NDLI: Thrombocytopenia induced by dabigatran: two case reports

Content Provider	Springer Nature : BioMed Central
Author	Kang, Hyun Goo Lee, Seung Jae Chung, Ji Yeon Cheong, Jin Sung
Abstract	Background Vitamin K inhibitors (e.g. warfarin) and indirect thrombin inhibitors (e.g. heparin) are widely used to prevent thromboembolic disorders (e.g. myocardial infarction, venous thromboembolism, and stroke). These agents have been mainstays of anticoagulation for people older than 60 years. However, their administration is associated with a risk of bleeding and requires careful monitoring of patients. Novel oral anticoagulants (NOACs), such as dabigatran, are significantly safer in preventing thromboembolism than warfarin and heparin (sporadically causes thrombocytopenia) and are more specific for their target protein, thrombin. The major advantage of dabigatran, a direct thrombin inhibitor, is that it reversibly inhibits both free and clot-bound thrombin by tight binding affinity and the predictable pharmacodynamic effect. A few studies, however, reported that dabigatran can cause thrombocytopenia, although the underlying mechanism remains unclear. Thus, an antidote for dabigatran was developed to prevent thrombocytopenia. Case presentation In this report, we discuss two cases of thrombocytopenia and purpura after dabigatran treatment. A 73-year-old man showed hemorrhagic necrotic skin lesions on his neck and right hand. He was administered dabigatran (220 mg/day) for cerebral infarction for three days and his platelet count decreased abruptly (6000/μL). This suggested that dabigatran had caused thrombocytopenia and purpura; therefore, dabigatran administration was discontinued. The results of a blood test, performed 14 days after stopping dabigatran treatment, showed that the platelet count had recovered to the normal range of more than 150,000/μL. A 75-year-old woman had taken warfarin continuously for 8 years. However, she had a new cerebral infarction. Therefore, warfarin treatment was replaced with dabigatran (300 mg/day). Her platelet count decreased (41,000/μL) significantly and dabigatran treatment was discontinued. The blood test results show that platelet counts gradually recovered to the normal range. Conclusions Dabigatran application may cause bleeding; therefore, careful monitoring during dabigatran treatment is required to prevent thrombocytopenia. An explanation is that the interaction of dabigatran with thrombin, because of its strong binding affinity, may cause the observed thrombocytopenia.
Related Links	https://bmcneurol.biomedcentral.com/counter/pdf/10.1186/s12883-017-0900-8.pdf
Ending Page	4
Page Count	4
Starting Page	1
File Format	HTM / HTML
ISSN	14712377
DOI	10.1186/s12883-017-0900-8
Journal	BMC Neurology
Issue Number	1
Volume Number	17
Language	English
Publisher	BioMed Central
Publisher Date	2017-06-29
Access Restriction	Open
Subject Keyword	Neurology Neurochemistry Neurosurgery Dabigatran Factor Xa inhibitor Thrombin inhibitor Thrombocytopenia
Content Type	Text
Resource Type	Case study
Subject	Neurology (clinical)
Journal Impact Factor	2.2/2023
5-Year Journal Impact Factor	2.5/2023

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