This is truly a remarkable achievement in the field of HCV treatment. It is only partially applicable to genotype 1a patients around the world, but nonetheless brings us closer to what we seek in HCV therapy: all-oral, highly effective treatment. This publication marks a turning point in the HCV drug development Torin 1 cost world. It demonstrates that a protease and an NS5A inhibitor together can achieve an extremely high SVR in null responders, at least in genotype 1b. It is the second trial to show that an SVR is possible without either IFN or RBV in null responders. In the patois of HCV drug development, we often speak of

an all-oral regimen as the Holy Grail we all seek. In history that term has had many meanings, particularly in Arthurian legends beginning in the late 12th century. The meaning that comes closest, though, Ganetespib in vitro to what we really intend is found in Wolfram von Eschenbach’s Parzival. He

portrays the grail as a stone that prevents anyone who sees it from dying. The development of an oral regimen of DAAs that can produce SVR in a high proportion of patients is the grail that we seek. It will prolong life and prevent death from liver disease, just as the epidemic is reaching crisis proportions. The two studies in this issue of Hepatology bring us much closer to providing the answer to the epidemic. “
“Background and Aims:  A pH of more than 6 is required for clot stability and hemostasis. Intravenous proton pump inhibitors have a rapid onset of action compared to oral and have been preferred for management of non-variceal bleeding. MCE Intravenous pantoprazole has been used extensively. Buffered esomeprazole (BE) is an oral preparation consisting of an inner core of non-enteric-coated

esomeprazole with a shell of sodium bicarbonate. The buffer protects against acid degradation of esomeprazole in addition to immediate antacid action. The aim of this study was to assess the efficacy of BE for raising and maintaining an intragastric pH of more than 6 in comparison to i.v. pantoprazole in equivalent dosing. Methods:  A randomized two-way cross-over study was conducted. Ten healthy volunteers were randomized to twice daily BE 40 mg or pantoprazole 40 mg i.v. bolus. Intragastric pH was measured with a wireless pH radiotelemetry capsule (Bravo, Medtronic). A 2-week washout period was given between doses. Results:  BE achieved a steady pH of more than 6 in a median time of 2 min (range 1–5 min) after the first dose. The mean % time that intragastric pH was more than 6.0 for BE was 96%, and 90% of the 24-h period compared to pantoprazole (47% and 18%), P = 0.000. A median pH (interquartile range) for the BE group was 6.2 (6.175–6.2) which was higher than i.v. pantoprazole 4.60 (4.5–5.0) (P = 0.005). Conclusion:  BE achieves and maintains a pH of more than 6 within minutes of administration. It was significantly superior to i.v. pantoprazole in equivalent dosing.