Summary
Background
With the development of direct‐acting anti‐virals (DAAs), almost all patients with chronic hepatitis C virus (HCV) infection can achieve sustained viral response (SVR).
Aim
To ...evaluate the short‐term risk of HCC among patients with SVR by DAAs, including those with cirrhosis or previous HCC.
Methods
This large‐scale, multicentre cohort study included 1,675 consecutive patients who achieved SVR by treatment with interferon‐free sofosbuvir‐based regimens, divided into groups with (n = 152) or without previous HCC (n = 1,523). The Kaplan‐Meier method and Cox proportional hazard analysis were used to calculate the cumulative HCC incidence and related factors of HCC.
Results
During the follow‐up period (median: 17 months), 46 (2.7%) patients developed HCC. The 1‐year cumulative rates of de novo HCC were 0.4% and 4.9% for the noncirrhosis and cirrhosis groups respectively (log‐rank test: P < 0.001). For cirrhotic patients, serum α‐fetoprotein level at the end of treatment (EOT‐AFP) was the strongest predictor of de novo HCC. The 1‐year cumulative de novo HCC rates were 1.4% and 13.1% in the EOT‐AFP < 9.0 ng/mL and ≥ 9.0 ng/mL groups (cut‐off value) respectively (log‐rank test: P < 0.001). The 1‐year cumulative rates of HCC recurrence were 6.5% and 23.1% for the noncirrhosis and cirrhosis groups respectively (log‐rank test: P = 0.023). For cirrhotic patients, previous HCC characteristics were significantly associated with HCC recurrence. In contrast, sex, age and metabolic features did not influence de novo HCC or recurrence.
Conclusions
For cirrhotic patients after elimination of HCV, serum EOT‐AFP level and previous HCC characteristics would be useful markers for predicting de novo HCC or recurrence.
Linked ContentThis article is linked to Tan and Lim paper. To view this article visit https://doi.org/10.1111/apt.14437.
Summary
Background
Antiviral treatment is recommended for chronic hepatitis C patients with advanced fibrosis to reduce and prevent cirrhosis‐related complications.
Aim
To evaluate the efficacy and ...safety of telaprevir (TVR)‐based triple therapy for patients with advanced fibrosis in a clinical practice setting.
Methods
This prospective, multicentre study consisted of 102 patients with advanced fibrosis (METAVIR score F3‐4) who were infected with HCV genotype 1b. All received 12 weeks of TVR in combination with 24 weeks of pegylated interferon (PEG‐IFN) α2b and ribavirin (RBV).
Results
The sustained virological response (SVR) rate was 69.6% (71 of 102). Notably, for treatment‐naïve and prior relapse patients the SVR rate was over 80%. Previous treatment response, interleukin 28B polymorphism (rs8099917) and rapid virological response (undetectable HCV RNA at week 4) were independently associated with SVR. To achieve SVR, an adequate dosage of PEG‐IFNα2b (≥1.2 μg/kg/week) and RBV (≥7.5 mg/kg/day) is preferable; however, the mean weight‐adjusted TVR dosage had little impact on treatment outcome. Although severe blood cytopaenia and a dermatological disorder were frequently found, the rate of discontinuation due to adverse effects was 12.7%. The inosine triphosphatase CC allele (rs1127354) was independently associated with the development of severe anaemia, and lower serum albumin level (<35 g/L) was associated with the occurrence of infection.
Conclusions
The great gain in the SVR rate by telaprevir‐based triple therapy offsets the problems with adverse effects; thus, it should be considered as a potent treatment protocol for patients with advanced fibrosis, especially for those with treatment‐naïve and prior relapse.
Summary
Favourable efficacy and safety profiles for simeprevir in combination with pegylated interferon alpha (PEG‐IFNα) and ribavirin (triple therapy) have been shown in clinical trials. This study ...was carried out to evaluate the effectiveness of simeprevir‐based triple therapy for patients with prior telaprevir treatment failure. This multicentre, observational cohort consisted of 345 consecutive Japanese patients infected with HCV genotype 1b, including 20 who had experienced telaprevir‐based triple therapy. Amino acid substitutions in the NS3/4A region were identified by direct sequencing at the time of relapse or breakthrough in treatment with telaprevir and at the initiation of treatment with simeprevir. Patients were stratified according to prior response to PEG‐IFNα and ribavirin. Of the 20 patients with telaprevir treatment failure, 10 (50.0%) achieved sustained virological response at week 12 after the end of treatment (SVR12). For patients treatment naïve 3/4 (75.0%) or with prior relapse 1/1 (100%) or partial response 5/6 (83.3%) to PEG‐IFNα and ribavirin, almost all achieved SVR12, mainly because of the improvement of treatment adherence, especially to direct‐acting antiviral agent and ribavirin. However, of the nine patients with prior null response to PEG‐IFNα and ribavirin, only one (11.1%) achieved SVR12, despite all having received an adequate treatment dosage, and five (55.6%) achieved rapid virological response. The treatment outcome of simeprevir‐based triple therapy for HCV genotype 1b patients with prior telaprevir failure depended on the prior response to PEG‐IFNα and ribavirin. For patients with prior null response to PEG‐IFNα and ribavirin, retreatment with simeprevir‐based triple therapy is not a useful option.
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