Serum Galectin-3 in Hepatitis C Virus Infection Declines after Successful Virus Eradication by Direct-Acting Antiviral Therapy.

ABSTRACT

BACKGROUND AND AIMS: Serum galectin-3 is regarded as an inflammatory marker in patients with chronic liver diseases. Hepatitis C virus (HCV) infection is associated with higher levels of inflammatory molecules which ameliorate by efficient treatment with direct-acting antivirals (DAAs). The aim of this study was to compare serum galectin-3 levels between HCV patients before treatment with DAAs and at the time of sustained virologic response at 12 weeks post-treatment (SVR12). METHODS: Hepatitis B and human immunodeficiency virus-negative HCV infected patients not treated with HCV therapies before were recruited at the University Hospital of Regensburg. Galectin-3 was measured by enzyme-linked immunosorbent assay in the serum of patients with chronic HCV infection, before treatment initializing, at four and twelve weeks after the start of DAA therapy and at SVR12. Associations of serum galectin-3 with C-reactive protein (CRP), leukocyte count and measures of liver disease severity were analyzed. Liver fibrosis was assessed by acoustic radiation force impulse, the aspartate aminotransferase/platelet ratio index, and the fibrosis-4 score. RESULTS: In the serum of 81 HCV patients, galectin-3 did not correlate with viral load, viral genotype, CRP, leukocyte count, or the model for end stage liver disease score. Therapy with DAAs effectively diminished viral load within four weeks in all patients. The median value of the serum galectin-3 was 3.0 (Q12.0, Q34.0) ng/ml before therapy and declined to 2.4 (Q1 1.7, Q3 3.4) ng/ml at SVR12 (p<0.001; paired samples of 67 patients). At SVR12, serum galectin-3 was not correlated with CRP (r=0.057, p=0.646) or leu-kocyte count (r=0.222, p=0.071) and did not change with increasing fibrosis stage. The associations between serum galectin-3 and body mass index, liver steatosis or diabetes could not be observed. CONCLUSIONS: Elimination of HCV by DAA treatment lowered serum galectin-3 compared to the pre-treatment levels suggesting that HCV infection causes an increase of this immune-regulatory protein.