Anticoagulants
Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod in The Primary FRCA Structured Oral Examination Study Guide 2, 2017
What types of heparin do you know?Naturally occurring heparinA highly sulphated glycosaminoglycan carbohydrate weighing between 3000 and 50 000 Daltons.It is produced by basophils and mast cells.Unfractionated heparin (UFH)Synthetic agent weighing between 5000 and 25 000 Daltons.It binds to and potentiates the action of antithrombin III 1000-fold.Activated antithrombin III inhibits thrombin and other serine proteases that promote blood clotting.
Procoagulant Activity in Gastroenterology
Gary A. Levy, Edward H. Cole in Procoagulant Activity in Health and Disease, 2019
Despite the evidence for activation of coagulation and fibrin generation at all phases of clinical activity, cross-linked fibrin degradation products (FDP), as measured by latex agglutination, were within the normal range (<250 mg/ml). In contrast, in the D-dimer assay for FDP, a sensitive marker of fibrinolysis,27 levels correlate significantly with the fibrinopeptide-A levels, suggesting reactive fibrinolysis in some patients. Plasminogen activator inhibitor type 1 (PAI-1) levels showed no significant difference between active and inactive disease, although 5 of the 14 (35%) patients had a PAI-1 level above the upper limit of normal at some stage during the study period. In those patients with the highest PAI-1 levels, the D-dimers were all within the normal range, suggesting impaired fibrinolysis in this group. In all patients, antithrombin III levels were within the normal range. The protein C antigen levels were significantly lower in the active phase of disease than in remission. Two patients had a free protein S level below the lower limit of normal.
Inflammation
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Hemorrhagic syndromes are connected with inherited defects of coagulation factors (Table 2). In these disorders the defect is mainly due to the synthesis of an abnormal protein rather than the lack of production.376 Deficiences of Factors VII, VIII, and IX are the most frequently occurring disease conditions. Both defects are related to extrinsic and intrinsic pathways of coagulation 89,157 Factor VIII and Factor IX deficiencies are X chromosomelinked disorders, and they are mainly found in males. The management of Factor VIII inhibitors in nonhemophilic patients seems to be essential.157 Hereditary antithrombin III deficiency is connected with venous thrombosis.309 In certain conditions, such as colon adenocarcinoma, the production of acquired factors has been observed.81
Ameliorative effect of flavonoid-rich extracts from Gongronema latifolium against diabetic cardiomyopathy via serpin A3 and socs3-a in streptozocin treated rats
Published in Biomarkers, 2022
Babatunji Emmanuel Oyinloye, Basiru Olaitan Ajiboye, Oluwafolakemi Johnson, Olutunmise Victoria Owolabi, Jerius Nkwuda Ejeje, Bartholomew I. C. Brai, Olaposi Idowu Omotuyi
The SERPINC1 gene encodes antithrombin (previously known as antithrombin III), which is a type of serine protease inhibitor (serpin). Serpins control several types of chemical reactions by blocking the activity of certain proteins. Antithrombin is found in the bloodstream and is important for controlling blood clotting (Song et al. 2020). While one part of antithrombin binds to thrombin and other clotting proteins, another part of the protein binds to a substance called heparin (Gindele et al. 2021). Antithrombin changes its shape when it binds to heparin. This change in shape allows antithrombin to inactivate clotting proteins at a much faster rate. Over secretion of this protein leads to serpin polymerisation, which does not only reduce the amount of active inhibitor but also leads to accumulation of the polymers, causing cell death and organ failure (Ingwersen 2020).
Trend of fluctuations of antithrombin in plasma of patients with COVID-19: a meta-analysis and systematic review
Published in Expert Review of Hematology, 2022
Mehrdad Rostami, Hassan Mansouritorghabeh
A total of 28 studies involving 2729 patients with COVID‐19 included in the meta‐analysis [3,24–50]. Of the 28 articles, merely 9 articles reported the use of an activity assay for antithrombin testing (32.14%) and 18 articles did not report the method used to detect (67.85%). In addition, the reference range of the used kits for the detection of antithrombin was variable somehow. Among 28 articles, 15 had a reference range for antithrombin reported. The broader reference range was 70–140%, and the most common reference range was 80–120%. The latter reference range was the most commonly reported and was used as a mean of the reference ranges for the analyses. A large heterogeneity was found between studies (I2 = 96.39%, p = 0.00). Consequently, a random-effects model was used for the analysis. The analysis showed that the pooled mean antithrombin level for all patients was 89.65% (95% CI: 86.52–92.79, normal range: 80–120%), as shown in Figure 2. Subgroup analysis based on patient ward showed a statistically significant decrease in antithrombin level in ICU COVID‐19 patients (All patients group: mean = 92.46%, 95% CI: 89.16–95.76; I2 = 96.56%; ICU patients group: mean = 83.59%, 95% CI: 78.24–88.95; I2 = 85.63%). Testing for differences between subgroups showed a statistically significant difference between levels of antithrombin in ICU and non-ICU patients (p = 0.01).
First Report of an α Chain Variant [Hb Coombe Park (HBA2: c.382A>G)] from India, Coinherited with a Novel SERPINC1 Gene Mutation: A Double Whammy?
Published in Hemoglobin, 2022
Sona B. Nair, Arundhati S. Athalye, Madhavi Panphalia, Firuza R. Parikh
Hereditary antithrombin (AT) deficiency, an important physiological inhibitor of blood coagulation proteases such as thrombin and factor Xa, are associated with high risk of a pro-thrombotic tendency is caused by mutations/variants in the SERPINC1 gene [4]. It is an autosomal disorder with a dominant inheritance pattern and affects about 1/2000 to 1/3000 individuals [5]. Antithrombin deficiency can be classified as a type I (quantitative) and type II (qualitative or functional) deficiency [6]. To date, several mutations have been reported in the SERPINC1 gene affecting the AT structure and function [7]. Antithrombin deficiency is mainly due to heterozygous mutations, as homozygous mutations are very rare and incompatible with life, though there have been reports of few homozygous cases [5].