Purpose: The introduction of direct-acting antivirals (DAAs) has revolutionized the treatment of chronic hepatitis C viral (HCV) infection. This study aims to establish real-world treatment efficacy of Sofosbuvir-based (SOF-B) and Ombitasvir/Paritaprevir/Ritonavir-based (OPR-B) regimens. Patients and methods: This prospective, non-randomized observational real-life study was conducted in Salmaniya Medical Complex, Bahrain, and included consecutive patients with chronic HCV infection (genotypes 1-4) who were treated with direct-acting antivirals. Sustained virologic response to therapy was assessed at week 12 post end of treatment (SVR12). Results: Of the 167 patients included, 60.5% (n=101) were treated with SOF-B and 39.5% (n=66) with OPR-B regimens for 12 weeks (n=148; 88.6%) or 24 weeks (n=19; 11.4%). SVR12 was achieved in 156 (93.4%) patients, 4 patients failed to achieve SVR despite completion of treatment, and 7 patients discontinued treatment due to non-compliance and were included in the analysis on an intention-to-treat basis. There was no difference between SOF-B and OPR-B regimens (95/101; 94.1%) and (61/66; 92.4%), respectively (p=0.68). However, SVR12 rates were significantly higher in patients without liver cirrhosis (103/104; 99.0%) compared to patients with cirrhosis (53/63; 84.1%; p<0.001), and in patients who received 12-week-regimen (141/148; 95.3%) compared to those who received 24-week regimen (15/19; 78.9%; p<0.024). However, logistic regression analysis identified cirrhosis at baseline to be the only independent predictor of non-SVR12 (OR: 16.1, 95% confidence interval 1.96-131.91, p=0.01). Apart from Hb, INR, and ALP, all other laboratory parameter improved following treatment (p<0.05). Conclusion: Both SOF-B and OPR-B regimens achieved high SVR12 rates in this real-life cohort of patients with chronic HCV infection, similar to what is reported in other real-world studies. Cirrhosis was the only independent predictor of poor response.
Keywords: DAAs; HCV; cirrhosis; liver disease; sustained viral response; treatment.