Clinical Evidence and Consequences of the Association Between Hemostatic Functions and Malignancies
László Muszbek in Hemostasis and Cancer, 2019
The relationship between thromboembolic disorders and neoplastic diseases has been recognized since 1865 when Trousseau first reported a high incidence of venous thrombosis in patients with carcinoma of the stomach. In an attempt to explain this association several investigators have demonstrated procoagulant activities in tumor (among them leukemic) cells and mucous secreted by tumors, and it has been shown that tumor cells also activated platelets. A beneficial therapeutic effect of anticoagulants and possibly antiplatelet drugs became substantiated. On the other hand, numerous clinical and experimental studies indicate a role for hemostatic components, first of all fibrin and platelets in tumor growth and metastasis formation. Fibrin anchors tumor cells to intra- and extravascular sites and platelet-derived tumor-directed growth factors may be involved in tumor progression and spread. Again, the anticoagulants and antiplatelet agents could interact these biological effects. Several mostly clinical aspects of this two-way interaction are touched upon.
Venous Thrombosis
Hau C. Kwaan, Meyer M. Samama in Clinical Thrombosis, 2019
The major side effect of oral anticoagulant therapy is bleeding. Bleeding during well-controlled oral anticoagulant therapy is usually due to surgery or other forms of trauma, or to local lesions such as peptic ulcer or carcinoma.11–14 Spontaneous bleeding may occur if warfarin sodium is given in an excessive dose resulting in marked prolongation of the PT; this bleeding may be severe and even life-threatening. The risk of bleeding can be substantially reduced, without loss of effectiveness for preventing recurrent venous thromboembolism, by monitoring the PT to achieve a less intense anticoagulant effect (1.25 to 1.5 times control using a rabbit brain thromboplastin such as Simplastin or Dade-C, corresponding to an INR of 2.0 to 3.0).14
Left atrial appendage exclusion
Debabrata Mukherjee, Eric R. Bates, Marco Roffi, Richard A. Lange, David J. Moliterno, Nadia M. Whitehead in Cardiovascular Catheterization and Intervention, 2017
An additional surgical approach includes thorascopic extracardiac obliteration. An initial experience with 15 patients was reported by Blackshear et al.59 With this approach, a double-lumen intratracheal tube is used. Selective intubation and ventilation of the right lung result in reduction in the volume of the left lung. Using video-assisted thorascopic instruments, the pericardium is opened and the tip of the LAA can be grasped. A loop is then manipulated to position it at the base of the appendage where it is cinched to occlude the appendage. In this small series, success was achieved in 14 of 15 patients; one patient developed bleeding and was converted to open thoracotomy. In all patients, there was a contraindication to anticoagulant therapy.
Pullulan based derivatives: synthesis, enhanced physicochemical properties, and applications
Published in Drug Delivery, 2022
Surendra Agrawal, Divya Budhwani, Pravina Gurjar, Darshan Telange, Vijay Lambole
Anticoagulants are used to stop the thickening of the blood and the formation of clots. Heparin is one of the popular anticoagulants. Pullulan derivatization via sulfation has been done with the aim to develop an alternative to heparin. Sulfated pullulan can be obtained by the reaction of pullulan and sulfur trioxide–pyridine complex in DMF (dimethylformamide) at 75 °C and 95 °C for 3–8 h. Sulfate pullulan can also be obtained from pullulan reaction with SO3-DMF (N,N-dimethyl formamide) complex, but due to SO3–DMF complex, resultant pullulan becomes more reactive and less viscous; therefore, SO3–Py (pyridine) complex is more preferred to achieve stable and viscous derivative. Pullulan sulfate C-6 is the most preferential position for sulfation, followed by C-3, while C-4 remained mostly unsulfated (Mähner et al., 2001). It was reported that pullulan sulfate prevents coagulation by interfering with several stages of coagulation (Alban et al., 2002).
Do the benefits of prophylactic inferior vena cava filters outweigh the risks in trauma patients? A meta-analysis*
Published in Acta Chirurgica Belgica, 2022
Mahir Gachabayov, Lulejeta A. Latifi, Rifat Latifi
Major trauma is a well-known risk factor for venous thromboembolism (VTE) [1]. It arises as a result of a cascade of normal physiologic response to shock and tissue injury leading to increased activated protein C levels, endothelial glycocalyx disruption, platelet dysfunction, and subsequent traumatic coagulopathy [2]. Pulmonary embolism (PE) is the third leading cause of death in multiple trauma patients who survived the first 24 h [3]. Long bone fractures with severe extremity trauma were shown in a multicenter study to be associated with even higher risk of PE in general and early PE (within 72 h), in particular [4]. Moreover, the authors reported that early anticoagulation did not decrease the rates of early PE. In addition, anticoagulants may be unacceptable in trauma patients due to the increased risk of bleeding. An alternative strategy to decrease the risk of PE can be inferior vena cava filters (IVCF), which function by trapping thromboemboli as they travel to the heart from the deep veins of lower extremities.
Acute upper gastrointestinal bleeding: a population-based, five-year follow-up study
Published in Scandinavian Journal of Gastroenterology, 2021
Johann P. Hreinsson, Armann Jonsson, Einar S. Bjornsson
In February to March 2017, electronic medical records of cases and controls were retrospectively reviewed and data collected on; comorbidities according to the Charlson comorbidity index [12], rebleeding and its cause as well as date of death. Additionally, the following laboratory values were collected for bleeders at the index bleeding: haemoglobin, haematocrit, platelets, creatinine and international normalized ratio (INR). Pharmaceuticals noted were non-steroidal anti-inflammatory drugs (NSAIDs), low-dose aspirin (LDA), anticoagulants, antiplatelets and proton-pump inhibitors (PPIs). Anticoagulants included, warfarin, dabigatran, apixaban, rivaroxaban, heparin, low-molecular-weight heparins, and fondaparinux. Antiplatelets included low-dose aspirin, clopidogrel, dipyridamole, prasugrel, ticagrelor, ticlopidine, eptfibatide, and anagrelide. Proton-pump inhibitors included esomeprazole, omeprazole, rabeprazole, and lansoprazole. Bleeding was considered clinically significant if the patients required blood transfusion (Hb <100 g/l), became hemodynamically unstable, were admitted to intensive care, required surgery, or died.
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