- Risk Assessment and Treatment Guide for Obstetric Thromboprophylaxis: Comprehensive Review of Current Guidelines. [Journal Article]
- AJAm J Perinatol 2018 Sep 19
- CONCLUSIONS: This compilation of guidelines integrates the complicated topic into a simple comprehensive guide where women can be identified early and accurately for appropriate VTE prophylaxis to protect them during and after pregnancy.
- Management of Microsurgical Patients using Intraoperative Unfractionated Heparin and Thromboelastography. [Journal Article]
- JRJ Reconstr Microsurg 2018 Sep 19
- CONCLUSIONS: The TEG is a useful adjunct for monitoring coagulation status in microsurgical breast reconstruction. When thrombosis at the anastomosis occurs, TEG correlates with a more rapid rebound from an intraoperative hypocoagulable state to a postoperative hypercoagulable state, when using the TEG. The TEG is a valuable tool for a more dynamic assessment of the patients' changing coagulation status.
- A Case of Recurrent First Trimester Miscarriages Due to Inherited Multifactorial Thrombophilia in an Otherwise Asymptomatic Patient: A Clinical Dilemma. [Journal Article]
- JOJ Obstet Gynaecol India 2018; 68(5):414-416
- Common Conditions Requiring Long-Term Anticoagulation in Neurosurgical Patients. [Review]
- NCNeurosurg Clin N Am 2018; 29(4):529-535
- Long-term anticoagulant therapy prevents thrombosis. Management of neurosurgical patients with conditions such as atrial fibrillation, mechanical heart valves, and other prothrombotic states necessit...
Long-term anticoagulant therapy prevents thrombosis. Management of neurosurgical patients with conditions such as atrial fibrillation, mechanical heart valves, and other prothrombotic states necessitates application of a strategy to mitigate hemorrhagic complications of anticoagulation. Development of direct oral anticoagulants, which include the direct thrombin and factor X inhibitors, yields new considerations to be had, in particular, the introduction of reversal agents. This article reviews the more common chronic clinical entities that require the use of prolonged anticoagulant therapy with special consideration for neurosurgical patients. It also includes a discussion of established treatment strategies across available treatment options.
- Genetics of Hypercoagulable and Hypocoagulable States. [Review]
- NCNeurosurg Clin N Am 2018; 29(4):493-501
- Hemostasis is the normal process of blood coagulation in vivo to stop pathologic bleeding. Virchow triad includes venous stasis, hypercoagulability, and vascular injury. Natural anticoagulants includ...
Hemostasis is the normal process of blood coagulation in vivo to stop pathologic bleeding. Virchow triad includes venous stasis, hypercoagulability, and vascular injury. Natural anticoagulants include protein C, protein S, and antithrombin. Factor V Leiden is the most common inherited thrombophilia, followed by prothrombin gene mutation. All inherited thrombophilias are passed down in an autosomal dominant fashion. Patients harboring the antiphospholipid antibodies have an increased risk for thrombosis. von Willebrand disease is the most common inherited bleeding disorder; the pattern of inheritance is autosomal. Hemophilia A and B are the only hereditary bleeding disorders inherited in a sex-linked recessive pattern.
- Hemostasis, bleeding and thrombosis in liver disease. [Journal Article]
- JTJ Transl Sci 2017; 3(3)
- The presence of cirrhosis poses an increased risk of both thrombosis and bleeding in individuals with chronic liver disease. This duality is a result of a dynamic disequilibrium between procoagulant ...
The presence of cirrhosis poses an increased risk of both thrombosis and bleeding in individuals with chronic liver disease. This duality is a result of a dynamic disequilibrium between procoagulant and anticoagulant states in individuals with cirrhosis. The mechanism of this imbalance in cirrhosis remains unclear. It is known that the progression of cirrhosis leads to decreased synthetic function and a concurrent lack of natural anticoagulants. Other proposed mechanisms contributing to this hemostatic imbalance include decreased platelet production, increased platelet destruction from hypersplenism, decreased synthesis of Vitamin K-dependent and independent clotting factors and anticoagulant factors, and alterations in purinergic signaling pathways. Given the current state of flux in our understanding of bleeding and thrombophilia in cirrhosis, the recommendations for treatment of these conditions are still evolving. We provide a current update on the proposed pathophysiology of altered hemostasis and thrombophilia in cirrhosis. We discuss recent studies in portal vein thrombosis (PVT) and venous thromboembolism (VTE), which are the common thrombotic consequences of cirrhosis, resulting in substantive morbidity and mortality. To address these, we discuss new prophylactic interventions and current treatment options to manage the heightened risk of thrombosis in cirrhosis, while limiting hemorrhagic complications.
- An Electronic Best Practice Alert Based on Choosing Wisely Guidelines Reduces Thrombophilia Testing in the Outpatient Setting. [Journal Article]
- JGJ Gen Intern Med 2018 Sep 13
- Extracellular Vesicle Characteristics in β-thalassemia as Potential Biomarkers for Spleen Functional Status and Ineffective Erythropoiesis. [Journal Article]
- FPFront Physiol 2018; 9:1214
- β-thalassemia major (β-TM) is a therapeutically challenging chronic disease in which ineffective erythropoiesis is a main pathophysiological factor. Extracellular vesicles (EVs) are membrane-enclosed...
β-thalassemia major (β-TM) is a therapeutically challenging chronic disease in which ineffective erythropoiesis is a main pathophysiological factor. Extracellular vesicles (EVs) are membrane-enclosed vesicles released by cells into biological fluids; they are involved in intercellular communication and in multiple physiological and pathological processes. The chaperone heat-shock protein 70 (HSP70), which is released from cells via EVs, aggravates ineffective erythropoiesis in β-TM. We propose that β-TM EVs may show specific signatures, reflecting disease mechanisms, stages and severity. Our study aims were to define EV profiles in β-TM patients, investigate the influence of hypersplenism and splenectomy on EV features, and explore the association of circulating EVs with ineffective erythropoiesis and iron-overload parameters. We characterized circulating EVs in 35 transfusion-dependent β-thalassemia patients and 35 controls using several techniques. Nanoparticle-tracking analysis revealed increased EV concentration in patients vs. controls (P = 0.0036), with smaller EV counts and sizes in patients with hypersplenism. Flow cytometry analysis showed lower levels of RBC and monocyte EVs in patients vs. controls. RBC-EV levels correlated with patient hematocrit, reflecting degree of anemia. The procoagulant potential of the EVs evaluated by flow cytometry revealed lower levels of endothelial protein C receptor-labeled EVs in patients vs. controls, and increased tissue factor-to-tissue factor pathway inhibitor-labeled EV ratio in splenectomized patients, suggesting a hypercoagulable state. Protein content, evaluated in EV pellets, showed increased levels of HSP70 in patients (P = 0.0018), inversely correlated with transfusion requirement and hemoglobin levels, and positively correlated with reticulocyte, erythropoietin and lactate dehydrogenase levels. This first description of EVs in patients with hypersplenism reveals the spleen's importance in EV physiology and clearance. Circulating EV-HSP70 levels were associated with markers of ineffective erythropoiesis, hemolysis and hematological disease severity. EV analysis in β-TM-reflecting spleen status, hypercoagulability state and ineffective erythropoiesis-may serve as a biomarker of disease dynamics, supporting both anticipation of the risk of complications and optimizing treatment.
- Recurrent cerebellar infarction associated with hereditary heterozygous protein C deficiency in a 35-year-old woman: A case report and genetic study on the pedigree. [Journal Article]
- ETExp Ther Med 2018; 16(3):2677-2681
- Deficiency of protein C may cause deep venous thrombosis and pulmonary embolism, leading to ischemic stroke. The present study reports on a case of a young adult with recurrent cerebellar infarction ...
Deficiency of protein C may cause deep venous thrombosis and pulmonary embolism, leading to ischemic stroke. The present study reports on a case of a young adult with recurrent cerebellar infarction due to hereditary heterozygous protein C deficiency and performs a literature review. A 35-year-old Asian woman was admitted t o the Department of Neurology of The First Affiliated Hospital of Guangxi Medical University (Nanning, China) due to right limb paralysis and vomiting. The diagnosis of stroke was confirmed by computed tomography and magnetic resonance imaging, which indicated acute cerebral infarction of the right cerebellar hemisphere and cerebellar vermis, as well as a previous cerebral infarction on the left cerebellar hemisphere. This patient had taken aspirin orally for 4 years following surgical therapy for small intestine thrombosis and was regularly taking hydroxychloroquine sulfate to treat systemic lupus erythematosus. The protein C (PROC) levels were 57.6%, while protein S and antithrombin levels were normal. Gene sequencing analysis of the patient and the patient's pedigree revealed a heterozygous mutation, c.565C>T, on the PROC gene in the patient and the patient's father. In conclusion, the clinical manifestations of hereditary PROC deficiency may vary between individuals. The heterozygous mutation locus c.565C>T on the PROC gene is associated with thrombophilia. Awareness of the association between natural anticoagulants and thrombophilia may promote the prevention and therapy of stroke.
New Search Next
- Antiphospholipid syndrome - an update. [Journal Article]
- VASAVasa 2018 Sep 12; :1-14
- Antiphospholipid syndrome (APS) is an autoantibody-mediated acquired thrombophilia. It is characterized by the presence of antiphospholipid antibodies (APL) that are directed against phospholipid-bin...
Antiphospholipid syndrome (APS) is an autoantibody-mediated acquired thrombophilia. It is characterized by the presence of antiphospholipid antibodies (APL) that are directed against phospholipid-binding plasma proteins, such as beta-2-glycoprotein I (b2GPI). Its main manifestations are recurrent vascular thromboses (so-called "thrombotic APS") and pregnancy complications ("obstetric APS"). According to the current consensus criteria, a persistently positive functional lupus anticoagulant (LA) assay and/or the presence of anti-b2GPI and/or anti-cardiolipin antibodies, together with clinical symptoms, is mandatory for the diagnosis of APS. Other clinical features, such as thrombocytopenia, Coombs-positive haemolytic anaemia, heart valve disease, renal microangiopathy and neurologic disorders are also common in APL-positive patients. APS can be associated with other autoimmune disorders, such as systemic lupus erythematosus. In rare cases, catastrophic APS (CAPS) occurs, with the development of excessive thrombosis at multiple sites, usually affecting small vessels and leading to multi-organ dysfunction and organ failure. Treatment usually comprises antithrombotic therapy using antiplatelet and anticoagulant agents. However, there is no consensus concerning the intensity or duration of therapy. Despite apparently adequate anticoagulation, the risk of recurrent thrombosis remains high. For patients with CAPS, a combined therapeutic approach that includes anticoagulation, glucocorticoids, plasma exchange and/or intravenous immunoglobulin seems to be the best treatment option.