Cobas ampliprep cobas taqman hcv test

The patients were carefully monitored for clinical symptoms and adverse events (AEs) including serious adverse events (SAEs) during the treatment and follow-up. Laboratory data including routine blood tests, biochemical liver and renal function and HCV RNA were regularly monitored at baseline, week 4 of therapy, the end of therapy (week 12 or week 24), and at week 12 after the completion of therapy. Additional laboratory tests might be performed in some patients with the request of patient and the consultation of referring physician. Efficacy was measured by sustained virologic response at post-treatment week 12 (SVR12). Serum HCV RNA was quantified by reverse-transcription polymerase chain reaction (RT-PCR) using the Cobas AmpliPrep/COBAS TaqMan HCV Test (Roche Diagnostics, Branchburg, NJ, USA), which has a lower limit of 15 IU/mL for HCV RNA quantification. HCV genotype was determined using RT-PCR with genotype-specific primers from the 5′noncoding region of the virus. Routine blood tests and biochemical liver and renal functions were determined using standard procedures. The primary endpoint was SVR12, which was defined as serum HCV RNA undetectable at 12 weeks after the end of therapy. The secondary endpoints were the treatment-related AEs and laboratory abnormalities.

Cytokine and growth factor concentrations in patients with CHC were determined at four different time points. The first time point represented serum samples obtained from patients with CHC before antiviral treatment. Serum samples from the same patients were also collected after four, eight and 12 weeks of treatment (second, third and fourth time point). The samples were stored at −80 °C to avoid repeated freeze and thaw cycles. Quantification of HCV RNA was performed with COBAS AmpliPrep/COBAS TaqMan HCV Test (Roche Diagnostics, Manheim, Germany) as recommended by the manufacturer.

Viral nucleic acid extraction and quantification were performed using the COBAS® AmpliPrep/COBAS® TaqMan® HCV Test (Roche Molecular Diagnostics, Almere, Netherlands), according to manufacturer’s instructions.

Patients with CHC who received a complete course of DAA therapy from September 2012 to December 2017 were enrolled in this retrospective analysis. Inclusion criteria were as follows: age ≥ 18 years, presence of the serum anti-hepatitis C virus (HCV) antibody for > 6 months and detectable HCV RNA (detection limit = 15 IU/mL; COBAS Ampliprep/COBAS TaqMan HCV test, Roche Diagnostics, Branchburg, NJ, USA), and completion of DAA therapy. Exclusion criteria were as follows: presence of liver disease caused by other etiologies, decompensated liver disease, hepatocellular carcinoma at baseline, comorbid diseases or cancer, and concurrent use of eltrombopag or immunomodulatory agents. Demographic data, complete blood count analysis results, and biochemical data were collected at baseline, week 2, week 4, EOT, and PW12. Paired LSMs were performed using acoustic radiation force impulse elastography (ARFI) at baseline and PW12 in a subgroup of patients (n = 199). This study was conducted in accordance with the 1975 Declaration of Helsinki. All patients provided written informed consent prior to enrollment, and this study was approved by the Research Ethics Committee of China Medical University Hospital, Taichung, Taiwan (CMUH106-REC2–105).