ArticleGut and liver2026
Risk Assessment for Carotid Atherosclerosis in Asymptomatic Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease.
Article in Gut and liver, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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Abstract
Background/Aims: Cardiovascular disease remains a major cause of mortality in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). This study evaluated the association between subclinical carotid atherosclerosis (SCA) and MASLD or MASLD and increased alcohol intake (MetALD) in asymptomatic individuals. Methods: This cross-sectional study included 56,889 adults undergoing health check-ups in South Korea. Hepatic steatosis was diagnosed by ultrasound, and SCA was defined by carotid plaques or increased intima-media thickness. Liver fibrosis was evaluated using the fibrosis-4 index and elastography. Results: SCA was identified in 13.5%. MASLD and MetALD were significantly associated with SCA in models adjusted for demographic and lifestyle factors (adjusted odds ratio [aOR], 1.26; 95% confidence interval [CI], 1.19 to 1.33; aOR, 1.43; 95% CI, 1.30 to 1.58; respectively, p<0.001 for both). However, these associations attenuated and lost statistical significance when metabolic risk factors were further adjusted. The risk of SCA increased with greater hepatic steatosis and liver fibrosis severity. In patients with MASLD, aORs were 1.70 (hepatic steatosis index >36), 1.23 (fibrosis-4 index ≥1.3), and 1.78 (liver stiffness measurement ≥5.6 kPa), compared to individuals without MASLD. Similar trends were observed in the MetALD group. Additionally, hypertension and clustering of ≥3 cardiometabolic risk factors were significantly associated with SCA in the MASLD group, supporting the role of metabolic burden in SCA development. Conclusions: MASLD and MetALD were associated with increased SCA risk, particularly in individuals with hepatic steatosis and fibrosis. These findings suggest that metabolic burden and liver disease severity jointly contribute to subclinical atherosclerosis risk.
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