Coagulation factor haemostasis

Vlasuk GP. Structural and functional characterization of tick anticoagulant peptide (TAP) a potent and selective inhibitor of blood coagulation factor Xa. Thrombosis and Haemostasis 1993 70 212-216. 

Coagulation factor V is a glycoprotein essential for haemostasis by accelerating the activation of prothrombin. Factor V is secreted as a single-chain polypeptide of 330 kDa... 

Lechner D, Eichinger S, Wanivenhaus A, Kyrle PA. Peri-interventional control of haemostasis in a patient with combined coagulation factor V- and factor VIII-deflciency and anaphylaxis to fresh frozen plasma—a rare indication for recombinant factor Vila. Haemophilia 2010 16(4) 704-5. 

When HES is infused, the smaller molecules are excreted by the kidneys, while the larger molecules are metabolised by o-amylase, and taken up by the reticuloendothelial system (RES) and the skin. Even though HES molecules disappear from the blood within 10-72 hours, dependent on their molecular weight, they can be detected in the RES for at least one month. Anaphylactic reactions to HES are lower than with other colloids and they have minimal effects on coagulation. Controversy exists regarding the use of HES in patients with renal insufficiency, and dose recommendations are based on the risk of renal tubular overload and the influence on haemostasis (possible decrease in factor Vll/von Willebrand factor). The risk is greater with the higher MW solutions, and appears to be lower with the new HES 130/0.4. 

Sato K, Kawasaki T, Hisamichi N et al. (1998) Antithrombotic effects of YM-60828, a newly synthesized factor Xa inhibitor, in rat thrombosis models and its effects on bleeding time. Br J Pharmacol 123 92-96 Yamazaki M, Asakura H, Aoshima K et al. (1994) Effects of DX-9065a, an orally active, newly synthesized and specific inhibitor of factor Xa, against experimental disseminated intravascular coagulation in rats. Thromb Haemostasis 72 393-396... 

By means of the complex process of haemostasis, the organism seeks to protect itself spontaneously against bleeding and the corresponding loss of blood. Three components are available to this end (J.) blood vessels themselves (= vascular haemostasis), (2.) platelets and endothelial cells (= cellular haemostasis), and (J.) blood-clotting factors (= plasmic blood coagulation). 

If no haemorrhagic diathesis is present or when no invasive measures or techniques which might possibly distress the patient are planned, coagulation disorders generally require no treatment. The equilibrium between haemostasis and fibrinolysis, which is based on lower clotting factor levels, is indeed somewhat unstable, yet it does not normally lead to spontaneous haemorrhaging. 

Aberg M, Hedner U, Bergentz SE (1977) The effect of dextran on haemostasis and coagulation with special regard to factor VIII. Acta Univ Ups Symp 3 23-30 Adar R, Schneiderman W (1977) Severe anaphylaxis in cirrhotic patients receiving dextran 40. JAMA 237 119-120... 

R. J. Linhardt, A. Al-Hakim, S. Ampofo and D. Loganathan, in "New Trends in Haemostasis Coagulation Proteins Endothelium, and Tissue Factors," G. Schettler, L. Heene and J. Harenberg, Eds., Springer Verlag, 1990, pp. 12-26. 

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