Non-HDL to HDL cholesterol ratio as a biomarker associated with decompensation in chronic liver disease

Aim: Chronic liver disease (CLD) is characterized by progressive impairment of hepatic function and frequent lipid metabolism abnormalities, with reductions in high-density lipoprotein cholesterol (HDL-C) and other lipoprotein fractions shown to parallel worsening liver dysfunction and predict adverse clinical outcomes such as decompensation and mortality. Established prognostic scores like Model for End-Stage Liver Disease (MELD) and Child-Turcotte-Pugh (CTP) capture aspects of disease severity, but composite lipid indices such as the non-HDL/HDL-C ratio (NHHR), which balance atherogenic and protective lipoproteins, have emerged as potentially informative biomarkers in metabolic and liver disorders. This study evaluated the association of NHHR with clinical decompensation in CLD. Methods: This cross-sectional study included 220 adults with CLD of mixed etiologies. Baseline demographics, liver disease severity scores, and fasting lipid profiles were obtained. NHHR was calculated, and patients were categorized into tertiles. Spearman correlation coefficients were calculated to examine relationships between NHHR and clinical severity markers. Multivariable logistic regression was used to evaluate the association between NHHR and clinical decompensation. Model performance was compared using receiver operating characteristic curves, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Results: Among 220 patients with CLD (mean age 54.5 ± 11.9 years, 63% male), 96 (43.6%) had decompensated disease. Higher NHHR tertiles were associated with increasing MELD-3.0 scores (P = 0.028) and lower serum albumin (P < 0.001). NHHR correlated positively with MELD-3.0, bilirubin, and international normalized ratio (INR) and inversely with albumin and platelet count. Decompensation prevalence rose across NHHR tertiles (31.1% to 53.4%, P < 0.001). NHHR was independently associated with decompensation (adjusted OR 1.55, 95% CI 1.21–1.98, P < 0.001) and improved model discrimination (AUC 0.79 vs. 0.73). Conclusions: NHHR is independently associated with clinical decompensation in CLD and provides incremental prognostic value beyond traditional predictors, suggesting its potential utility in clinical risk assessment and stratification.