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Coleman C.I.,University of Connecticut | Tangirala M.,Bayer Health Care Pharmaceuticals | Evers T.,Bayer AG

A retrospective cohort analysis of the US MarketScan claims databases was performed to compare persistence and discontinuation rates between the vitamin K antagonist warfarin and the non-vitamin K antagonist oral anticoagulants rivaroxaban and dabigatran in patients with non-valvular atrial fibrillation. The analysis included adult patients with non-valvular atrial fibrillation newly initiated on rivaroxaban, dabigatran, or warfarin between November 1, 2011 and December 31, 2013, with a baseline CHA2 DS2 -VASc score≥ 2, two or more non-valvular atrial fibrillation diagnosis codes (427.31), and ≥6 months' continuous medical and pharmacy benefit enrollment before oral anticoagulant initiation. Propensity score matching was performed to match patients receiving rivaroxaban with those receiving dabigatran (1:1) and warfarin (1:1). Patients were followed until the first event of inpatient death, end of continuous enrollment, or end of study period. Medication persistence was defined as absence of a refill gap of >60 days. Discontinuation was defined as no additional refill for >90 days and through to end of follow-up. Hazard ratios (HRs) of oral anticoagulant persistence and discontinuation were estimated using Cox proportional hazard models. In total, 3,2634 patients were included (n = 10878/oral anticoagulant group). Rivaroxaban was associated with better persistence than both dabigatran (HR 0.64, 95% confidence interval [CI] 0.62-0.67) and warfarin (HR 0.62, 95% CI 0.59-0.64) and lower discontinuation than dabigatran (HR 0.61, 95% CI 0.58-0.64) and warfarin (HR 0.65, 95% CI 0.62-0.68). Realworld analysis of oral anticoagulant use may reveal whether the relatively high persistence/ low discontinuation demonstrated for rivaroxaban translates into lower rates of stroke. © 2016 Coleman et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Source

Llovet J.M.,Institute dInvestigacions Biomediques Sugust Pi i Sunyer IDIBAPS | Llovet J.M.,Catalan Institution for Research and Advanced Studies | Llovet J.M.,Mount Sinai School of Medicine | Pena C.E.A.,Bayer Health Care Pharmaceuticals | And 4 more authors.
Clinical Cancer Research

Purpose: Validated biomarkers of prognosis and response to drug have not been identified for patients with hepatocellular carcinoma (HCC). One of the objectives of the phase III, randomized, controlled Sorafenib HCC Assessment Randomized Protocol (SHARP) trial was to explore the ability of plasma biomarkers to predict prognosis and therapeutic efficacy. Experimental Design: In SHARP, 602 patients with advanced HCC were randomized to receive either oral sorafenib 400 mg twice a day per os or matching placebo daily on a continuous basis. Ten plasma biomarkers implicated in the pathogenesis of HCC were measured in 491 patients at baseline and in 305 after 12 weeks of treatment. The candidate biomarkers were analyzed to identify correlates of prognosis or predictors of response to sorafenib. Results: In both the entire patient population and the placebo cohort, baseline angiopoietin 2 (Ang2) and VEGF concentrations independently predicted survival. Clinical variables such as macroscopic vascular invasion, Eastern Cooperative Oncology Group (ECOG) performance status, and baseline α-fetoprotein and alkaline phosphatase concentrations also independently predicted survival in these groups. In the sorafenib cohort, trends toward enhanced survival benefit from sorafenib were observed in patients with high s-c-KIT or low hepatocyte growth factor concentration at baseline (P of interaction = 0.081 and 0.073, respectively). Conclusions: The angiogenesis biomarkers Ang2 and VEGF were independent predictors of survival in patients with advanced HCC. In contrast, none of the biomarkers tested significantly predicted response to sorafenib. ©2012 AACR. Source

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