肱踝关节脉搏波速度（baPWV）作为亚临床动脉粥样硬化的标志物，并计算无创纤维化指数FIB-4来评估纤维化的可能性。结果：在I期研究中，肝纤维化与CAS风险增加（OR = 1.17, 95%CI1.01-1.37, P = 0.045）和baPWV升高（OR = 1.49, 95%CI 1.06-2.09, P = 0.022）相关。在II期研究中，在中位24个月的随访期间，466例（17.45%）MASLD患者发生了CAS。与稳定的低概率患者相比，进展到中高概率晚期纤维化的患者发生CAS的风险更高（HR = 1.89, 95%CI1.42-2.51， P）。结论：持续或进展到中高概率纤维化与亚临床动脉粥样硬化的风险增加相关，而回归到低概率纤维化并没有显著降低这一风险。

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

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.