The impact of single-nucleotide polymorphisms on liver stiffness and controlled attenuation parameter in patients treated with direct-acting antiviral drugs for hepatitis C infection.

Single-nucleotide polymorphisms (SNPs) of patatin-like phospholipase domain-containing 3 (), tolloid-like protein 1 () and interleukin-28 () have been identified as susceptibility factors for liver steatosis, inflammation and fibrosis in patients with hepatitis C virus (HCV) infection. Here, whether these polymorphisms affected predispositions to changes in liver stiffness (LS) and controlled attenuation parameter (CAP) following direct-acting antiviral (DAA) therapy was assessed. The changes in LS and steatosis in 77 HCV-infected patients receiving DAA therapy were compared with , and genotypes, using CAP, FibroScan and Virtual Touch tissue quantification (VTTQ) before treatment and 12 weeks after the end of the treatment. VTTQ results showed that LS significantly decreased in CC (P=0.035), AA (P=0.011) and TT (P=0.005) genotypes; no significant differences were observed in CG/GG, AT/TT and TG/GG. FibroScan results showed that LS significantly decreased in AA (P=0.028) and TT (P=0.032), with no significant difference in CC. No significant differences were observed in CG/GG, AT/TT and TG/GG groups. CAP was significantly increased in CG/GG (P=0.039 and P<0.05) and TT (P=0.014); no significant difference was observed in CC and all genotypes of and TG/GG. Therefore, these results indicated that SNPs could predict changes in LS and steatosis after DAA therapy.