Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents.
Level 4 - case-series / case-control
Cross-sectional observational study
PubMed 28214020 · doi:10.1016/j.jhep.2016.12.025
What was done
Investigators evaluated 271 obese children and adolescents with proven non-alcoholic fatty liver disease (NAFLD). NASH was diagnosed using a NAFLD activity score >= 5 and confirmed with the fatty liver inhibition of progression (FLIP) algorithm. Daily dietary fructose intake (g/day) was estimated via food frequency questionnaire, and serum uric acid (mg/dl) was measured. Multivariable binary logistic regression was used to evaluate independent predictors of NASH and hyperuricemia after adjusting for covariates and confounders.
What was found
NASH was present in 37.6% of the cohort. Hyperuricemia (uric acid >= 5.9 mg/dl) was present in 47% of patients with NASH compared to 29.7% of non-NASH patients (p=0.003). In adjusted multivariable models, both serum uric acid concentration (OR=2.488, 95% CI: 1.87-2.83, p=0.004) and fructose consumption (OR=1.612, 95% CI: 1.25-1.86, p=0.001) were independently associated with NASH. Fructose consumption was also independently associated with hyperuricemia (OR=2.021, 95% CI: 1.66-2.78, p=0.01) and was the only factor independently linked with serum uric acid concentration.
Why it matters
This study links both dietary fructose intake and serum uric acid independently to histological NASH in pediatric NAFLD, suggesting potential dietary and metabolic targets for disease progression.
Limits
The cross-sectional design cannot establish causality or temporal relationships. Dietary fructose intake was assessed using self-reported food frequency questionnaires, which are prone to recall and measurement error. The cohort was restricted to obese children and adolescents with existing NAFLD, limiting generalizability to wider populations.
Cited by
- context Serum uric acid levels exceeding 5 milligrams per deciliter indicate excess dietary fructose consumption and hepatic fructose overload.