Association of the cholesterol-HDL-glucose index with prevalent metabolic dysfunction-associated steatotic liver disease and its incremental metabolic-hepatic assessment value: a hospital-based cross-sectional study.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly encountered in routine health examinations, where simple metabolic indices may help contextualize hepatic steatosis within broader cardiometabolic risk. The cholesterol-HDL-glucose (CHG) index integrates fasting glycemia and cholesterol-related information, but its association with prevalent MASLD and its incremental metabolic-hepatic assessment value in real-world health examination settings remain incompletely defined. Methods: We performed a cross-sectional analysis of an independent hospital-based analytic cohort comprising adults who underwent routine health examinations at the Health Examination Center of the Second Affiliated Hospital of Shandong First Medical University between 2024 and 2025. The final de-identified analytic dataset included 977 participants with complete questionnaire, anthropometric, laboratory, and abdominal ultrasonography data. The primary outcome was prevalent MASLD, operationally defined as ultrasonographic steatosis plus at least 1 cardiometabolic risk factor. We evaluated the association between CHG and prevalent MASLD using multivariable logistic regression, dose-response analyses, ROC comparisons with metabolic and steatosis-related indices, incremental model assessment, and sensitivity analyses. Results: The mean (SD) age was 44.13 (11.11) years, and 524 participants (53.6%) were men. MASLD was present in 343 participants (35.1%). Mean CHG was significantly higher in participants with MASLD than in those without MASLD [5.35 (0.22) vs 5.07 (0.25); Conclusions: Higher CHG was independently and dose-dependently associated with prevalent MASLD in adults undergoing hospital-based health examinations. CHG appears to capture a clinically relevant metabolic-hepatic signal, but the incremental gain beyond already strong clinical models is modest. Given the limited evidence supporting population-wide screening for steatosis alone, CHG should be interpreted as a low-cost adjunct for opportunistic metabolic-hepatic risk assessment rather than as a stand-alone diagnostic test or evidence sufficient for broad community MASLD screening. Prospective multicenter validation with longitudinal hepatic and cardiometabolic endpoints is warranted before CHG is adopted for risk-guided pathways.