Summary In randomized controlled trials of patients with chronic HCV infection, elbasvir/grazoprevir (EBR/GZR) demonstrated high cure rates and a good safety profile. This study assessed the effectiveness and safety of EBR/GZR, with and without ribavirin, in a real‐world HCV patient cohort. HEPA‐C is a collaborative, monitored national registry of HCV patients directed by the Spanish Association for the Study of the Liver and the Networked Biomedical Research Centre for Hepatic and Digestive Diseases. Patients entered into HEPA‐C between December 2016 and May 2017, and treated with EBR/GZR with at least end‐of‐treatment response data, were included. Demographic, clinical and virologic data were analysed, and adverse events (AEs) recorded. A total of 804 patients were included in the study. The majority were male (57.9%), with a mean age of 60 (range, 19‐92) years. Genotype (GT) distribution was GT 1, 86.8% (1a, 14.3%; 1b, 72.5%); GT 4, 13.2% and 176 patients (21.9%) were cirrhotic. Overall, among 588 patients with available data, 570 (96.9%) achieved sustained virologic response at 12 weeks post‐treatment (SVR12). SVR12 rates by genotype were GT 1a, 97.7%; GT 1b, 98.6%; and GT 4, 98.1%. No significant differences in SVR12 according to fibrosis stage were observed. Eighty patients experienced an AE, resulting in treatment discontinuation in three. In this large cohort of patients with chronic HCV managed in a real‐world setting in Spain, EBR/GZR achieved high rates of SVR12, comparable to those observed in randomized controlled trials, with a similarly good safety profile.

SUMMARY BackgroundSustained virological response rates of up to 52% have been obtained with peginterferon a2a (40 kDa) plus ribavirin in patients suffering from chronic hepatitis C genotype 1 in randomized-controlled trials.

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The effects of vanadate on the contractility of the guinea-pig isolated trachea was examined. Vanadate (0.1 mM) produced a sustained contraction that was abolished in Ca(2+)-free EGTA (0.1 mM)-containing physiological salt solution but was resistant to verapamil (1 microM). Vanadate (0.1 mM) depressed tracheal responses to CaCl2 (in Ca(2+)-free depolarizing solution), KCl, acetylcholine, histamine and 5-hydroxytryptamine. For vanadate (10 microM), the inhibition of spasmogenic responses only reached statistical significance for histamine and 5-hydroxytryptamine. Caffeine (1 mM)-induced spasm (trachea at 20 degrees C in the presence of indomethacin (2.8 microM)) was not affected by vanadate (10 microM-0.1 mM). Vanadate (0.1 mM) slightly depressed the responses to KCl (50 mM), acetylcholine (1 mM), histamine (1 mM) or 5-hydroxytryptamine (0.1 mM) observed in Ca(2+)-free EGTA (0.1 mM)-containing physiological salt solution. Vanadate (0.5 mM) depressed Ca2+ (20 microM)-induced contraction of trachea which had been chemically skinned of its plasmalemmal membranes. The mechanism of the inhibitory effect of vanadate on tracheal responses to a variety of spasmogens remains obscure, but, under in-vitro conditions, vanadate clearly does not induce hyper-reactivity of airway smooth muscle to spasmogens.

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