Thrombocytopenia Induced by Direct Oral Anticoagulants: a Clinical Case and Literature Review

Abstract

The last decade has dramatically changed the strategy of anticoagulant therapy in patients with atrial fibrillation. Direct oral anticoagulants have replaced vitamin K antagonists: either direct thrombin blockers (dabigatran) or factor IIa blockers (apixaban, rivaroxaban, edoxaban). According to the regulatory domestic and foreign documents, the use of direct oral anticoagulants in patients with atrial fibrillation has priority in comparison with vitamin K antagonists, since they have a predictable anticoagulant effect, the possibility of taking fixed doses without the need for routine anticoagulant monitoring, rapid onset and termination of action, relatively low potential for food and drug interactions. Direct oral anticoagulants are used for the prevention of thromboembolic complications in patients with atrial fibrillation, for the prevention of deep vein thrombosis in patients who have undergone surgery on the knee or hip joints, for emergency treatment and secondary prevention of deep vein thrombosis and pulmonary embolism. Alertness to side effects tends to focus on the likelihood of bleeding, with the possibility of other side effects of direct oral anticoagulants receiving less attention or going unnoticed. These mainly include liver damage, kidney damage and a number of other rare adverse reactions. The finding of isolated thrombocytopenia in patients taking direct oral anticoagulants may be associated with a high risk of life-threatening bleeding. The article analyzes published data on the occurrence of thrombocytopenia associated with the intake of direct oral anticoagulants, and presents a clinical case of thrombocytopenia while taking apixaban.

Potential of anticoagulant therapy in cardiology practice for thrombocytopenia. Literature review

“…Тем более, что ТП в инструкциях к ПОАК указана как редкая побочная реакция с частотой развития от ≥1/1000 до <1/100 пациентов. При этом единичные случаи ТП всё же были зарегистрированы и описаны как в зарубежной, так и в отечественной литературе [16][17][18]. В частности, в статье Татарского Б. А. и др.…”

“…после отмены препарата. Авторы указывают, что, возможно, развитие ТП также было связано с межлекарственным взаимодействием дабигатрана и индукторов Р-гликопротеина [18].…”