Inhibitor incidence after intensive FVIII replacement for surgery in mild and moderate haemophilia A: a prospective national study in the Netherlands

Inhibitor development is currently the most severe complication in mild/moderate haemophilia A patients, causing increased bleeding tendency, hospitalization and mortality. It has been suggested that receiving high doses of factor VIII (FVIII) concentrates for surgical procedures is an important risk factor for inhibitor development in these patients. The current multicentre study aimed to determine prospectively the incidence of inhibitor development after intensive FVIII replacement therapy for surgical procedures in patients with mild/moderate haemophilia A. All consecutive patients with mild/moderate haemophilia A were included when they required at least 10 similar to 000 iu of FVIII concentrates (or 250 iu/kg) for 5 or more days for a surgical procedure. Potential clinical risk factors for inhibitor development and results of inhibitor tests were collected. Forty-six patients with a median age of 54 similar to years (interquartile range, 4059 similar to years) were included in the study. F8 genotyping revealed 20 different missense mutations. Patients received either recombinant (65%) or plasma-derived FVIII concentrates (35%) by intermittent bolus injections (41%) or continuous infusion (57%). Two patients developed a low titre inhibitor post-operatively. The incidence of inhibitor development following intensive treatment for surgery in this unselected prospective cohort of mild/moderate haemophilia A patients was 4% (95% confidence interval, 0.514.8)

Platelet reactivity in patients with venous thrombosis who use rosuvastatin: a randomized controlled clinical trial

Background Statins may exert a protective effect against the risk of venous thrombosis (VT), but the mechanism is unclear. Objectives In this open-label, randomized clinical trial ( NCT01613794), we aimed to determine the ex vivo effect of rosuvastatin on platelet reactivity in patients with a history of VT. Methods Platelet reactivity, in platelet reaction units (PRUs), was measured at baseline and after 28 days with VerifyNow, which uses arachidonic acid to determine thromboxane-mediated platelet aggregation, in 50 consecutive patients included in our study (25 receiving rosuvastatin and 25 without intervention). Results Forty-seven of 50 (94.0%) consecutively enrolled patients had two valid PRU measurements. The mean PRUs in rosuvastatin users were 609 at baseline and 613 at the end of the study (mean change 5; 95% confidence interval [CI] - 18 to 27). The mean PRUs in non-users were 620 at baseline and 618 at the end of the study (mean change - 2; 95% CI - 15 to 12). The mean difference in PRU change between users and non-users was 6 (95% CI - 20 to 33). After exclusion of patients who used antiplatelet medication, or had thrombocytopenia, similar results were obtained, i.e. no apparent effect of rosuvastatin on PRUs, with a mean difference in PRU change between users and non-users of - 1 (95% CI - 20 to 19). Conclusions Rosuvastatin does not affect platelet reactivity when arachidonic acid is used as an agonist in patients with a history of VT

Agreement between Coaguchek XS and STA-R Evolution (Hepato Quick) INR results depends on the level of INR

Introduction: Introducing point-of-care (POC) INR measurement to monitor anticoagulant therapy may be beneficial for both patients and anticoagulation clinics. However, agreement between POC and laboratory INR results is still unclear, especially at sub-and supratherapeutic levels. Therefore we investigated the analytical and clinical agreement between POC INR results of the Coaguchek XS and laboratory INR results of the STA-R Evolution. Materials and Methods: Paired POC and laboratory INR results were obtained and analyzed in 3257 patients aged 18-104 years between August 2008 and March 2014. Results: Mean difference between POC and laboratory results ranged from -0.18 (95% CI-0.20;-0.16) INR point for POC results 2.0-3.0, up to 1.14 (95% CI 0.87; 1.42) INR point for POC results 7.1-8.0. In the therapeutic range (POC INR 2.0-4.0), mean difference between POC and laboratory results was -0.13 (95% CI -0.15;-0.12) INR point. At subtherapeutic (POC INR <2.0) and supratherapeutic (POC INR >4.0) INR levels, mean differences were-0.13 (95% CI-0.15;-0.11) and 0.72 (95% CI 0.63; 0.80) INR point, respectively. Clinical agreement regarding therapeutic range was present in 92.0% (POC within range), 67.7% (POC below range) and 87.6% (POC above range) of the paired measurements. We observed >= 15% INR difference between the POC and laboratory result in 14.8% (POC INR 2.0-4.0), 17.0% (POC INR < 2.0) and 47.8% (POC INR >4.0) of the paired measurements. Conclusions: POC and laboratory INR results were strongly correlated within the therapeutic range and differences between results become larger with increasing INR. Clinical disagreement between laboratory and POC results occurs often at both sub-and supratherapeutic INR levels. (C) 2015 Elsevier Ltd. All rights reserved