Chronic hepatitis B with type 2 diabetes mellitus: Association between glycemic control and liver fibrosis

The interplay between abnormal glucose metabolism and the progression of liver fibrosis in patients with both chronic hepatitis B (CHB) and type 2 diabetes mellitus (T2DM) remains unclear. Previous studies have suggested that the coexistence of these conditions may exacerbate liver inflammation and fibrosis; however, the impacts of dynamic changes in glucose metabolism indicators, hypoglycemic medication regimens, and glycemic control status on liver fibrosis require further elucidation.

To explore the effect of glycemic control on hepatic fibrosis in patients with CHB and T2DM.

A total of 420 patients with CHB and T2DM admitted to the Public Health Clinical Center of Chengdu between October 2018 and January 2022 were retrospectively included and classified according to liver stiffness measurement and glycemic control for between-group comparisons.

Significant differences were observed in the alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, AST/ALT ratio, total bilirubin, direct bilirubin, diabetes treatment program, and thrombin time values among the liver fibrosis groups (adjusted P < 0.05). Significant differences in albumin and gamma-glutamyl transferase levels were observed among the groups categorized by glucose status at admission (adjusted P < 0.05). A positive correlation between fasting plasma glucose (FPG) and liver stiffness measurement was found to be mediated by ALT and AST. Fibrinogen and the international normalized ratio were positively correlated with glycated hemoglobin A1c, while the fibrosis-4 score, ALT, AST/ALT ratio, type III procollagen N-terminal peptide, ferritin, and activated partial thromboplastin time were correlated with FPG at admission. Additionally, AST was positively correlated with FPG at discharge (P < 0.05).

Specific glucose metabolic parameters, hypoglycemic agents, and glycemic control status markers are associated with hepatic fibrosis in patients with both CHB and T2DM. Close blood glucose monitoring, optimized use of hypoglycemic agents, and continuous maintenance of good glycemic control may slow the progression of liver fibrosis in patients with CHB and T2DM.