Inflammation
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
The end-point of blood coagulation is the transformation of fibrinogen to fibrin by the action of thrombin.40,67,160,245 This can be divided into two systems based on the mechanisms by which thrombin is formed from prothrombin. According to the extrinsic mechanism, tissue thromboplastin is derived from the injured cells, and it converts prothrombin to thrombin in the presence of several factors (Table 4) such as calcium, Factor VII, Factor V, and Factor X (Figure 23). In the intrinsic mechanism, blood generates an activating agent that rapidly transforms prothrombin to thrombin using calcium, platelets, Factor XII, Factor XI, Factor IX, Factor VIII, Factor V, and Factor X.40 The thrombin so formed then activates the conversion of fibrinogen to fibrin.
Benzylpenicillin (Penicillin G)
M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson in Kucers’ The Use of Antibiotics, 2017
If administered in large doses of 6 g daily to uremic patients, or 24 g daily to those with normal renal function, Pen G can induce coagulation disorders. These may appear soon after Pen G administration is commenced and persist for about 4 days after it is stopped. Factors involved are platelet dysfunction, disturbed conversion of fibrinogen to fibrin and increased antithrombin III activity (Andrassy et al., 1976; Manian et al., 1990). Pen G therapy can also be associated with the development of acquired inhibitors of blood coagulation, particularly blocking inhibitors. These are proteins, but not necessarily antibodies, that can interfere with many aspects of the coagulation reaction. They are rarely, if ever, associated with overt bleeding. The prothrombin time is normal, but the activated partial thromboplastin time is usually prolonged. Uncommonly, Pen G hypersensitivity may be associated with the presence of specific clotting factor inhibitors which inactivate single factors. Inhibitors specifically directed against factors V, VIII, IX, and XI have been described, factor VIII inhibitors being the most common. These factor inhibitors appear to be antibodies, and their presence may be associated with severe bleeding (Orris et al., 1980).
Hypercoagulability And Thrombosis
Genesio Murano, Rodger L. Bick in Basic Concepts of Hemostasis and Thrombosis, 2019
Changes in circulating coagulation factors have also been well documented in both thrombosis and situations leading to thrombosis. Increased coagulation factors are often noted postoperatively, as well as in the postpartum period, in patients suffering fractures or trauma, in ulcerative colitis, in malignancy, in acute thrombosis, and in recurrent deep vein thrombophlebitis.9-11 Like the finding of increased platelet adhesion, however, many increases in coagulation factors that have been described have been measured after the fact, and the significance of this finding remains unclear. The coagulation factors most commonly increased in the above-mentioned disorders are fibrinogen, Factor VIII, Factor V, and Factor VII, and many investigators have measured “increased thromboplastin generation”12
Serine protease from Indian Cobra venom: its anticoagulant property and effect on human fibrinogen
Published in Toxin Reviews, 2022
K. N. Neema, Vivek Hamse Kameshwar, Zohara Nafeesa, Divya Kumar, Priya Babu Shubha, M. N. Nagendra Prasad, Shivananju Nanjunda Swamy
According to APTT assay, in the presence of calcium ions, thromboplastin activates coagulation factors of the intrinsic pathway in the plasma leading to clot formation. Clotting time is proportional to the concentration of factors VIII, IX, XI, and XII as well as common pathway factors II, V, and X. Whereas PT measures the time taken by the citrated plasma to clot in the presence of tissue thromboplastin and Ca2+ which activates extrinsic pathway of the human blood coagulation cascade. This assists in estimating the cause and extent of the hemorrhagic disorder. When thromboplastin reagent is added to citrated plasma, a clotting cascade is initiated forming a gel clot. The time required for clot formation would be prolonged if there is a deficiency of factor (s) activity in the extrinsic pathway of the coagulation cycle. Venom protease prolonged the clotting time for re-calcification Figure 3(c) and activated partial thromboplastin time (APTT) but have negligible variations for PT test as shown in Table 1, which suggests that serine protease from Naja naja venom, works on intrinsic pathway but has minimal effect on the extrinsic pathway.
Analysis of clinical characteristics and prognostic factors associated with EBV-associated HLH in children
Published in Hematology, 2022
Kun-yin Qiu, Shu-yi Guo, Yang-hui Zeng, Xiong-yu Liao, Shao-fen Lin, Jian-pei Fang, Dun-hua Zhou
We collect general information such as gender, age, family history and clinical symptoms such as fever, hepatomegaly, splenomegaly, superficial lymph node enlargement, jaundice, skin rash, plasma cavity effusion, central nervous system (CNS) symptoms. As for laboratory findings, we collect blood routine, liver function which included alanine aminotransferase (ALT), glutathione aminotransferase (AST), albumin (ALB), γ-glutamyl transferase (γ-GGT), serum total bilirubin (TBIL), and triglycerides (TG). Coagulation function include prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB). In addition, inflammatory factors which included soluble interleukin 2 receptor (sIL2R/sCD25), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), tumour necrosis factor-α (TNF-α), serum ferritin (SF), hemophagocytosis, whole blood/plasma EBV-DNA load and gene mutation associated with HLH.
Warfarin monitoring with viscoelastic haemostatic assays, thrombin generation, coagulation factors and correlations to Owren and Quick prothrombin time
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Caroline U. Nilsson, Karin Strandberg, Peter Reinstrup
TGA was measured on Ceveron alpha® (Technoclone, Vienna, Austria) with a fluorescent substrate and the TGA RC High® reagents (Technoclone). Coagulation is initiated through the addition of tissue factor and phospholipids in the commercial reagent (high concentration of recombinant human phospholipid micelles containing ∼5 pM recombinant human tissue factor). The thrombin formed is measured over time, and the results are presented as lag time (until the thrombin formation starts) in seconds, and the maximal amount of thrombin formed as an area under curve (AUC; or endogenous thrombin potential (ETP)) in nM × min. Different types of thromboplastin are used for the various analyses described above, but for each method the same type of commercial thromboplastin was used. CVs and normal reference ranges for all the respective plasma analyses are seen in Table 1.
Related Knowledge Centers
- Coagulation
- Partial Thromboplastin Time
- Phospholipid
- Placenta
- Reagent
- Prothrombin Time
- Tissue Factor
- Thrombin
- Calcium Chloride