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Design

Baseline characteristics in Cohort A (cirrhosis, pre-transplantation), median or %

Baseline characteristics (post-transplantation), median or %

Virologic response

Virologic resistance

• Relapse in 7% (3/42) with baseline NS5A resistance-associated variants versus 4% (10/269) in patients without baseline NS5A RAVs
• No relapse in patients treated 24 weeks
• Of the 13 relapses,
  • 11 (85%) had emergence of NS5A RAVs
    • M28T
    • Q30H/R
    • H58D
    • Y93H/C

Liver transplantation in Cohort A

• N = 7 (4 during study treatment and 3 after completing treatment)

Deaths, N = 13

• Cohort A, Child-Pugh B, N = 3 ; Child-Pugh C, N = 3
• Cohort B, Child-Pugh A, N = 2 ; Child-Pugh B, N = 5 ; Child-Pugh C, N = 0

Serious Adverse events, N = 77 (23%)

• 30 (28.3% in cohort A
• 47 (20.5%) in cohort B

Discontinuation for adverse event, N = 13 (4%)

• 5 in Cohort A
• 8 in cohort B
• Reasons for discontinuation : sepsis or infection (n = 3), acute renal failure (N = 2), gastric hemorrhage (N = 1), ALT + AST increase (N = 1), dyspnea (N = 1)

Summary

• LDV/SOF + RBV for 12 weeks is an effective treatment for patients with advanced liver disease, including those with decompensated liver function before and after liver transplantation.
  • Extending treatment to 24 weeks was not associated with improved outcomes, although there were no relapses in these groups
• Rates of SVR₁₂ were over 85% in every group of patients with Child-Pugh class B decompensated cirrhosis - in those who had and had not undergone liver transplantation-, as well as those who received 12 and 24 weeks of treatment.
• Similar response rates were observed in Child-Pugh class C patients who had not undergone liver transplantation
• Results are very encouraging for fibrosing cholestatic hepatitis which may now be a manageable complication of liver transplantation
• SVR₁₂ in patients with decompensated cirrhosis was associated with early improvements in Child-Pugh and MELD scores
• Patients with decompensated liver disease experienced high frequencies of RBV hematotoxicity