Cureus · 2026
Serum Uric Acid and Disease Severity in Chronic Liver Disease: A Cross-Sectional Study of Its Association With Child-Pugh Class.
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Rathi Pratik, Pande Vivek, Shaikh Fahad Idrees, Deshmukh Rituraj Y, Hussain Arman, Zainab, Chandwani Malvika, Satish Bhala, Bezbaruah Verbena
Аннотация
BACKGROUND: Chronic liver disease (CLD) is a major cause of morbidity and mortality worldwide, with India accounting for the highest absolute number of cirrhosis-related deaths globally. Serum uric acid (SUA), the end product of purine metabolism, is increasingly recognised as a marker of oxidative stress and metabolic derangement and has been reported to be elevated in CLD. The Child-Pugh score remains the most widely used bedside tool for assessing hepatic functional reserve. Data regarding the association of SUA with Child-Pugh class and CLD-related complications in Indian tertiary care settings remain limited.
OBJECTIVES: The study aimed to estimate SUA levels in patients with CLD at admission, determine their association with disease severity according to Child-Pugh class, and assess their association with CLD-related complications.
METHODS: This cross-sectional, observational study was conducted over 18 months in the Department of General Medicine at a tertiary care teaching hospital. Ninety-two consecutive patients with CLD aged 18-65 years were enrolled. Fasting SUA, liver function tests, haemogram, and coagulation parameters were recorded, and disease severity was graded using the Child-Pugh classification. Continuous variables were compared using the independent-samples t-test or one-way analysis of variance (ANOVA) with Bonferroni-corrected pairwise comparisons. Categorical associations were assessed using Pearson's chi-square test or Fisher's exact test, as appropriate. A two-tailed p-value <0.05 was considered statistically significant.
RESULTS: The mean age was 47.6 years, with a male predominance (76.1%). Alcoholic liver disease was the most common aetiology (65.2%). Sixty-four (69.6%) patients had elevated SUA (>7.2 mg/dL, the cutoff applied uniformly to both sexes), with an overall mean SUA of 7.1 ± 1.9 mg/dL. Mean SUA increased progressively across Child-Pugh classes A (5.2 ± 1.1 mg/dL), B (6.9 ± 1.3 mg/dL), and C (8.4 ± 1.6 mg/dL) (ANOVA F(2,89)=37.38, p<0.001), with all pairwise comparisons significant after Bonferroni correction (all p<0.001). SUA was also significantly associated with Child-Pugh class in categorical analysis (χ²(2)=22.00, p<0.001). Patients with complications had higher mean SUA than those without complications (8.0 ± 1.5 vs. 5.6 ± 1.2 mg/dL; t(90)=8.08, p<0.001), and elevated SUA was significantly associated with any complication (χ²(1)=17.63, p<0.001). Child-Pugh class was similarly associated with complications (χ²(2)=15.68, p<0.001). Among individual complications, elevated SUA was significantly associated with hepatic encephalopathy (χ²(1)=6.15, p=0.013) but not with variceal bleeding, hepatorenal syndrome, spontaneous bacterial peritonitis, or portal hypertension (all p>0.05).
CONCLUSION: Hyperuricaemia was common in this CLD cohort and was significantly associated with Child-Pugh class and the overall presence of complications. These findings support a hypothesis-generating association between SUA and disease severity rather than an established prognostic or independent role. Except for hepatic encephalopathy, SUA was not significantly associated with individual complications. Larger prospective multicentric studies adjusting for renal function and other confounders are needed before SUA can be considered a clinical adjunct marker.
OBJECTIVES: The study aimed to estimate SUA levels in patients with CLD at admission, determine their association with disease severity according to Child-Pugh class, and assess their association with CLD-related complications.
METHODS: This cross-sectional, observational study was conducted over 18 months in the Department of General Medicine at a tertiary care teaching hospital. Ninety-two consecutive patients with CLD aged 18-65 years were enrolled. Fasting SUA, liver function tests, haemogram, and coagulation parameters were recorded, and disease severity was graded using the Child-Pugh classification. Continuous variables were compared using the independent-samples t-test or one-way analysis of variance (ANOVA) with Bonferroni-corrected pairwise comparisons. Categorical associations were assessed using Pearson's chi-square test or Fisher's exact test, as appropriate. A two-tailed p-value <0.05 was considered statistically significant.
RESULTS: The mean age was 47.6 years, with a male predominance (76.1%). Alcoholic liver disease was the most common aetiology (65.2%). Sixty-four (69.6%) patients had elevated SUA (>7.2 mg/dL, the cutoff applied uniformly to both sexes), with an overall mean SUA of 7.1 ± 1.9 mg/dL. Mean SUA increased progressively across Child-Pugh classes A (5.2 ± 1.1 mg/dL), B (6.9 ± 1.3 mg/dL), and C (8.4 ± 1.6 mg/dL) (ANOVA F(2,89)=37.38, p<0.001), with all pairwise comparisons significant after Bonferroni correction (all p<0.001). SUA was also significantly associated with Child-Pugh class in categorical analysis (χ²(2)=22.00, p<0.001). Patients with complications had higher mean SUA than those without complications (8.0 ± 1.5 vs. 5.6 ± 1.2 mg/dL; t(90)=8.08, p<0.001), and elevated SUA was significantly associated with any complication (χ²(1)=17.63, p<0.001). Child-Pugh class was similarly associated with complications (χ²(2)=15.68, p<0.001). Among individual complications, elevated SUA was significantly associated with hepatic encephalopathy (χ²(1)=6.15, p=0.013) but not with variceal bleeding, hepatorenal syndrome, spontaneous bacterial peritonitis, or portal hypertension (all p>0.05).
CONCLUSION: Hyperuricaemia was common in this CLD cohort and was significantly associated with Child-Pugh class and the overall presence of complications. These findings support a hypothesis-generating association between SUA and disease severity rather than an established prognostic or independent role. Except for hepatic encephalopathy, SUA was not significantly associated with individual complications. Larger prospective multicentric studies adjusting for renal function and other confounders are needed before SUA can be considered a clinical adjunct marker.