China
Africa
Explore chapters and articles related to this topic
The Potential of Plants as Treatments for Venous Thromboembolism
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Lilitha L. Denga, Namrita Lall
Hypercoagulability (thrombophilia) is a state of increased risk for thrombosis. A hypercoagulable state describes a pathologic state whereby coagulation is exaggerated in the bloodstream due to hyperactivity of pro-coagulant factors or a deficiency in anticoagulants (Schafer 2007). Hypercoagulability is caused by genetic factors which are inherited or it can be acquired through physiological responses to stress or trauma (Khan and Dickerman 2006; Thomas 2001). In many VTE cases, a hypercoagulable state develops due to an interaction between inherited and acquired factors.
A patient with calf pain
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
There are many causes of hypercoagulability, including: Pregnancy: stasis and increased clotting factorsOral contraceptive pill (OCP) or hormone replacement therapy (HRT): increased clotting factorsOngoing infection and inflammation: thrombocytosisNephrotic syndrome: reduced antithrombin III levelsMalignancyDehydration: including DKA.
The Rational Basis of Thrombosis Models
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
It is evidently exceptional to show that an acquired hypercoagulable state could start without vascular lesion, and the other way around, with every vascular lesion or even functional perturbation anywhere in the vascular tree, blood clotting and platelet activation resulting in a local or disseminated thrombosis even at distant sites should be expected as a possible consequence. In fact, most hypercoagulability tests represent an indirect indication of the presence or recent presence of vascular lesion somewhere in the circulatory bed.
An update on novel therapies for treating patients with arterial thrombosis
Published in Expert Review of Hematology, 2023
Udaya S Tantry, Sanchit Duhan, Eliano Navarese, Bogumil Ramotowski, Parshotam Kundan, Kevin P Bliden, Paul Gurbel
It has been shown that the ‘thrombin pathway’ may play a pivotal role in the generation and propagation of thrombus in selected patients with arterial diseases. These patients may have hypercoagulability phenotype and can be treated with very low dose FXa inhibitor on top of standard DAPT. The latter concept may provide improved net clinical benefit with a lower risk for bleeding in patients with hypercoagulability. Finally, FXIa and FXIIa inhibition may provide additional antithrombotic effect with lower risk of bleeding. However, strong evidence from large scale clinical trials is needed before their implementation. These novel agents may provide more choices to overcome some of the unmet needs of current antithrombotic agents and provide better net clinical benefits in patients with arterial thrombosis.
Reducing inappropriate inpatient thrombophilia testing through an electronic health record intervention
Published in Baylor University Medical Center Proceedings, 2023
Charis Durham, John Kim, Roma Bhandarkar, Daphne Garcia Galan, Alwin Alias, James Hall, Gerald Ogola, Micah Burch
On retrospective chart review, 271 patients underwent a hypercoagulability workup in the inpatient setting during the 6-month preintervention period. There was approximately a 6-month delay in implementing the intervention after the acquisition of baseline data due to hospital administrative and information technology processing and guidance prior to approval. After implementing the electronic orders intervention in early December 2020, 238 patients were identified who underwent hypercoagulability workup during the 6-month postintervention period. This represented a 12% reduction in the number of patients tested, but the study was not powered to evaluate the statistical significance of this difference. There was a statistically significant reduction in the total number of laboratory tests ordered, from 1185 in the preintervention group to 910 in the postintervention group (Table 1), which amounts to a 13% decrease (P = 0.003). The individual tests were evaluated as well, demonstrating a statistically significant reduction in some of the individual tests ordered but also an increased incidence of orders placed for APS workup. It is difficult to assess how the COVID-19 pandemic and resulting hospital surges may have impacted the number of tests ordered and number of patients tested.
Contributions of von Willebrand factor to clinical severity of sickle cell disease: a systematic review and metanalysis
Published in Hematology, 2022
T. U. Nwagha, Martins Nweke, E. D. Ezigbo
VWF is a glycoprotein that is known to mediate platelet adhesion, increased platelet adhesion and aggregation, and impaired fibrinolytic activity, all of which contribute to a state of hypercoagulable and prothrombotic disease [5]. VWF is a large sticky multimeric protein that contributes to vascular hemostasis and functions as a marker of endothelial dysfunction [6]. The larger the protein, the more adhesive it is to function. A VWF deficiency or defect can result in von Willebrand disease and bleeding. On the other hand, an increase in VWF can promote thrombosis by creating a favourable environment [7]. Hypercoagulability has been linked to a variety of clinical symptoms, including severe vasoocclusive crises, hemolytic anemia, and oxidative stress [3,5]. In SCD, a similar relationship has been discovered between an elevated level of extracellular hemoglobin (Hb) and the development of the disease. Extracellular Hb binds to VWF and inhibits its cleavage by ADAMTS-13, resulting in the accumulation of ultra-large VWF multimers in the circulation and in the endothelium, as well as the stimulation of prothrombotic events [8].