Comparison of Zinc Levels in Liver Cirrhosis and Evaluating the Severity Using Child-Pugh Score

Introduction Liver cirrhosis represents the final common pathway for chronic liver diseases, characterized by extensive fibrosis and hepatocyte dysfunction. Zinc, an essential micronutrient with critical roles in protein synthesis, enzymatic reactions, and antioxidant defense, has been implicated in liver pathophysiology. This study aimed to evaluate serum zinc levels in patients with liver cirrhosis and correlate them with disease severity as measured by the Child-Pugh classification. Methods This hospital-based cross-sectional study was conducted among 85 patients with liver cirrhosis attending the outpatient and inpatient departments of BLDE University's Shri BM Patil Medical College Hospital. Clinical evaluation and biochemical investigations were performed, including serum zinc levels and Child-Pugh scoring. Zinc deficiency is defined as serum levels below 51 μg/dL. Statistical analysis included descriptive statistics, chi-square tests, and analysis of variance (ANOVA) to assess relationships between variables. Results The study cohort comprised predominantly middle-aged men (95.3%), with alcoholic etiology (n=76, 89.4%) being the leading cause of cirrhosis. Advanced disease was common, with 67.1% of patients categorized as Child-Pugh Class C. Zinc deficiency was observed in 97.6% (n=83) of patients, with mean zinc levels showing a significant progressive decrease from Child-Pugh Class A (50.4±4.31 μg/dL) to Class B (42.32±4.86 μg/dL) to Class C (37.02±3.68 μg/dL) (p<0.001). There was a perfect parallelism between zinc and albumin deficiency (n=83, 97.6%). The mortality rate during the study period was 15.3% (n=13). Conclusion This study reveals a markedly high prevalence of zinc deficiency among patients with liver cirrhosis and establishes a significant inverse correlation between serum zinc levels and disease severity. The observed progressive decline in zinc concentrations with advancing Child-Pugh scores indicates that zinc deficiency may function both as a clinical marker of disease progression and as a contributing factor to hepatic deterioration. These findings highlight the potential value of incorporating routine zinc assessment in the evaluation of cirrhotic patients. Moreover, zinc supplementation may be considered as an adjunctive therapeutic strategy, particularly in those with advanced-stage disease.