A mouse model to study thrombotic complications of thalassemia

Kalish, Yosef; Malyutin, Zeev; Shai, Ela; Dana, Mutaz; Avraham, Limor; Jahshan, Nivin; Rachmilewitz, Eliezer A.; Fibach, Eitan; Varon, David

doi:10.1016/j.thromres.2014.12.023

Cited by 9 publications

(11 citation statements)

References 33 publications

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“…El aumento de la adhesión plaquetaria en la β-talasemia, se correlaciona con eventos trombóticos clínicos, lo cual podría deberse al contacto directo con los glóbulos rojos patológicos que expresan niveles anormalmente altos de fosfolípidos cargados negativamente, principalmente fosfatidilserina en su membrana [53]. Por otro lado, existen otros factores que contribuyen al estado de hipercoagulabilidad crónica en la talasemia dentro de los cuales se encuentran la deficiencia de inhibidores del factor de la coagulación como la proteína C y la proteína S, la disfunción cardíaca, hepática y las deficiencias hormonales debidas a la acumulación de hierro en órganos vitales [53].…”

Section: Estado De Hipercoagulabilidadunclassified

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Beta-Talasemia: Un mundo de complicaciones con nuevas alternativas de tratamiento.

Alzate

2019

archmed

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Introducción: β-talasemia, es causada por mutaciones en el gen de la globina HBB, que codifica la subunidad β de la HbA. La enfermedad es conocida por ser altamente prevalente en el área que se extiende desde África subsahariana, a través de la región mediterránea y Medio Oriente. En Colombia, se han reportado varios estudios independientes de hemoglobinopatías en ciudades como Cartagena, Buenaventura, Cali, San Andrés y Providencia debido a su gran población afrodescendiente sobre la cual las Talasemias y otras hemoglobinopatías tienen incidencia directa. Objetivo: recolectar datos acerca de las características clínicas, complicaciones y clasificaciones de β-talasemia con el fin de brindar una fuente de información que permita realizar un diagnóstico eficaz y en consecuencia un tratamiento que busque llegar a la curación completa de los pacientes que sufren esta condición, con el mínimo de complicaciones para los mismos. Conclusión: la β-Talasemia es una hemoglobinopatía estructural que tiene un porcentaje de prevalencia e incidencia importante en el mundo. En Colombia no se tiene claro cuál es la epidemiología real para esta condición puesto que no se han realizado estudios que abarquen una muestra adecuada y significativa. Esta enfermedad genera múltiples complicaciones en diferentes órganos, que no solo están asociadas al desarrollo de la enfermedad, sino también a la terapia de trasfusión a largo plazo. Por esta razón, los nuevos tratamientos están encaminas a lograr en un futuro la curación completa, reduciendo al máximo las complicaciones.

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Section: Estado De Hipercoagulabilidadunclassified

“…El estrés oxidativo también puede llevar a un estado de hipercoagulabilidad crónico ya que puede estimular la activación y agregación de las plaquetas e inducir la externalización de la fosfatidilserina [53].…”

Section: Estado De Hipercoagulabilidadunclassified

Beta-Talasemia: Un mundo de complicaciones con nuevas alternativas de tratamiento.

Alzate

2019

archmed

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“…Negatively charged phospholipids can also stimulate thrombin generation . Chronic platelet activation and increased platelet aggregation are among the factors that are thought to contribute to a hypercoagulable state in patients with NTDT . Patients with NTDT, especially those who are splenectomized, have elevated markers of hemostatic activity .…”

Section: The Pathophysiology Underlying the Clinical Morbidities In Ntdtmentioning

confidence: 99%

“…Chronic platelet activation and increased platelet aggregation are among the factors that are thought to contribute to a hypercoagulable state in patients with NTDT . Patients with NTDT, especially those who are splenectomized, have elevated markers of hemostatic activity . RBCs from patients with NTDT show increased adhesion to endothelial cells in vitro , and this is thought to contribute to the pathogenesis of hypercoagulable and microcirculatory disorders in patients with NTDT .…”

Section: The Pathophysiology Underlying the Clinical Morbidities In Ntdtmentioning

confidence: 99%

Morbidities in non‐transfusion‐dependent thalassemia

Saliba

Taher

2016

Annals of the New York Academy of Sciences

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Patients with non-transfusion-dependent thalassemia (NTDT) experience a wide array of clinical complications despite their independence from frequent, regular red blood cell (RBC) transfusions. According to the current understanding of NTDT, these clinical complications stem from the interaction of multiple pathophysiological factors: ineffective erythropoiesis, iron overload, and hypercoagulability. The state of chronic anemia and hypoxia-resulting from ineffective erythropoiesis and hemolysis-leads to the expansion of the erythroid marrow and extramedullary hematopoiesis. The chronic ineffective erythropoiesis also triggers increased intestinal iron absorption and deposition in the liver and endocrine glands despite the lack of transfusional iron load. Patients with NTDT also have a higher incidence of thromboembolic disease, pulmonary hypertension, and silent cerebral ischemia. The treatment of NTDT relies on occasional or more frequent blood transfusions for certain indications (severe infection, pregnancy, and surgery), iron chelation therapy, splenectomy, and hydroxyurea. Splenectomy is no longer routinely performed in all patients with NTDT in light of its association with increased risk of NTDT-related complications. This review focuses on the clinical morbidities associated with NTDT, summarizes the mainstays of treatment, and sheds light on future therapeutic directions in the field.

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“…Intraperitoneal administration being a commonly used route in pharmacological studies in murine models and ASA treatment [6], [9], [12], [14], [16], [19], [25], we also evaluated this type of administration. However, we did not either observe any effect of ASA on thrombus formation under this particular condition.…”

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confidence: 99%

Evaluation of commonly used tests to measure the effect of single-dose aspirin on mouse hemostasis

Decouture

Leuci

Dizier

et al. 2019

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Discrepancies in preclinical studies of aspirin (ASA) antiplatelet activity in mouse models of bleeding and arterial thrombosis led us to evaluate commonly reported methods in order to propose a procedure for reliably measuring the effects of single dose ASA on mouse hemostasis. FVB and C57Bl6 mice received 100 mg/kg of ASA or vehicle orally 30 min or 3 h prior to investigate either hemostasis using the tail bleeding assay or carotid thrombosis induced by FeCl 3 , or to blood sampling for isolated platelet aggregation and TXB 2 generation. Expected inhibition of COX1 by ASA was ascertained by a strong decrease in TXB 2 production, and its effect on platelet function and hemostasis, by decreased collagen-induced aggregation and increased bleeding time, respectively. Strikingly, we determined that anti-hemostatic effects of ASA were more predictable 30 min after administration than 3 h later. Conversely, ASA did not alter time to arterial occlusion of the carotid upon FeCl 3-induced thrombosis, suggesting ASA not to be used as reference inhibitor drug in this model of arterial thrombosis.

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A mouse model to study thrombotic complications of thalassemia

Cited by 9 publications

References 33 publications

Beta-Talasemia: Un mundo de complicaciones con nuevas alternativas de tratamiento.

Beta-Talasemia: Un mundo de complicaciones con nuevas alternativas de tratamiento.

Morbidities in non‐transfusion‐dependent thalassemia

Evaluation of commonly used tests to measure the effect of single-dose aspirin on mouse hemostasis

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