Document Type : Original Article
Authors
1
Department of Internal Medicine, , Faculty of Medicine, Minia University, Minya, Egyp
2
Department of Internal Medicine, , Faculty of Medicine, Minia University, Minya, Egypt
3
Department of Clinical Pathology, Faculty of Medicine, Minia University, Minya, Egypt
Abstract
Background and aims: Treatment of hepatitis C virus (HCV) changed dramatically with the
introduction of oral direct-acting antiviral drugs due to their high antiviral potency and safety profile.
Sofosbuvir plus daclatasvir combination therapy was extensively investigated in HCV genotypes 1, 2,
and 3, while published data regarding its real-life application in the treatment of genotype 4 is lacking.
Therefore, we conducted this study to assess the outcomes and predictors of treatment response with
sofosbuvir plus daclatasvir with or without ribavirin in Egyptian patients with genotype 4 hepatitis C
virus infection. Patients and methods: This prospective study included 200 Egyptian patients with
chronic genotype 4 HCV, treated with sofosbuvir plus daclatasvir with or without ribavirin for 12
weeks. Evaluation of number of non-responders, their demographics, and evaluation of C-X-C motif
chemokine- 10(CXCL-10) level, interleukin 12 (IL 12) and natural killer (NK) cell phenotype
pretreatment and12 weeks of treatment. Results: A total of 92.5% of all patients achieved SVR12.
SVR12 rates of 96.29% and 84.61% were reported in non-cirrhotic and cirrhotic patients, respectively.
Older age, cirrhosis, low platelet count, high level of CXC-L 10 , lower NK cell frequency and lower
frequency of the NK subset CD56−CD16+
were the predictors of treatment non-response. Conclusion:
Based on this prospective study, sofosbuvir plus daclatasvir with or without ribavirin for 12 weeks
appears to have favorable outcomes in the treatment of genotype 4 HCV-infected Egyptian patients.
Older age, cirrhosis, and low platelet count, high level of CXC-L 10 , lower NK cell frequency and lower
frequency of the NK subset CD56-CD16+ are independent risk factors of treatment non-response.
Keywords
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