Oral Direct-acting Agent Therapy for Hepatitis C Virus Infection a Systematic Review

Review

. 2017 May ii;166(9):637-648.

doi: 10.7326/M16-2575. Epub 2017 Mar 21.

Oral Direct-Acting Agent Therapy for Hepatitis C Virus Infection: A Systematic Review

Affiliations

  • PMID: 28319996
  • PMCID: PMC5486987
  • DOI: 10.7326/M16-2575

Free PMC article

Review

Oral Direct-Acting Amanuensis Therapy for Hepatitis C Virus Infection: A Systematic Review

Oluwaseun Falade-Nwulia  et al. Ann Intern Med. .

Costless PMC article

Abstract

Groundwork: Rapid improvements in hepatitis C virus (HCV) therapy accept led to the approval of multiple oral straight-acting antiviral (DAA) regimens by the U.S. Nutrient and Drug Administration (FDA) for handling of chronic HCV infection.

Purpose: To summarize published literature on the efficacy and safety of oral DAAs for handling of persons with chronic HCV infection.

Data sources: MEDLINE and EMBASE from inception through 1 Nov 2016.

Report selection: 42 English-linguistic communication studies from controlled and single-grouping registered clinical trials of adults with HCV infection that evaluated at least viii weeks of an FDA-approved interferon-free HCV regimen that included at least ii DAAs.

Data extraction: Two investigators abstracted data on written report design, patient characteristics, and virologic and safety outcomes sequentially and assessed quality independently.

Data synthesis: Six DAA regimens showed high sustained virologic response (SVR) rates (>95%) in patients with HCV genotype 1 infection without cirrhosis, including those with HIV co-infection. Constructive treatments for HCV genotype 3 infection are limited (2 DAA regimens). Patients with hepatic decompensation, particularly those with Kid-Turcotte-Pugh class C disease, had lower SVR rates (78% to 87%) than other populations. The improver of ribavirin was associated with increased SVR rates for sure DAA regimens and patient groups. Overall rates of serious adverse events and treatment discontinuation were low (<10% in the general population); regimens that included ribavirin had more than mild or moderate adverse events than those without.

Limitations: Twenty-3 studies had moderate adventure of bias (10 were open-label unmarried-group trials, 11 had limited information on darkening of the allocation scheme, and 5 had selective outcome reporting). All but 1 of the studies were manufacture-funded. Heterogeneity of interventions precluded pooling.

Conclusion: Multiple oral DAA regimens show high rates of prophylactic, tolerability, and efficacy for treatment of HCV genotype one infection, particularly amid persons without cirrhosis.

Principal funding source: Patient-Centered Outcomes Research Institute. (PROSPERO: CRD42014009711).

Conflict of interest argument

Authors not named here have disclosed no conflicts of interest.

Figures

Figure 1
Figure 1. Summary of testify search and selection

FDA = U.S. Food and Drug Administration; SVR = sustained virologic response.

Figure 2
Figure ii. HCV genotype 1a and 1b SVR12 rates and 95% CIs, by oral DAA regimen and clinical trial

DAA = direct-acting antiviral; DAV = dasabuvir; DCV = daclatasvir; EBV = elbasvir; GZP = grazoprevir; HCV = hepatitis C virus; LDV = ledipasvir; OBV = ombitasvir; PLAC = placebo; PTV–r = paritaprevir–ritonavir; RBV = ribavirin; SIM = simeprevir; SOF = sofosbuvir; SVR12 = sustained virologic response at 12 wk; VEL = velpatasvir.

Figure 3
Effigy three. HCV genotype 2 to 6 SVR12 rates and 95% CIs, by oral DAA regimen and clinical trial

DAA = direct-interim antiviral; DAV = dasabuvir; DCV = daclatasvir; EBV = elbasvir; GZP = grazoprevir; HCV = hepatitis C virus; LDV = ledipasvir; OBV = ombitasvir; PTV–r = paritaprevir–ritonavir; RBV = ribavirin; SIM = simeprevir; SOF = sofosbuvir; SVR12 = sustained virologic response at 12 wk; VEL = velpatasvir.

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Source: https://pubmed.ncbi.nlm.nih.gov/28319996/

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