Abstract
Background/Objectives: Oxidative stress contributes to the pathogenesis of cirrhosis, but its value as a clinical biomarker remains uncertain. Methods: We retrospectively analysed 90 patients with decompensated cirrhosis. Serum malondialdehyde (MDA) and 8-epi-prostaglandin F2α (8-iso-PGF2α) were measured at admission. Biomarker levels were compared between Child-Pugh classes B and C, across hepatic encephalopathy grades, and ascites severity, using Mann-Whitney, Kruskal-Wallis, and Spearman correlation tests. Results: Median MDA did not differ significantly between Child-Pugh classes B and C (2.67 [2.10-3.20] vs. 2.45 [1.98-3.05] μmol/L; p = 0.331), nor across ascites categories (p = 0.453). Similarly, 8-iso-PGF2α values did not vary between Child-Pugh classes (255.8 [220.0-310.0] vs. 250.1 [210.0-295.0] pg/mL; p = 0.784) or ascites groups (p = 0.828). Spearman analysis showed no significant correlations with albumin, INR, bilirubin, creatinine, or age, except for a non-significant trend with bilirubin (ρ = -0.18, p = 0.09). Importantly, MDA levels increased significantly across encephalopathy grades (p = 0.021), suggesting a link between systemic oxidative stress and neuropsychiatric impairment. Conclusions: In this clinical cohort, oxidative stress biomarkers did not provide discriminatory value for staging by Child-Pugh or ascites, but MDA was associated with encephalopathy severity. These findings highlight both the limitations and potential clinical relevance of oxidative stress markers in cirrhosis management.