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Spontaneous (Unexplained) Thrombosis: The Inherited Basis for the Thrombohemorrhagic Balance
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Heparin cofactor II (HC II)—Another plasma factor, HC II has also been identified as a thrombin inhibitor. HC II seems to depend on another endothelial GAG, dermatan sulfate, to exert its effect.20,21
Coagulation Theory, Principles, and Concepts
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Heparin cofactor II is another plasma protein inhibitor of thrombin. Like antithrombin III, its activity as an inhibitor is enhanced by the presence of heparin. Unlike antithrombin III, it does not have a high-affinity binding site for heparin, i.e., the pentasaccharide site for antithrombin III binding. It therefore requires higher concentrations of heparin to achieve the same degree of thrombin inhibition. Heparin cofactor II activity is also enhanced by several other polyanionic compounds, including heparan and chondroitin sulfates. Dermatan sulfate, on the other hand, seems to possess a specific binding site for heparin cofactor II. This does not, however, offer any significant advantages over heparin. On a weight basis, considerably less heparin is required than dermatan sulfate to achieve the same degree of thrombin inhibition. Recently, dermatan disulfates have been found to enhance heparin cofactor II’s activity even more than dermatan sulfate. There has been some interest in using dermatan-like compounds in place of heparin in such areas as cardiovascular surgery, where it has been reported that bleeding problems occur less frequently with dermatans than with heparins (88–91).
Pharmacodynamics of Anticoagulants
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Dennis Mungall, Richard H. White
The use of an in vitro coagulation test to measure the in vivo effect of heparin poses several problems, since the result reflects a dynamic process that is affected by a number of variables, including the blood volume, the hematocrit, the circulating level AT-III and heparin cofactor II, binding of heparin to other plasma proteins, temperature, plasma pH, and the presence of platelet factor 4, which inactivates heparin. Other factors that can also affect the result of a coagulation test include the type of anticoagulant used in the blood collection, the nature and concentration of the substrate used to activate coagulation (e.g., the thromboplastin reagent), the buffer used, the presence of naturally occurring inhibitors, such as a lupus anticoagulant, the order of adding the various reagents, length of incubation time during performance of the test, the pH of the reagents, time between obtaining the blood sample and test measurement, and whether a manual or automated system is used.226 Generally speaking, heparin prolongs the time required for blood to clot by inhibiting amplification of the coagulation cascade catalyzed by thrombin.
Clinical Significance of Endothelin-1 And C Reaction Protein in Restenosis After the Intervention of Lower Extremity Arteriosclerosis Obliterans
Published in Journal of Investigative Surgery, 2021
Weishuai Lian, Hongpeng Nie, Yifeng Yuan, Kun Wang, Weiqian Chen, Liangfu Ding
Restenosis after intervention of ASO is a complicated process. Several studies have demonstrated some possible roles of biomarkers in the process. Lu et al. reported that plasma heparin cofactor II activity was associated with the incidence of in-stent restenosis after the intervention of ASO, and patients with lower heparin cofactor II activity had higher restenosis rates [22]. Nomura et al. reported that factors of hemoglobin A1c, E-selectin, vascular cell adhesion molecule-1, and plasminogen activator inhibitor-1 were all biomarkers for ASO [8]. In a recent study, it was also found that plasma olfactomedin-2 increased in restenosis patients with ASO, who received intervention [23]. However, except for these studies, few studies have focused on other biomarkers in restenosis.
Verification of a proteomic biomarker panel to diagnose minor stroke and transient ischaemic attack: phase 1 of SpecTRA, a large scale translational study
Published in Biomarkers, 2018
Andrew M. Penn, Maximilian B. Bibok, Viera K. Saly, Shelagh B. Coutts, Mary L. Lesperance, Robert F. Balshaw, Kristine Votova, Nicole S. Croteau, Anurag Trivedi, Angela M. Jackson, Janka Hegedus, Evgenia Klourfeld, Amy Y. X. Yu, Charlotte Zerna, Christoph H. Borchers
Heparin cofactor II (HCII) functions to inactive thrombin and is therefore involved in the modulation of blood coagulation. HCII is responsible for approximately 20–30% of thrombin inactivation during coagulation (Rau et al.2007, Bhakuni et al.2016). HCII is unique in that, in the extravascular lumen, it inhibits only thrombin and no other proteins involved in the coagulation process (Parker and Tollefsen 1985). Plasma concentrations of HCII have been found to decrease with age (Aihara et al.2004), with higher levels associated with reduced risk of peripheral arterial disease in the elderly (Aihara et al.2009). Higher levels of HCII may also be preventative of ischaemic stroke (Toulon et al.2008). Aihara et al. (2004) found that after controlling for patient age, sex and diabetes status, higher HCII levels were more negatively correlated with carotid atherosclerosis than with HDL in elderly patients. The finding in our study that higher HCII levels were predictive of mimic conditions is in keeping with the results of these previous studies.
Congenital prothrombin defects: they are not only associated with bleeding but also with thrombosis: a new classification is needed
Published in Hematology, 2018
Antonio Girolami, Silvia Ferrari, Elisabetta Cosi, Bruno Girolami, Anna Maria Lombardi
Our knowledge about the dysforms have changed during the last few years. Actually the first data about the existence of a severe procoagulant state associated with a mild bleeding tendency dated back to 2002 [11]. In that year Akhavan et al. reported an 11 years old girl from Iran who had only a mild-to-moderate bleeding tendency despite having prothrombin level of less than 1% but an antigen level of 61%. On the suspicion of a dysfunctional protein further studies showed that the underlying mutation was Arg67His substitution (chymotrypsinogen numbering that is equivalent to the Arg382His mutation). Furthermore, it was demonstrated a decreased activation of protein C, a decreased binding to thrombomodulin, a severe impairment of thrombin inhibition by heparin cofactor II and, finally, a decrease of prothrombin activation by the FXa–FVa complex. The complex defect caused by the Arg67His mutation was cautiously concluded to affect both the coagulant and the anticoagulant activities of thrombin. It was thought that there was a balance between these two opposing forces [11]. This interesting observation remained silent for several years and the prothrombin defects were always considered to be responsible of a bleeding tendency. Several dysprothrombinemias were reported but no thrombosis event was ever mentioned [2,3,12–17].