Cholinesterase and the association between hepatic steatosis and liver fibrosis in patients with prior hepatitis E

This study aimed to evaluate the association between the hepatic steatosis and liver fibrosis burden in patients with prior hepatitis E virus (HEV) infection, and to further explore potential influencing factors and key predictive indicators to clarify the independent role of steatosis in fibrotic progression and its possible underlying mechanisms. We conducted a retrospective cross-sectional study including 453 hospitalized patients with a history of HEV infection. Hepatic steatosis and fibrosis were assessed using abdominal ultrasonography. Participants were categorized according to steatosis and fibrosis status for comparative analyses. Multivariable logistic regression models were applied to identify independent factors associated with liver fibrosis after adjustment for demographic and metabolic variables. Subgroup analyses stratified by age, sex, and metabolic comorbidities were performed to assess the stability and heterogeneity of the observed associations. In addition, mediation analysis was conducted to examine the potential role of serum cholinesterase (CHE) in the association between steatosis and liver fibrosis. Among patients with previous HEV infection, hepatic steatosis was positively associated with liver fibrosis. After multivariable adjustment, steatosis remained independently associated with fibrosis. Subgroup analyses indicated that this association was more pronounced in females, individuals aged ≥ 60 years, and patients with diabetes or hypertension. CHE showed a cross-sectional suppression pattern: steatosis was positively associated with CHE, CHE was inversely associated with fibrosis, and adjustment for CHE strengthened the steatosis–fibrosis association. Among hospitalized patients with prior HEV infection, hepatic steatosis severity is significantly associated with liver fibrosis burden, and this association varies across demographic and metabolic subgroups. As a marker reflecting hepatic functional reserve, CHE may statistically offset part of the observed association between steatosis and fibrosis.