Erratum to “Preventive Strategies against Bleeding due to Nonvitamin K Antagonist Oral Anticoagulants”

Abstract

In the paper titled "preventive strategies against bleeding due to nonvitamin K antagonist oral anticoagulants, " the authors' given first and last names were inverted. Here we provide the right authors' information as shown above.

Effect of tramadol and DOACs with special attention to dabigatran on concomitant use, on the risk of mayor bleeding using BIFAP database in Spain

“…Some of the preventive strategies against bleeding due to use of oral anticoagulants include improvement of appropriate prescription, tailoring DOAC doses, identifying drug interactions and identifying modifiable risk factors. For the latter, it has been proposed to screen conditions that may lead to major bleeding events before initiating the NOAC therapy such as history of gastrointestinal bleeding, esophageal varices, and so forth 36 . Several studies have evaluated the protective effect of acid suppressants on anticoagulant‐related gastrointestinal bleeding (GIB) which represented 82.6% of all our major bleed cases in our study.…”

“…For the latter, it has been proposed to screen conditions that may lead to major bleeding events before initiating the NOAC therapy such as history of gastrointestinal bleeding, esophageal varices, and so forth. 36 Several studies have evaluated the protective effect of acid suppressants on anticoagulant-related gastrointestinal bleeding (GIB) which represented 82.6% of all our major bleed cases in our study. The results from a meta-analysis showed how proton pump inhibitors (PPIs) showed a protective effect against GIB episodes, but there was no evidence towards dabigatran related GIB.…”

How to manage patients on rivaroxaban in the emergency department: a statement of the Italian society of emergency medicine advisory board

“…In detail, patients should receive Oral bioavailability [7] For 10 mg tablets: 80-100% (with or without food) For 15 and 20 mg tablets: 66% (without food); ≥ 80% (with food) Peak concentration (hours to C max ) [8] 2-4 Volume of distribution [9] ∼ 50 l (0.62 l/kg) -low tissue penetration Half-life (h) [8,10] 5-9 (healthy young individuals) 11-13 (elderly individuals) Clearance [11] Renal: 1/3 of the active unchanged drug After hepatic degradation to inactive metabolite 1/2 renal 1/2 biliary Enzymes involved in degradation [12] CYP 3A4/2J2 Transporters involved in renal secretion [12] P-glycoprotein and BCRP (ABCG2) Interactions [12] P-glycoprotein and CYP3A4 moderate inhibitors Protein binding (%) [13] 92-95% (mainly serum albumin) Dialyzable No information on all of the topics shown in Fig. 1 [25,26]. Patients should also be warned about the importance of not discontinuing treatment, unless otherwise stated by a physician, and about conditions that may cause dehydration.…”

Management of Non-Vitamin K Antagonist Oral Anticoagulants in the Perioperative Setting

“…Dabigatran etexilate is metabolized in dabigatran in the plasma and liver via CYP450-independent mechanisms [ 38 ], but DE acts as a substrate for P-gp. Therefore, strong inhibitors or inducers of P-gp may alter the absorption of DE [ 39 ]. Rivaroxaban and apixaban are metabolized by CYP3A4/5 and are both substrates for P-gp.…”

“…Rivaroxaban and apixaban are metabolized by CYP3A4/5 and are both substrates for P-gp. Thus, drugs that strongly inhibit or induce CYP3A4 or P-gp or both influence the pharmacokinetic (PK) profile of these NOACs [ 39 , 40 ].…”