Early virologic response (EVR) is defined as a ≥2 log reduction or complete absence of serum HCV RNA at week 12 of therapy compared with the baseline level. Failure to achieve EVR is the most accurate predictor of not achieving SVR. Undetectable virus at the end of therapy is referred to as end-of-treatment virologic response (ETVR), which does not accurately predict SVR but is necessary for it to occur. Virologic Cell Cycle inhibitor breakthrough refers to the reappearance of HCV RNA while still on therapy, and virologic relapse is the reappearance of
HCV RNA in serum after treatment is discontinued after ETVR is achieved. Previous studies have shown that weight-based ribavirin is more effective than a fixed dose of ribavirin in inducing SVR, and a suboptimal dose of ribavirin is an important cause of virologic relapse; thus, weight-based ribavirin is recommended to reduce the virologic relapse rate.10 In the paper by Shin et al. factors associated with virologic relapse are explored in a cohort of Korean CHC patients who received PEG-IFN plus RBA treatment (weight-based dose for HCV genotype 1 patients and fixed dose for genotype 2 or 3 patients) and achieved ETVR. Baseline factors between patients with and without
SVR were compared and analyzed. They found that risk factors for relapse were age older than 50 years and, in genotype 1 cases, higher baseline HCV RNA level (≥2 000 000 IU/mL), while lower mTOR inhibitor adherence to PEG-IFN (<80%) was important in genotype 2 or 3 patients. These findings
not only confirm the importance of compliance and adherence to treatment, but also suggest that genotype 1 patients older than 50 years and with higher baseline HCV RNA level (≥2 000 000 IU/mL), have a lower chance of treatment success. The authors speculated that such cases may benefit from longer treatment duration than currently recommended. However, several issues are worthy of discussion. First, early viral kinetic parameters, such as RVR and EVR have been documented to be the most important factors predictive of therapeutic response in CHC patients treated with combination therapy. However, such viral kinetic data are lacking in most patients in this study. Second, Basso et al.11 indicated that only alanine aminotransferase Amisulpride (ALT) elevation in the later course of antiviral therapy of HCV RNA-negative patients was associated with virologic relapse, whereas pretreatment demographic (age, gender), clinical (ALT levels, histological grade and stage, body mass index) and viral (load, genotype) parameters failed to correlate with this phenomenon. It is known that older age, higher baseline viral load, and poor adherence to therapy are predictors of SVR. Thus the present results reported here are not surprising and cannot be simply interpreted as factors required for the implementation of prolonged therapy.