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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
The coagulation cascade (Figure 17.2) is a series of reactions that regulate hemostasis. The plasma portion of blood carries a set of serine proteases that exist in an inactivated state. These serine proteases are known as coagulation factors or procoagulants (Schenone, Furie, and Furie 2004). Inactive coagulation factors are represented by Roman numerals and are appended with a lowercase “a” once activated. The activity of the coagulation factors can increase by as much as five orders of magnitude when activated (Smith, Travers, and Morrissey 2015). The coagulation cascade consists of two pathways: the intrinsic and extrinsic.
Postoperative Bleeding
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Studies on the coagulation cascade have allowed for identification and targeting of specific areas of the pathway for therapy. Tranexamic acid (TXA) is one solution that has been heavily studied. TXA is a lysine derivative, and its mechanism of action is inhibition of plasminogen. It is an anti-fibrinolytic, ultimately stabilizing the clot. It has been studied in multiple patient populations with promise, including patients with trauma, traumatic brain injury and gastrointestinal bleeding as well as perioperative cardiac surgery and ob-gyn patients (Roberts et al., 2013).
Diagnosis and Treatment Model of the COVID-19 Rehabilitation Unit
Published in Wenguang Xia, Xiaolin Huang, Rehabilitation from COVID-19, 2021
During the treatment of COVID-19, first-line clinicians found that nearly 20% of patients had abnormal coagulation functions, affecting the coagulation and fibrinolysis system through various ways. Eventually, it leads to the activation of the coagulation cascade and the inhibition of the fibrinolysis process, which promotes the formation of blood clots. It is essential to pay attention to and prevent deep vein thrombosis (deep venous thrombosis, DVT) and pulmonary thromboembolism (PTE) that occurs after formation. We made the following, with reference to Recommendations for Prevention and Treatment of Venous Thromboembolism Related to COVID-19 (Trial).
Snakebite-associated thrombotic microangiopathy: a spotlight on pharmaceutical interventions
Published in Expert Review of Clinical Pharmacology, 2023
Tina Noutsos, Geoffrey K Isbister
The underlying etiology of snakebite-associated TMA is unclear, but it is consistently associated with VICC. VICC is triggered via a diverse variety of different mechanisms and develops rapidly after envenoming [24]. The procoagulant toxins target circulating proteins (clotting factors) of the coagulation cascade (Figure 2, Table 1). Procoagulant toxins activate various clotting factors, leading to activation of the coagulation cascade, factor consumption, and the resultant consumption coagulopathy of VICC [9]. Most snakes known to cause VICC are vipers and certain Australasian elapids [5]. The important procoagulant toxins activate prothrombin, factor X, and/or factor V, or act as thrombin-like enzymes (Figure 2) [9]. VICC presents with a reduced or unrecordable fibrinogen; prolonged or unrecordable prothrombin time (PT) (or its international normalized standardized equivalent, the international normalized ratio [INR]) and activated partial thromboplastin time (APTT); and an elevated D-dimer [8]. With respect to the natural history of VICC, its onset after envenoming is very rapid. In complete VICC, near or total depletion of fibrinogen and an unrecordable INR and APTT typically occur within one to two hours of the snakebite [8]. VICC recovery occurs at a rate suggestive of factor replenishment via new factor resynthesis after neutralization of venom toxins: the INR returns to below 2.0 in 10 to 30 hours, fibrinogen recovers to >1 g/L after 20 to 40 hours, and the labile factor V and VIII return to > 50% within 5 to 15 hours [8,24].
Hemophilia A gene therapy: current and next-generation approaches
Published in Expert Opinion on Biological Therapy, 2022
Steven W. Pipe, Gil Gonen-Yaacovi, Oscar G. Segurado
Hemophilia is classified as a group of X-linked inherited hemorrhagic disorders resulting from the absence of or defects in critical factors in the coagulation cascade [1]. Patients with hemophilia exhibit compromised thrombin generation and fibrin clot formation, which leads to bleeding episodes, most commonly into the joints (hemarthrosis). The 2 main types of hemophilia (A and B) relate to deficiency or dysfunction of the specific clotting factors VIII or IX, respectively, with the severity depending on the level of clotting factor activity. Hemophilia affects mainly males, and hemophilia A accounts for the large majority of cases (~80%), affecting approximately 1 of every 5000 live-born males. Hemophilia B is 5 times less common than hemophilia A, having an incidence of approximately 1 in 30,000 births [2,3]. Over a million people around the world are estimated to have hemophilia, including more than 30,000 in the United States (US) [4]. The prevalence is higher among Whites than Blacks or Hispanics [5].
Exploring the pathways of inflammation and coagulopathy in COVID-19: A narrative tour into a viral rabbit hole
Published in International Reviews of Immunology, 2022
Nitsan Landau, Yehuda Shoenfeld, Liat Negru, Gad Segal
Other coagulation cascade anomalies include increased concentrations of tissue factor (TF), factor VIII, factor V, Plasminogen-activator inhibitor type 1 (PAI-1), plasmin-anti-plasmin (PAP) and a marked increase in Von Willebrand factor (VWF). Changes are also reported in natural anticoagulants: thrombin-anti-thrombin (TAT), protein S and protein C [3, 21–23]. Few studies further evaluated nonconventional hemostasis assays and reported that tissue plasminogen activator (tPA), tissue factor pathway inhibitor (TFPI) and vascular endothelial growth factor (VEGF) were also significantly increased in the critical versus noncritical COVID-19 patients [24, 25]. One study reported ADAMTS-13 levels to be greatly reduced [26]. Various autoimmune antibodies that are linked to hypercoagulable states are reported: anti-phospholipid antibodies (aPL) [27, 28], as well as autoimmune antibodies to Annexin A2 [29]. Furthermore, sustained pro-thrombotic changes in COVID-19 patients were reported even 4 months after hospital discharge; The PT, factor V, VWF, fibrinogen, D-dimer, and TAT levels were elevated on admission but normalized on checkup, whereas plasma levels of factor VIII and PAI-1 were elevated both on admission and at follow-up [22].