Embolic stroke of undetermined source in a young woman

Prodan, Călin I.; Vijayvargiya, Pooja; Feisal, James K.; Khawandanah, Mohamad; Yang, Jiang; George, James N.

doi:10.1002/ajh.25557

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…11 Low ADAMTS13 activity may occur during remission from acquired TTP and may also be associated with increased risk for stroke. 12,13 MI was reported in only 5 case report patients (3%) (median age, 20 years; range, 22 months to 50 years). 4 Thirteen case report patients had died (8%) (median age, 23 years; range, newborn to 79 years).…”

Section: Resultsmentioning

confidence: 97%

Stroke and myocardial infarction in hereditary thrombotic thrombocytopenic purpura: similarities to sickle cell anemia

Borogovac

George

2019

Blood Advances

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Section: Resultsmentioning

confidence: 97%

Stroke and myocardial infarction in hereditary thrombotic thrombocytopenic purpura: similarities to sickle cell anemia

Borogovac

George

2019

Blood Advances

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“…Since aspirin is an effective treatment to reduce the risk for stroke, 56,57 it may be beneficial during remission of iTTP when risk of stroke may be increased. [9][10][11][12] Aspirin may also provide effective stroke prophylaxis for patients with hereditary TTP. The risk for increased bleeding caused by aspirin prophylaxis should be minimal, even if TTP patients become thrombocytopenic.…”

Section: Discussionmentioning

confidence: 99%

“…Following recovery from an acute episode, patients may have persistent low levels of ADAMTS13 that are associated with increased risk for transient cerebral ischemic attacks 9 and stroke. [10][11][12] There is currently no effective long-term prophylactic management to decrease risk for thrombosis during clinical remission. Patients with hereditary TTP (hTTP) are at risk for thrombosis throughout their lives.…”

Section: Introductionmentioning

confidence: 99%

Deletion of platelet CLEC-2 decreases GPIbα-mediated integrin αIIbβ3 activation and decreases thrombosis in TTP

Shao

Hoover

Shi

et al. 2022

Blood

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Microvascular thrombosis in patients with thrombotic thrombocytopenic purpura (TTP) is initiated by GPIba-mediated platelet binding to von Willebrand factor (VWF). Binding of VWF to GPIba causes activation of the platelet surface integrin aIIbb3. However, the mechanism of GPIba-initiated activation of aIIbb3 and its clinical importance for microvascular thrombosis remain elusive. Deletion of platelet C-type lectin-like receptor 2 (CLEC-2) did not prevent VWF binding to platelets but specifically inhibited platelet aggregation induced by VWF binding in mice. Deletion of platelet CLEC-2 also inhibited aIIbb3 activation induced by the binding of VWF to GPIba. Using a mouse model of TTP, which was created by infusion of anti-mouse ADAMTS13 monoclonal antibodies followed by infusion of VWF, we found that deletion of platelet CLEC-2 decreased pulmonary arterial thrombosis and the severity of thrombocytopenia. Importantly, prophylactic oral administration of aspirin, an inhibitor of platelet activation, and therapeutic treatment of the TTP mice with eptifibatide, an integrin aIIbb3 antagonist, reduced pulmonary arterial thrombosis in the TTP mouse model. Our observations demonstrate that GPIba-mediated activation of integrin aIIbb3 has an important role in the formation of thrombosis in TTP. These observations suggest that prevention of platelet activation with aspirin may reduce the risk for thrombosis in patients with TTP.

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“…This is effective for prevention of preeclampsia 57 and may also decrease risk for thrombosis associated with TTP. Also, because ADAMTS13 deficiency during remission increases the risk for relapse 58 and stroke, 59,60 we measure the woman's ADAMTS13 activity before becoming pregnant. If ADAMTS13 activity is < 20%, we recommend rituximab to increase ADAMTS13 activity prior to pregnancy.…”

Section: Severe Thrombocytopenia and Maha Caused By Complications Of ...mentioning

confidence: 99%

Severe thrombocytopenia and microangiopathic hemolytic anemia in pregnancy: A guide for the consulting hematologist

et al. 2021

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A hematologist receives a call from a maternal-fetal medicine (MFM) physician about a previously healthy patient who became ill at 25 weeks' gestation. Her mental status is deteriorating. There are signs of fetal distress. Platelet count and hemoglobin are falling. The MFM physician is considering the hemolysis, elevated liver enzymes and low platelet count (HELLP) syndrome. For the hematologist, everything seems unfamiliar. Our goal is to provide hematologists with the fundamental knowledge required for understanding and managing these patients who become suddenly and seriously ill during pregnancy and in whom thrombocytopenia and microangiopathic hemolytic anemia are part of their presentation.

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Embolic stroke of undetermined source in a young woman

Cited by 4 publications

References 22 publications

Stroke and myocardial infarction in hereditary thrombotic thrombocytopenic purpura: similarities to sickle cell anemia

Stroke and myocardial infarction in hereditary thrombotic thrombocytopenic purpura: similarities to sickle cell anemia

Deletion of platelet CLEC-2 decreases GPIbα-mediated integrin αIIbβ3 activation and decreases thrombosis in TTP

Severe thrombocytopenia and microangiopathic hemolytic anemia in pregnancy: A guide for the consulting hematologist

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