Effects of hepatitis C virus genotypes and viral load on glucose and lipid metabolism after sustained virological response with direct-acting antivirals.

Objective: The objective of this study, carried out at the university hospital of the Federal University of Rio Grande, was to assess whether the treatment of chronic hepatitis C with direct-acting antivirals and the sustained virological response will affect the metabolic influences of the hepatitis C virus and whether these effects will vary according to genotypes and virus load.

Methods: This is an intervention pre-post study, carried out from March 2018 to December 2019, evaluating 273 hepatitis C virus patients treated with direct-acting antivirals. Inclusion criteria included being monoinfected with hepatitis C virus and achieving sustained virological response . Exclusion criteria included the presence of decompensated cirrhosis or co-infected with hepatitis B virus or human immunodeficiency virus. Genotypes, genotype 1 subtypes, and hepatitis C virus viral load were analyzed. Glucose metabolism was evaluated by the Homeostasis Model Assessment-insulin resistance indices: Homeostasis Model Assessment-β, TyG, and HbA1c, measured at the beginning of treatment and in sustained virological response. Statistical analysis with a T test by paired comparison of the means of the variables in the pretreatment and in the sustained virological response.

Results: Homeostasis Model Assessment-insulin resistance analysis: there were no significant differences between pretreatment and sustained virological response. Homeostasis Model Assessment-β analysis: significant increase in genotype 1 patients (p<0.028). TyG index analysis: significant increase in genotype 1b (p<0.017), genotype 3 (p<0.024), and genotype non-1 with low viral load (p<0.039). HbA1c analysis: significant decrease in genotype 3 (p<0.001) and genotype non-1 patients with low viral load (p<0.005).

Conclusion: We detected significant metabolic influences after sustained virological response: impairment in lipid profile and improvements in the glucose metabolism. We found significant differences in genotype dependence, genotype 1 subtypes, and viral load.