Blood-Coagulating Factors

Interference with blood-coagulating factors may result from a deficiency of the factors or from the appearance of antagonists. 

The deficiencies in blood coagulation may involve one or more of the factors responsible for the process and can be classified as deficiencies in (1) the thromboplastin systems, (2) prothrombin formation, and (3) the conversion of fibrinogen to fibrin. 

The distribution of hemophilia among the descendants of Queen Victoria is by now too well known to be described here, suffice to say that the disease is transmitted through a sex-linked recessive gene. 

in most cases, the female transfers the gene but does not manifest the deficiency in her phenotype. Only in a few cases is the deficiency apparent in females. This is usually explained by assuming that the gene is not completely recessive. 

McFarland was the first to report the development of hemophilia in a 45-year-old patient who had received repeated transfusions. Several case reports have appeared. At first it was believed that the hemorrhagic diathesis resulted from the accumulation of coagulation inhibitors heparin was often incriminated. Only in the 1950 s was the immunological pathogenesis of the disease accepted. Inhibitors of factors VIII (hemophilia A) and IX (hemophilia B) have been reported. The acquired inhibitors to factor VIII have been studied most extensively. In fact, the inhibitors have been purified. They are believed to be y-globulins with a sedimentation constant of 7 S. 

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Griffin JH Role of surface in surface-dependent SO activation of Hageman factor (blood coagulation factor XII). Proc Natl Acad Sci USA 1978 75 1998-2002. 

The main goal of recessively inherited coagulation disorder (RICD) treatment is to prevent and control spontaneous and surgery-related bleeding episodes. Specifically, therapeutic options improve hemostasis via replacement of deficient blood coagulation factors while minimizing the development of immune tolerance.20... 

Possible effects of coffee on blood coagulation factors need further study, even though possible links may exist. 

Volume 222. Proteolytic Enzymes in Coagulation, Fibrinolysis, and Complement Activation (Part A Mammalian Blood Coagulation Factors and Inhibitors)... 

Isaacs, B.S., Husten, E.J., Esmon, C.T., and Johnson, A.E. (1986) A domain of membrane-bound blood coagulation factor Va is located far from the phospholipid surface. A fluorescence energy transfer measurement. Biochemistry 25, 4958-4969. 

Lee, K.Y., Birckbichler, P.J., and Patterson Jr., M.K. (1988) Colorimetric assay of blood coagulation factor XIII in plasma. Clin. Chem. 34, 906-910. 

Table 12.2 Recombinant blood coagulation factors that have been approved for the management of coagulation disorders...

Blood-Coagulation Factor VIII Genetics, Physiological Control, and Bioassay G. I. C. Ingram... 

It is believed that heparin acts by neutralizing a number of active blood coagulation factors, thus disrupting the transformation of prothrombin into thrombin. Heparin is used to prevent thrombo-formation in myocardial infarctions, thrombosis, and embolism, for maintaining liquid conditions in the blood in artificial blood drcnlation and hemodialysis. Synonyms of this drug are arteven, hepalen, leparan, Uquemin, panheprin, vetren, and many others. 

Dermal/Ocular Effects. Very few reports mention any effect of carbon tetrachloride inhalation on the skin. Inhalation exposure to carbon tetrachloride for several days in the workplace caused a blotchy, macular rash in one man (but not in six others) (McGuire 1932). Similarly, a hemorrhagic rash occurred in a woman exposed to carbon tetrachloride fumes for several days in the workplace (Gordon 1944), and black and blue marks were seen in a patient exposed intermittently to carbon tetrachloride vapors for several years (Straus 1954). Because observations of dermal effects are so sporadic, it is difficult to judge whether these effects are related to carbon tetrachloride exposure, or are incidental. Conceivably, they may have been secondary to reduced synthesis of blood coagulation factors resulting from carbon tetrachloride-induced hepatotoxicity. No studies were located regarding ocular effects in humans or animals after inhalation exposure to carbon tetrachloride. 

Blood coagulation factors Haemophilia and other related blood disorders Human blood... 

Tetrahydropyrazolo[3,4-f]pyridines have been prepared as cannabinoid modulators <2007W0112399>. The pyra-zolo[3,4-4pyridine, Apixaban (BMS-562247), has been found to be a highly potent, selective, efficacious, and orally bioavailable inhibitor of blood coagulation factor xa <2007JMC5339>. Several pyrazolo[3,4-f]pyridines have been found to be potent inhibitors of human eosinophil phosphodiesterase <2007JMC344>. 

Blood coagulation factors antihemophilic factor (recombinant) eptacog alfa (activated) factor IX contentrate (human) factor IX (recombinant) moroctocog alfa... 

Antihemophilic factor USP [USP] Blood-coagulation factor VIII, complex [CAS] Factor VIII, recombinant [SY]... 

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. 

Waxman L, Smith DE, Arcuri KE, Vlasuk GP. Tick anticoagulant peptide (TAP) is a novel inhibitor of blood coagulation factor Xa, Science 1990 248 593. 

Dunwiddie CT, Waxman L, Vlasuk GP, Friedman PA. Purification and characterization of inhibitors of blood coagulation factor Xa from hematophagous organisms. Methods in Enzymol 1993 233 291-312. 

Schreuder H, Arkema A, deBoer B, Kalk K, Dijkema R, Mulders J, Theunissen H, Hoi W. Crystallization and preliminary crystallographic analysis of antistasin, a leech-derived inhibitor of blood coagulation factor Xa. JMol Biol 1993 231 1137-1138. 

Protein C functions as an anticoagulant by proteolytically inactivating two protein cofactors of blood coagulation, factors V and VIII.402 It too circulates in a zymogen form and is activated by limited proteolysis. Protein C appears to contain about 16 sites for Ca2+, all of equal affinity, while activated protein C binds about nine Ca2+. Conformational rearrangement during activation results in loss of binding sites. 

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