Blood-coagulation Inhibitors after Snakebite

BMJ ◽  
1964 ◽  
Vol 1 (5398) ◽  
pp. 1639-1639
Author(s):  
J. Ghitis ◽  
G. Beltran
2005 ◽  
Vol 77 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Robson Q. Monteiro

The high specificity of blood coagulation proteases has been attributed not only to residues surrounding the active site but also to other surface domains that are involved in recognizing and interacting with macromolecular substrates and inhibitors. Specific blood coagulation inhibitors obtained from exogenous sources such as blood sucking salivary glands and snake venoms have been identified. Some of these inhibitors interact with exosites on coagulation enzymes. Two examples are discussed in this short revision. Bothrojaracin is a snake venom-derived protein that binds to thrombin exosites 1 and 2. Complex formation impairs several exosite-dependent activities of thrombin including fibrinogen cleavage and platelet activation. Bothrojaracin also interacts with proexosite 1 on prothrombin thus decreasing the zymogen activation by the prothrombinase complex (FXa/FVa). Ixolaris is a two Kunitz tick salivary gland inhibitor, that is homologous to tissue factor pathway inhibitor. Recently it was demonstrated that ixolaris binds to heparin-binding exosite of FXa, thus impairing the recognition of prothrombin by the enzyme. In addition, ixolaris interacts with FX possibly through the heparin-binding proexosite. Differently from FX, the ixolaris-FX complex is not recognized as substrate by the intrinsic tenase complex (FIXa/FVIIIa). We conclude that these inhibitors may serve as tools for the study of coagulation exosites as well as prototypes for new anticoagulant drugs.


1963 ◽  
Vol 102 (2) ◽  
pp. 171-179 ◽  
Author(s):  
L. Lorand ◽  
R.F. Doolittle ◽  
K. Konishi ◽  
S.K. Riggs

Author(s):  
Job Harenberg ◽  
Marina Marchetti ◽  
Anna Falanga

Vaccination against the SARS-CoV-2 may lead to immunologic reactions activating the haemostatic system and resulting in both venous and arterial thromboembolism. Aquired autoimmune Haemophilia following SARS-CoV-2 vaccines were now reported 15 to 19 days (or later) after vaccination and resolution of symptoms by adequate treatment of the immunologic reaction. From patients’ point of view, anticoagulants and SARS-CoV-2 vaccines share their capacity to induce thrombosis as well as bleeding and clinicians are subjected to Scylla and Charybdis when they treat patients not only with anticoagulants but also with SARS-CoV-2 vaccines. Careful analysis of coincidence and causality requires attention when reporting on acquired coagulation inhibitors regarding severity, treatments, duration and statistical risk.


Structure ◽  
2001 ◽  
Vol 9 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Herbert Nar ◽  
Margit Bauer ◽  
Angela Schmid ◽  
Jean-Marie Stassen ◽  
Wolfgang Wienen ◽  
...  

2001 ◽  
Vol 5 (1) ◽  
pp. 70-73
Author(s):  
David Green
Keyword(s):  

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
B Engelmann ◽  
J Bischof ◽  
AL Dirk ◽  
N Friedrich ◽  
E Hammer ◽  
...  

2001 ◽  
Vol 21 (03) ◽  
pp. 82-96 ◽  
Author(s):  
D. Hoppensteadt ◽  
O. Iqbal ◽  
R. L. Bick ◽  
J. Fareed

SummaryThrombotic disorders are the most common cause of death in the United States. About two million individuals die each year from an arterial or venous thrombosis or related disorders. About 80% to 90% of all cases of thrombosis can now be defined with respect to cause. Of these, over 50% occur in patients who harbor a congenital or acquired blood coagulation protein or platelet defect which caused the thrombotic event. It is obviously of major importance to define those individuals harboring such a defect as this allows: 1) appropriate antithrombotic therapy to decrease risks of recurrence; 2) determination of the length of time the patient must remain on therapy for secondary prevention; and 3) allow for testing of family members of those harboring a blood coagulation protein or platelet defect which is hereditary (about 50% of all coagulation and platelet defects mentioned above). Aside from mortality, significant additional morbidity occurs from both arterial or venous thrombotic events, including, but not limited to paralysis (non-fatal thrombotic stroke), cardiac disability (repeated coronary events), loss of vision (retinal vascular thrombosis), fetal waste syndrome (placental vascular thrombosis), stasis ulcers and other manifestations of post-phlebitic syndrome, etc.


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