BIOCHEMICAL PHENOTYPES OF METABOLIC DYSFUNCTION–ASSOCIATED STEATOTIC LIVER DISEASE ACCORDING TO LIVER FIBROSIS SEVERITY IN PATIENTS WITH INSULIN RESISTANCE

Background: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a heterogeneous disorder characterized by variable combinations of insulin resistance, inflammation, hepatocellular injury, and liver fibrosis. Identification of biochemical phenotypes associated with fibrosis progression may improve early risk stratification and selection of patients requiring advanced non-invasive assessment. Objective: To evaluate differences in biochemical and inflammatory parameters among patients with MASLD stratified according to liver fibrosis severity. Materials and methods: A total of 200 patients with MASLD and insulin resistance were divided into three groups: patients without fibrosis (n=60), patients with mild fibrosis (n=80), and patients with pronounced fibrosis (n=60). Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), total bilirubin, albumin, glycated haemoglobin, C-reactive protein, ferritin, and platelet count were evaluated. Continuous variables were presented as mean ± standard deviation. Statistical comparisons were performed against the group without fibrosis, with P<0.05 considered statistically significant. Results: A progressive biochemical deterioration was observed with increasing fibrosis severity. Compared with patients without fibrosis, those with pronounced fibrosis had 81.7% higher AST, 75.1% higher ALT, 142.5% higher GGT, 80.5% higher C-reactive protein, and 98.3% higher ferritin levels. Glycated haemoglobin increased from 5.39±0.69% in patients without fibrosis to 6.46±0.80% in those with pronounced fibrosis. Platelet count decreased from 254.5±37.0×10⁹/L to 151.0±18.9×10⁹/L, while serum albumin decreased from 40.7±6.1 to 34.6±5.4 g/L. Total bilirubin increased from 12.9±2.2 to 22.1±3.5 μmol/L. Most differences were statistically significant at P<0.001. Conclusion: Progression of liver fibrosis in patients with MASLD and insulin resistance was associated with a distinct biochemical phenotype characterized by increasing hepatocellular injury, cholestatic enzyme activity, systemic inflammation, metabolic dysregulation, hyperferritinaemia, thrombocytopenia, and reduced serum albumin. Combined assessment of these routinely available parameters may support fibrosis risk stratification but should be complemented by validated fibrosis scores and elastography.