Dabigatran etexilate/rabeprazole/warfarin
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Device-related thrombosis and upper gastrointestinal bleeding: 4 case reports In a case series, 4 patients [2 men and 2 women; including 3 patients aged 66–78 years; not all ages stated] were described, who developed device-related thrombosis (DRT) during anticoagulant treatment with dabigatran etexilate (1 patient) and following concomitant administration of dabigatran etexilate and rabeprazole (3 patients). Additionally, one of the 4 patients developed upper GI bleeding secondary to warfarin [not all dosages, routes, times to reaction onsets and outcomes stated]. Case 1: A 78-year-old woman, who had a 10-year history of hypertension, had been receiving valsartan and amlodipine for BP management. She presented with palpitations and chest discomfort following exercise. Based on the investigations, she was diagnosed with paroxysmal atrial fibrillation (AF). As her CHA2DS2-VASc score was 4, she was temporarily treated with unspecified vitamin-K antagonists. At a follow-up, one year following warfarin initiation, she was found unsuitable for continuous long-term oral anticoagulant (OAC) and hence, underwent percutaneous left atrial appendage closure (LAAC). At that time, no signs of thrombus were observed on transesophageal echocardiogram (TEE). She was discharged with an 8-week course of oral dabigatran 110mg two times a day with TEE follow-up. Additionally, rabeprazole 10mg two times a day was prescribed to reduce the risk of GI bleeding. Six weeks later, TEE showed the formation of thrombus on the occluder surface. Her DRT was attributed to dabigatran etexilate. Additionally, an interaction between dabigatran etexilate and rabeprazole led to decreased plasma concentration of dabigatran etexilate. Rabeprazole increased the gastric pH leading to decreased dissolution of dabigatran etexilate in presence of rabeprazole. Consequently, dabigatran etexilate was switched to warfarin. Over the following 6 weeks, gradual reduction of thrombosis on the occluder was noted and the decision was made to continue warfarin. Case 2: A woman presented following an ischaemic stroke for further evaluation. She reported recurrent palpitations and chest pain for 2 years. She had a history of hypertension and had uncontrolled high BP at that time. Based on the investigations, the diagnosis of paroxysmal AF was made. Her CHA2DS2- VASc score was 5 and hence, she started receiving OAC therapy with warfarin. However, over the following year, she developed upper GI bleeding secondary to warfarin. Consequently, she underwent LAAC under unspecified general anaesthetics. She was discharged with a 8-week course of oral dabigatran 110mg two times a day (at the age of 66 years) along with a follow-up TEE. She also received rabeprazole 10mg two times a day due to GI bleeding secondary to warfarin. Six weeks later, TEE indicated thrombosis in the anterolateral surface of the occluder. Consequently, dabigatran etexilate was switched to rivaroxaban. Her DRT was attributed to dabigatran etexilate. Additionally, an interaction between dabigatran ete
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