Abstract
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a multisystem cardiometabolic condition. Because cardiometabolic abnormalities are components of the diagnostic framework, studies describing their prevalence in MASLD must distinguish phenotypic characterization from criterion-independent association testing.
Objective: To compare the clinical, biochemical, and routine-care liver-stiffness profiles of adults with and without MASLD in a tertiary-care setting and to describe how metabolic comorbidity burden varied across imaging-defined steatosis grades.
Methods: This retrospective comparative study included 850 adults. MASLD was operationally defined by both imaging-confirmed hepatic steatosis and at least one documented cardiometabolic risk factor. Between-group comparisons used independent-samples t tests, Mann–Whitney U tests, or chi-square tests, as appropriate. Adjusted odds ratios for comorbidities were treated as exploratory and criterion-dependent because type 2 diabetes mellitus, hypertension, and dyslipidemia contributed to MASLD ascertainment. Across steatosis grades, binary outcomes were evaluated by logistic trend models and continuous outcomes by linear regression with grade coded 1–3.
Results: Of 850 patients, 432 (50.8%) met the operational MASLD definition and 418 (49.2%) had no imaging evidence of steatosis. The MASLD group had higher body mass index, aminotransferases, gamma-glutamyl transferase, triglycerides, glycated hemoglobin, and liver stiffness, and lower high-density lipoprotein cholesterol. Type 2 diabetes mellitus and dyslipidemia were more frequent in the MASLD group; however, these comparisons are partly criterion-dependent and should not be interpreted as independent validation of association. Within the MASLD group, increasing steatosis grade was accompanied by higher metabolic comorbidity burden and worsening biochemical and liver-stiffness measurements.
Conclusion: In this tertiary-care cohort, the operational MASLD definition identified patients with an adverse hepatic and cardiometabolic profile. The graded patterns across steatosis severity support integrated metabolic and liver-risk assessment, but the retrospective cross-sectional design, incorporation of cardiometabolic factors into case definition, and non-histologic nature of liver-stiffness measurements limit causal and criterion-independent interpretation.
