Monocyte-to-high-density lipoprotein cholesterol ratio and carotid atherosclerosis in patients with metabolic dysfunction–associated steatotic liver disease: a comparative analysis of systemic inflammatory indices
摘要
Systemic inflammation indices have been linked to carotid atherosclerosis (CAS); however, their comparative performance and relative independence within the metabolic–inflammatory milieu of metabolic dysfunction-associated steatotic liver disease (MASLD) remain unclear. We aimed to identify the inflammatory index showing the strongest and most consistent association with CAS and to exploratorily assess potential mediating pathways.
MethodsIn this cross-sectional study of 24,683 adults with MASLD, eight systemic inflammation indices were calculated. Associations with ultrasonography-defined CAS were evaluated using multivariable logistic regression. All indices were entered into a mutually adjusted model to identify the most independent marker. Dose–response relationships, subgroup analyses, and exploratory mediation analyses were performed.
ResultsAfter full adjustment, the monocyte-to-high-density lipoprotein cholesterol ratio (MHR) showed the strongest association with CAS (odds ratio [OR] per 1-standard deviation increase: 1.092, 95% confidence interval [CI] 1.054–1.132). In the mutually adjusted model including all eight indices, only MHR remained independently associated with CAS (OR: 1.062, 95% CI 1.005–1.123). The MHR–CAS association was linear (P for nonlinearity = 0.416) and stronger among individuals without hypertension (P for interaction = 0.027). Exploratory mediation analysis suggested that approximately 4.0% of the association was statistically mediated by fasting plasma glucose (FPG)–related pathways, observed exclusively in non-lean MASLD.
ConclusionAmong commonly used systemic inflammation indices, MHR appears to be a robust and independent marker associated with carotid atherosclerosis in MASLD. Its association is linear, modified by hypertension status, and modestly linked to glucose-related pathways in a phenotype-specific manner, supporting its potential role as a complementary biomarker for vascular risk stratification in MASLD.
Clinical trial numberNot applicable.