POSTER PRESENTATIONS Methods: We have prospectively included the first 90 patients since the initiation of the program in April 2015. Results: 60% were males, mean age was 57 years (32–81). 88% of the patients were genotype 1. 71% were treatment naïve. 8% were F0-1, 22% F2, 26% F3 and 44% F4. Mean MELD score was 7 (6–15). Patients were treated with a combination of Ombitasvir/Paritaprevir/ritonavir alone (6%) or in combination with Dasabuvir (63%), or with Sofosbuvir combined with Ledipasvir (29%) or Daclatasvir (2%). 51% received ribavirin. Sustained virological response was achieved in 98% of the cases. Creatinine values were increased by 10% after 24 weeks from the end of treatment ( p < 0.000). The worsening occurred during the first 4 weeks of treatment, and then stabilized, but did not return to baseline values after cessation of therapy. Creatinine values among males and females were significantly different, but increased over time in a similar degree (10% rise in plasma cratinine for males, 9% for females). Patients with prior kidney injury presented worse renal impairment compared to those without such diagnosis (33% vs. 9%, p = 0.029). Patients who received ACE inhibitors or Angiotensin II receptor antagonists had significantly more renal impairment than those not on them (17% vs. 6%, p = 0.028), although these drugs did not induce renal impairment on their own. Creatinine increased with the degree of liver fibrosis, despite the fact that fibrosis did not alter the degree of renal impairment seen with DAA treatment. The type of DAA used did not influence the renal impairment seen, nor did the use of ribavirin. No changes were seen in creatinine with genotype, previous treatment for hepatitis C, presence of diabetes or hypertension, or treatment with biguanides or NSAIDs. Conclusions: The time course of renal impairment and the absence of differences between different DAA suggest that it could be reactive to viral clearance. Clinical relevance of such finding is unclear, as no long term follow up is available, but creatinine values did not return to normal 24 weeks after the end of treatment. Close monitoring of patients with preexisting renal injury or receiving ACE inhibitors or Angiotensin II inhibitors should be granted. SAT-233 High SVR rates with eight and twelve weeks of pangenotypic glecaprevir/pibrentasvir: integrated efficacy and safety analysis of genotype 1–6 patients without cirrhosis M. Puoti1, G. Foster2, S. Wang3, D. Mutimer4, E. Gane5, C. Moreno6, T.T. Chang7, S.S. Lee8, R. Marinho9, J.-F. Dufour10, S. Pol11, C. Hezode12, S.C. Gordon13, S.I. Strasser14, P.J. Thuluvath15, R. Liu3, T. Pilot-Matias3, F. Mensa3. 1AO Ospedale Niguarda Ca Granda, Milan, Italy; 2Queen Mary University of London, Barts Health, London, United Kingdom; 3ABBVIE, North Chicago, United States; 4Queen Elizabeth Hospital and NIHR Liver Biomedical Research Unit, Birmingham, United Kingdom; 5University of Auckland, Auckland, New Zealand; 6CUB Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium; 7National Cheng Kung University Hospital, Tainan City, Taiwan; 8University of Calgary, Calgary, Canada; 9 Hospital S. Maria, Medical School of Lisbon, Lisbon, Portugal; 10 Hepatology, University Clinic for Visceral Surgery and Medicine, Bern University Hospital, Bern, Switzerland; 11Groupe Hospitalier CochinSaint Vincent De Paul, Paris; 12Hôpital Henri Mondor, AP-HP, Université Paris-Est, Créteil, France; 13Henry Ford Health System, Detriot, United States; 14Royal Prince Alfred Hospital, Sydney, Australia; 15Mercy Medical Center & University of Maryland School of Medicine, Baltimore, United States E-mail:
[email protected] Background and Aims: The pangenotypic direct-acting antivirals (DAAs) glecaprevir (formerly ABT-493; NS3/4A inhibitor developed by AbbVie and Enanta) and pibrentasvir (formerly ABT-530; NS5A inhibitor), comprise the interferon (IFN)- and ribavirin (RBV)-free regimen G/P. In seven phase 2/3 clinical trials, G/P achieved SVR12 rates of 92–100% across all six major HCV genotypes (GTs). Here we present an integrated analysis from these studies on the efficacy of 8 and 12 weeks of G/P treatment in non-cirrhotic patients with GT1-6 infection.
Methods: Data were pooled from the phase 2 SURVEYOR-I and –II, and phase 3 EXPEDITION-4 and ENDURANCE 1, 2, 3 and 4 studies. Patients with chronic HCV GT 1, 2, 3, 4, 5 or 6 infection without cirrhosis received G/P without RBV for either 8 or 12 weeks. Patients were either treatment-naïve or treatment-experienced with IFNbased or sofosbuvir (SOF)-based regimens. Patients experienced with a DAA other than SOF were excluded. Efficacy was evaluated as the rate of sustained virologic response (HCV RNA
