Clinical & Medical Case Reports

Our patient was a 58-year-old man with HCV diagnosed four years ago. He had no co-morbidities and his brother was also diagnosed HCV. There were no risk factors. His fi brosis stage by Ishak was F5 four years ago and he was treatment- experienced with pegylated interferon- RBV. On initial evaluation, he was asymptomatic and examination was unremarkable. Laboratory testing revealed elevated transaminase levels and HCV genotype 1b with a viral load of 4.2+E6 IU/mL. The patient was treated with 12-week course of SOF (400 mg daily)/ LDV (90 mg daily) and RBV (1000 mg daily). In the first month of the therapy there was rapid normalization transaminase levels and clearance of the virus however, no side effects of therapy have found. The compliance of the treatment was certainly perfect. Three months after completing treatment, virological relapse was occurred with a HCV RNA 4.0+E5 IU/mL and his transaminase levels were slightly elevated.

 

Methods: The patient was categorized as CHC according to the European Association for the Study of the Liver Clinical Practice Guidelines. Blood sample with K2EDTA was immediately separated by centrifugation, liquated, and kept at -80ËšC until required. The presence of anti- HCV was tested for the sample which was anti-HCV positive through ELISA testing, using a commercial kit (Cobas E601 Analyzer Roche Diagnostic- Mannheim, Germany). In addition, for protease inhibitors; asunaprevir, boceprevir, faldaprevir, grazoprevir, pariteprevir, simeprevir, telaprevir, for NS5A inhibitors; daclatasvir, elbasvir, ledipasvir, ombitasvir, velpatasvir, and for NS5B inhibitors; dasabuvir and sofosbuvir were analyzed in the HCV NS3, NS5A and NS5B sequencing, respectively.

 

Discussion: Our patient was one among the rare occurrences of the cases in whom viral relapse occur after achieving end-of-treatment response with LDV/SOF. Inspite of the compliance of the treatment, infected with genotype 1b and addition of RBV, with no reinfection and no comorbidity; the patient had only three poor prognostic factors: cirrhosis, male gender and treatment was experienced. Molecular analysis demonstrated that Y93H as a cross - resistant mutation for NS5A region related resistance mutation was determined. In addition, S282G and C316S were determined as amino acid substitution for NS5B region. NS5A resistance associated mutation (Y93H) could be eff ective in relapse in LDV/SOF therapy. However, in Turkey, this case with Y93H mutation was the fi rst to be reported.