Antithrombin iii. Medical search

A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.

An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis.

Endogenous factors and drugs that directly inhibit the action of THROMBIN, usually by blocking its enzymatic activity. They are distinguished from INDIRECT THROMBIN INHIBITORS, such as HEPARIN, which act by enhancing the inhibitory effects of antithrombins.

A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.

An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance.

An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.

Activated form of factor X that participates in both the intrinsic and extrinsic pathways of blood coagulation. It catalyzes the conversion of prothrombin to thrombin in conjunction with other cofactors.

Storage-stable glycoprotein blood coagulation factor that can be activated to factor Xa by both the intrinsic and extrinsic pathways. A deficiency of factor X, sometimes called Stuart-Prower factor deficiency, may lead to a systemic coagulation disorder.

The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.

A sulfated plasma protein with a MW of approximately 66kDa that resembles ANTITHROMBIN III. The protein is an inhibitor of thrombin in plasma and is activated by dermatan sulfate or heparin. It is a member of the serpin superfamily.

A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.

Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.

A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.

Laboratory tests for evaluating the individual's clotting mechanism.

A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.

Agents that prevent clotting.

Endogenous substances, usually proteins, that are involved in the blood coagulation process.

Inflammation of a vein associated with a blood clot (THROMBUS).

The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.

Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.

An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)

Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.

A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.

An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)

Single-chain polypeptides of about 65 amino acids (7 kDa) from LEECHES that have a neutral hydrophobic N terminus, an acidic hydrophilic C terminus, and a compact, hydrophobic core region. Recombinant hirudins lack tyr-63 sulfation and are referred to as 'desulfato-hirudins'. They form a stable non-covalent complex with ALPHA-THROMBIN, thereby abolishing its ability to cleave FIBRINOGEN.

A reagent used mainly to induce experimental liver cancer. According to the Fourth Annual Report on Carcinogens (NTP 85-002, p. 89) published in 1985, this compound "may reasonably be anticipated to be a carcinogen." (Merck, 11th ed)

The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.

Activated form of factor IX. This activation can take place via the intrinsic pathway by the action of factor XIa and calcium, or via the extrinsic pathway by the action of factor VIIa, thromboplastin, and calcium. Factor IXa serves to activate factor X to Xa by cleaving the arginyl-leucine peptide bond in factor X.

Formation and development of a thrombus or blood clot in the blood vessel.

Clotting time of PLASMA mixed with a THROMBIN solution. It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. BATROXOBIN, a thrombin-like enzyme unaffected by the presence of heparin, may be used in place of thrombin.

The rate dynamics in chemical or physical systems.

An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC 4.2.2.7.

Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.

Immunoelectrophoresis in which a second electrophoretic transport is performed on the initially separated antigen fragments into an antibody-containing medium in a direction perpendicular to the first electrophoresis.

Colorless, endogenous or exogenous pigment precursors that may be transformed by biological mechanisms into colored compounds; used in biochemical assays and in diagnosis as indicators, especially in the form of enzyme substrates. Synonym: chromogens (not to be confused with pigment-synthesizing bacteria also called chromogens).

A sulfated pentosyl polysaccharide with heparin-like properties.

The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.

A naturally occurring glycosaminoglycan found mostly in the skin and in connective tissue. It differs from CHONDROITIN SULFATE A (see CHONDROITIN SULFATES) by containing IDURONIC ACID in place of glucuronic acid, its epimer, at carbon atom 5. (from Merck, 12th ed)

Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.

Coagulant substances inhibiting the anticoagulant action of heparin.

Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin.

A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Carbohydrates consisting of between two (DISACCHARIDES) and ten MONOSACCHARIDES connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form.

A member of the serpin superfamily found in plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin.

Activated form of factor XI. In the intrinsic pathway, Factor XI is activated to XIa by factor XIIa in the presence of cofactor HMWK; (HIGH MOLECULAR WEIGHT KININOGEN). Factor XIa then activates factor IX to factor IXa in the presence of calcium.

The parts of a macromolecule that directly participate in its specific combination with another molecule.

Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.

Glycoproteins with a molecular weight of approximately 620,000 to 680,000. Precipitation by electrophoresis is in the alpha region. They include alpha 1-macroglobulins and alpha 2-macroglobulins. These proteins exhibit trypsin-, chymotrypsin-, thrombin-, and plasmin-binding activity and function as hormonal transporters.

A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.

The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.

The natural enzymatic dissolution of FIBRIN.

Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).

An order of wholly aquatic MAMMALS occurring in all the OCEANS and adjoining seas of the world, as well as in certain river systems. They feed generally on FISHES, cephalopods, and crustaceans. Most are gregarious and most have a relatively long period of parental care and maturation. Included are DOLPHINS; PORPOISES; and WHALES. (From Walker's Mammals of the World, 5th ed, pp969-70)

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

Two small peptide chains removed from the N-terminal segment of the beta chains of fibrinogen by the action of thrombin. Each peptide chain contains 20 amino acid residues. The removal of fibrinopeptides B is not required for coagulation.

Extracellular protease inhibitors that are secreted from FIBROBLASTS. They form a covalent complex with SERINE PROTEASES and can mediate their cellular internalization and degradation.

A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1-antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of SERINE ENDOPEPTIDASES, and some serpins occur in plants where their function is not known.

Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or N-acetylgalactosamine.

Stable blood coagulation factor involved in the intrinsic pathway. The activated form XIa activates factor IX to IXa. Deficiency of factor XI is often called hemophilia C.

Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).

Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.

Heparin derivatives. The term has also been used more loosely to include naturally occurring and synthetic highly-sulphated polysaccharides of similar structure. Heparinoid preparations have been used for a wide range of applications including as anticoagulants and anti-inflammatories and they have been claimed to have hypolipidemic properties. (From Martindale, The Extra Pharmacopoeia, 30th, p232)

Inflammation of a vein, often a vein in the leg. Phlebitis associated with a blood clot is called (THROMBOPHLEBITIS).

Amidines substituted with a benzene group. Benzamidine and its derivatives are known as peptidase inhibitors.

7-Hydroxycoumarins. Substances present in many plants, especially umbelliferae. Umbelliferones are used in sunscreen preparations and may be mutagenic. Their derivatives are used in liver therapy, as reagents, plant growth factors, sunscreens, insecticides, parasiticides, choleretics, spasmolytics, etc.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.

Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.

Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).

A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.

A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.

The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).

The sum of the weight of all the atoms in a molecule.

Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.

Compounds that contain a 1-dimethylaminonaphthalene-5-sulfonyl group.

A family of proteinase-activated receptors that are specific for THROMBIN. They are found primarily on PLATELETS and on ENDOTHELIAL CELLS. Activation of thrombin receptors occurs through the proteolytic action of THROMBIN, which cleaves the N-terminal peptide from the receptor to reveal a new N-terminal peptide that is a cryptic ligand for the receptor. The receptors signal through HETEROTRIMERIC GTP-BINDING PROTEINS. Small synthetic peptides that contain the unmasked N-terminal peptide sequence can also activate the receptor in the absence of proteolytic activity.

Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.

Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.

Pregnane derivatives containing two double bonds anywhere within the ring structures.

The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.

Precursor of plasmin (FIBRINOLYSIN). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent.

Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.

Proteins prepared by recombinant DNA technology.

Sperm chemotaxis. (1/874)

Communication between spermatozoa and egg before contact by chemotaxis appears to be prevalent throughout the animal kingdom. In non-mammalian species, sperm chemotaxis to factors secreted from the egg is well documented. In mammals, sperm chemotaxis to follicular factors in vitro has been established in humans and mice. The attractants of female origin in non-mammalian species are heat-stable peptides or proteins of various sizes, or other small molecules, depending on the species. Species specificity of the attractants in non-mammalian species may vary from high species specificity, through specificity to families with no specificity within a family, to absence of specificity. The mammalian sperm attractants have not been identified but they appear to be heat-stable peptides. The claim that progesterone is the attractant for human spermatozoa has failed to be substantiated, neither have claims for other mammalian sperm attractants been verified. The molecular mechanism of sperm chemotaxis is not known. Models involving modulation of the intracellular Ca2+ concentration have been proposed for both mammalian and non-mammalian sperm chemotaxis. The physiological role of sperm chemotaxis in non-mammalian species appears to differ from that in mammals. In non-mammalian species, sperm chemotaxis strives to bring as many spermatozoa as possible to the egg. However, in mammals, the role appears to be recruitment of a selective population of capacitated ('ripe') spermatozoa to fertilize the egg. (+info)

Age-related changes in blood coagulation and fibrinolysis in mice fed on a high-cholesterol diet. (2/874)

To investigate the pathogenesis of hyperlipidemia-induced atherosclerosis, we examined age-dependent changes in platelet activity, blood coagulation and fibrinolysis in susceptibility to a high cholesterol diet (HCD) feeding in male ICR mice. Pretreatment of platelet-rich-plasma from HCD feeding mice for 3 days with epinephrine (300 microM) resulted in a marked enhancement of adenosine 5'-diphosphate (ADP: 0.1 microM) or collagen (0.7 microgram/ml)-stimulated aggregation compared with the same in control mice. Yohimbine as alpha 2-adrenergic blocker antagonized these aggregations in a dose-dependent manner. A significant increase in plasma total cholesterol and VLDL (very low-density lipoprotein)-LDL (low-density lipoprotein)-cholesterol and the liver/body weight ratio was observed in mice fed on HCD for 3 months (3-month HCD mice). In the early phase of this experiment, a significant increase in fibrinogen was observed. In the middle phase, increases in the activity of antithrombin III (ATIII) and alpha 2-plasmin inhibitor (alpha 2-Pl) followed. Plasminogen content gradually decreased in both normal diet and HCD mice throughout the experiment. The activity of plasminogen activator inhibitor (PAI) decreased in 3-month HCD mice. Morphological observation of the aortic arch from 3-month HCD mice revealed apparent atheromatous plaques not seen in control mice. These results suggest that 3-month HCD mice can be a convenient hyperlipidemia-induced atherosclerotic model and the changes in platelet activity, coagulation and fibrinolysis in the early phase may be a cause of pathologic changes in this model. (+info)

Single and combined prothrombotic factors in patients with idiopathic venous thromboembolism: prevalence and risk assessment. (3/874)

The inherited thrombophilias--deficiencies of protein C, protein S, and antithrombin III--and the prothrombotic polymorphisms factor V G1691A and factor II G20210A predispose patients toward venous thromboembolism (VTE). The aim of this study was to determine the prevalence of single and combined prothrombotic factors in patients with idiopathic VTE and to estimate the associated risks. The study group consisted of 162 patients referred for work-up of thrombophilia after documented VTE. The controls were 336 consecutively admitted patients. In all subjects factor V G1691A, factor II G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T were analyzed by specific polymerase chain reactions and restriction enzymes. Activities of antithrombin III and protein C, free protein S antigen, and lupus anticoagulant were determined in a subset of 109 patients who were not receiving oral anticoagulants. The prevalences of heterozygotes and homozygotes for factor V G1691A and factor II G20210A among patients and controls were 40.1% versus 3.9% and 18.5% versus 5.4%, respectively (P=0.0001). The prevalence of homozygotes for MTHFR C677T in patients was 22.8% and in controls, 14.3% (P=0.025). Heterozygous and homozygous factor V G1691A, factor II G20210A, and homozygous MTHFR C677T were found to be independent risk factors for VTE, with odds ratios of 16.3, 3.6, and 2.1, respectively. Two or more polymorphisms were detected in 27 of 162 patients (16.7%) and in 3 of 336 controls (0.9%). Logistic regression analysis disclosed odds ratios of 58.6 (confidence interval [CI], 22.1 to 155.2) for joint occurrence of factor V and factor II polymorphisms, of 35.0 (CI, 14.5 to 84.7) for factor V and MTHFR polymorphisms, and of 7.7 (CI, 3.0 to 19.6) for factor II and MTHFR polymorphisms. Among 109 patients in whom a complete thrombophilic work-up was performed, 74% had at least 1 underlying defect. These data indicate that in most patients referred for evaluation of thrombophilia due to idiopathic VTE, 1 or more underlying genetic predispositions were discernible. The presence of >1 of the prothrombotic polymorphisms was associated with a substantial risk of VTE. (+info)

Oxidation of methionine residues in antithrombin. Effects on biological activity and heparin binding. (4/874)

Commercially available human plasma-derived preparations of the serine protease inhibitor antithrombin (AT) were shown to contain low levels of oxidation, and we sought to determine whether oxidation might be a means of regulating the protein's inhibitory activity. A recombinant form of AT, with similarly low levels of oxidation as purified, was treated with hydrogen peroxide in order to study the effect of oxidation, specifically methionine oxidation, on the biochemical properties of this protein. AT contains two adjacent methionine residues near the reactive site loop cleaved by thrombin (Met314 and Met315) and two exposed methionines that border on the heparin binding region of AT (Met17 and Met20). In forced oxidations with hydrogen peroxide, the methionines at 314 and 315 were found to be the most susceptible to oxidation, but their oxidation did not affect either thrombin-inhibitory activity or heparin binding. Methionines at positions 17 and 20 were significantly oxidized only at higher concentrations of peroxide, at which point heparin affinity was decreased. However at saturating heparin concentrations, activity was only marginally decreased for these highly oxidized samples of AT. Structural studies indicate that highly oxidized AT is less able to undergo the complete conformational change induced by heparin, most probably due to oxidation of Met17. Since this does not occur in less oxidized, and presumably more physiologically relevant, forms of AT such as those found in plasma preparations, oxidation does not appear to be a means of controlling AT activity. (+info)

Dose response of intravenous heparin on markers of thrombosis during primary total hip replacement. (5/874)

BACKGROUND: Thrombogenesis in total hip replacement (THR) begins during surgery on the femur. This study assesses the effect of two doses of unfractionated intravenous heparin administered before femoral preparation during THR on circulating markers of thrombosis. METHODS: Seventy-five patients undergoing hybrid primary THR were randomly assigned to receive blinded intravenous injection of either saline or 10 or 20 U/kg of unfractionated heparin after insertion of the acetabular component. Central venous blood samples were assayed for prothrombin F1+2 (F1+2), thrombin-antithrombin complexes (TAT), fibrinopeptide A (FPA), and D-dimer. RESULTS: No changes in the markers of thrombosis were noted after insertion of the acetabular component. During surgery on the femur, significant increases in all markers were noted in the saline group (P < 0.0001). Heparin did not affect D-dimer or TAT. Twenty units per kilogram of heparin significantly reduced the increase of F1+2 after relocation of the hip joint (P < 0.001). Administration of both 10 and 20 U/kg significantly reduced the increase in FPA during implantation of the femoral component (P < 0.0001). A fourfold increase in FPA was noted in 6 of 25 patients receiving 10 U/kg of heparin but in none receiving 20 U/kg (P = 0.03). Intraoperative heparin did not affect intra- or postoperative blood loss, postoperative hematocrit, or surgeon's subjective assessments of bleeding. No bleeding complications were noted. CONCLUSIONS: This study demonstrates that 20 U/kg of heparin administered before surgery on the femur suppresses fibrin formation during primary THR. This finding provides the pathophysiologic basis for the clinical use of intraoperative heparin during THR. (+info)

Effect of thrombin inhibition in vascular dementia and silent cerebrovascular disease. An MR spectroscopy study. (6/874)

BACKGROUND AND PURPOSE: Silent cerebrovascular disease (CVD) has been proposed as a predisposing condition for clinically overt stroke and vascular dementia. Recently, we found increased thrombin generation in silent CVD patients. Here, we report the effect of thrombin inhibition using a potent selective thrombin inhibitor on the cerebral metabolism and function in peripheral arterial occlusive disease (PAOD) patients with or without silent CVD. METHODS: We examined 17 mild chronic PAOD patients, including 2 cases of vascular dementia. We divided the patients into 2 groups: 1 was the advanced CVD group with multiple lacunar infarction and/or advanced periventricular hyperintensity detected by brain MRI (n=12), and the other was the no CVD group that had none of these abnormalities (n=5). We assessed the cerebral biochemical compounds in the deep white matter area and cerebellar hemisphere (8 cm3) by proton MR spectroscopy before and after infusion of argatroban (10 mg/d IV) over 2 hours for 7 days. RESULTS: The ratio of N-acetylasparate (NAA) to total creatine (Cre) in the deep white matter area was significantly lower in the advanced CVD group than in the no CVD group, whereas there were no significant differences in this ratio in the cerebellar hemisphere between the 2 groups. In the former group, this decreased NAA/Cre ratio significantly increased after argatroban therapy, whereas there was no change in the latter group. The 2 patients with vascular dementia showed clinical improvement with marked increases in the NAA/Cre ratio and mini-mental score. CONCLUSIONS: These results suggest that increased thrombin generation may have some pathophysiological roles in developing vascular dementia and its chronic predisposing conditions. Thrombin inhibition may break this vicious cycle and lead to clinical improvement. (+info)

Comparison of the antithrombotic effect of PEG-hirudin and heparin in a human ex vivo model of arterial thrombosis. (7/874)

Polyethylene glycol (PEG)-hirudin is a derivative of hirudin with a long plasma half-life. We have compared the efficacy of PEG-hirudin with unfractionated heparin (UH) in preventing arterial thrombosis. Arterial thrombus formation was induced ex vivo in 12 healthy human volunteers by exposing a tissue factor-coated coverslip positioned in a parallel-plate perfusion chamber to flowing nonanticoagulated human blood drawn directly from an antecubital vein at an arterial wall shear rate of 2600 s-1 for 3.5 minutes. PEG-hirudin, UH, or saline (as control) were administered ex vivo through a heparin-coated mixing device positioned proximal to the perfusion chamber. Platelet and fibrin deposition was quantified by immunoenzymatic measure of the P-selectin and D-dimer content of dissolved plasmin-digested thrombi, respectively. UH was administered to a plasma concentration of 0.35 IU/mL. This concentration prolonged the activated partial thromboplastin time from 32+/-1 seconds to 79+/-4 seconds (P<0.01). UH did not significantly prevent platelet deposition. However, fibrin deposition was reduced by 39% (P<0.05). PEG-hirudin in plasma concentrations of 0.5, 2.5, and 5 microg/mL prolonged the activated partial thromboplastin time to 48+/-2, 87+/-4, and 118+/-4 seconds, respectively. In contrast to UH, PEG-hirudin prevented both platelet and fibrin deposition in a dose-dependent manner with a >80% reduction at 5 microg/mL (P<0.01). Furthermore, the plasma level of PEG-hirudin required to significantly prevent fibrin deposition (0.5 microg/mL) corresponded to a much shorter prolongation of activated partial thromboplastin time (48+/-2 seconds) than that needed for UH (79+/-4 seconds). Thus, our results are compatible with the view that thrombin is greatly involved in recruitment of platelets in evolving thrombi, and that PEG-hirudin is an effective agent for preventing arterial thrombosis in a human ex vivo experimental model. (+info)

Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction. (8/874)

OBJECTIVES: The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND: Increased plasma hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical data concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS: Blood samples were obtained from 64 patients (mean age 67 +/- 11 years; 49 male) with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasma concentrations of fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS: The follow-up time was 27 +/- 17 months, and 19 patients died of cardiac causes during the follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86; 95% confidence interval [CI] 1.55-15.19), left ventricular ejection fraction (hazard ratio 0.94; 95% CI 0.90-0.99), FPA (hazard ratio 1.54; 95% CI 1.13-2.10), F1+2 (hazard ratio 2.03; 95% CI 1.17-3.53) and TAT (hazard ratio 1.88; 95% CI 1.27-2.79) as significant factors associated with cardiac mortality. In multivariate analyses, only FPA level (hazard ratio 1.84; 95% CI 1.03-3.30) and left ventricular ejection fraction (hazard ratio 0.93; 95% CI 0.88-0.98) were independent predictors of cardiac mortality. CONCLUSIONS: Elevated FPA in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction. (+info)

Antithrombin Găman AM, Găman GD (2014). "Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature". ... Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. This deficiency may be ... The prevalence of antithrombin deficiency is estimated at ~0.02 to 0.2% of the general population, and 1-5% of patients with ... Testing for antithrombin activity can confirm deficiency if the levels are less than 70%. Deficiency can result from genetic ...

https://en.wikipedia.org/wiki/Antithrombin_III_deficiency

... is also termed antithrombin III (AT III). The designations antithrombin I through to antithrombin IV originate in ... Antithrombin III (AT III) refers to a substance in plasma that inactivates thrombin. Antithrombin IV (AT IV) refers to an ... AT III is generally referred to solely as "antithrombin" and it is antithrombin III that is discussed in this article. ... Native antithrombin can be converted to latent antithrombin (L-antithrombin) by heating alone or heating in the presence of ...

https://en.wikipedia.org/wiki/Antithrombin

... antithrombin III), which can be distinguished from autoimmune anti-thrombin. Anti-thrombin antibodies can react with both types ... Autoimmune anti-thrombin was also found to inhibit the binding of antithrombin III to thrombin. Such activities are more often ... "Antigenic changes produced by complex formation between thrombin and antithrombin-III". J. Immunol. 127 (1): 239-44. PMID ... "Monoclonal antibodies directed against human alpha-thrombin and the thrombin-antithrombin III complex". Thromb. Res. 36 (5): ...

https://en.wikipedia.org/wiki/Anti-thrombin_antibodies

PITX3 Antithrombin III deficiency; 613118; AT3 Antley-Bixler syndrome; 207410; FGFR2 Antley-Bixler syndrome-like with ... GNPTAB Mucolipidosis III alpha/beta; 252600; GNPTAB Mucolipidosis III gamma; 252605; GNPTAG Mucolipidosis IV; 252650; MCOLN1 ... SDHAF1 Mitochondrial complex III deficiency; 124000; BCS1L Mitochondrial complex III deficiency; 124000; UQCRB Mitochondrial ... type III; 130020; COL3A1 Ehlers-Danlos syndrome, type IV; 130050; COL3A1 Ehlers-Danlos syndrome, type VI; 225400; PLOD Ehlers- ...

https://en.wikipedia.org/wiki/List_of_OMIM_disorder_codes

... antithrombin-III, alpha-antitrypsin, and ovalbumin; epidermal growth factor and the light chain of coagulation factor X; and ... Dayhoff also served on the editorial boards of three journals: DNA, Journal of Molecular Evolution and Computers in Biology and ... apolipoproteins A-I, A-II, C-I and C-III. Based on this work, Dayhoff and her coworkers developed a set of substitution ...

https://en.wikipedia.org/wiki/Margaret_Oakley_Dayhoff

... particularly those caused by a decrease in blood antithrombin III levels due to leakage. Antithrombin III counteracts the ... is a greater predisposition for the formation of blood clots that are caused by a decrease in the levels of antithrombin III in ... Treatment is with oral anticoagulants (not heparin as heparin acts via anti-thrombin 3 which is lost in the proteinuria so it ... antithrombin or the immunoglobulins to pass through the cell membrane and appear in urine. Albumin is the main protein in the ...

https://en.wikipedia.org/wiki/Nephrotic_syndrome

Some examples of heparin binding proteins include antithrombin III. It is thought that much protein interaction with heparin is ... 3 (5984): 614-6. doi:10.1136/bmj.3.5984.614. JSTOR 20406780. PMC 1674425. PMID 51664. Rutjes, Anne W.S.; Jüni, Peter; Da Costa ... 157 (3): 180-91. doi:10.7326/0003-4819-157-3-201208070-00473. PMID 22868835. S2CID 5660398. Linhardt, Robert J.; Toida, ... ISBN 0-8247-9982-8. {{U.S. Pharmacopeia Heparin Stage Two Monograph Revisions Open Microphone Web Meeting March 3, 2009 ...

https://en.wikipedia.org/wiki/Heparinoid

Unlike thrombin, reptilase is resistant to inhibition by antithrombin III. Thus, the reptilase time is not prolonged in blood ...

https://en.wikipedia.org/wiki/Reptilase_time

Austin RC, Rachubinski RA, Ofosu FA, Blajchman MA (May 1991). "Antithrombin-III-Hamilton, Ala 382 to Thr: an antithrombin-III ... "Primary structure of antithrombin III (heparin cofactor): partial homology between alpha-1-antitrypsin and antithrombin III". ... Petitou M, van Boeckel CA (June 2004). "A synthetic antithrombin III binding pentasaccharide is now a drug! What comes next?". ... Hunt LT, Dayhoff MO (July 1980). "A surprising new protein superfamily containing ovalbumin, antithrombin-III, and alpha 1- ...

https://en.wikipedia.org/wiki/Serpin

UFH binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation. The ... Allingstrup M, Wetterslev J, Ravn FB, Møller AM, Afshari A (April 2016). "Antithrombin III for critically ill patients: a ... The antithrombin protein itself is used as a protein therapeutic that can be purified from human plasma or produced ... There are three major categories of heparin: unfractionated heparin (UFH), low molecular weight heparin (LMWH), and ultra-low- ...

https://en.wikipedia.org/wiki/Anticoagulant

However, the other major anticoagulants, protein C and antithrombin III, remain constant. Fibrinolysis is impaired by an ... and antithrombin III deficiency. Hypercoagulability in pregnancy, particularly due to inheritable thrombophilia, can lead to ... Both anti-IIa and anti-Xa activity may return up to three hours after protamine reversal, possibly due to release of additional ... Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal ...

https://en.wikipedia.org/wiki/Hypercoagulability_in_pregnancy

Castro MA, Goodwin TM, Shaw KJ, Ouzounian JG, McGehee WG (1996). "Disseminated intravascular coagulation and antithrombin III ... Deficiency of LCHAD (3-hydroxyacyl-CoA dehydrogenase) leads to an accumulation of medium and long chain fatty acids. When this ... It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the fetus, caused by long-chain 3- ... 20 (3): 420-422. doi:10.1023/A:1005310903004. PMID 9266371. S2CID 23046057.[permanent dead link] Wanders RJ, Vreken P, den Boer ...

https://en.wikipedia.org/wiki/Acute_fatty_liver_of_pregnancy

After the antithrombin III binds to Factor Xa, the Fondaparinux is released and can activate another antithrombin. Another drug ... Fondaparinux binds to antithrombin III and activates the molecule for Factor Xa inhibition. In fact, Fondaparinux imparts an ... Idraparinux also binds antithrombin III, however with a 30-fold increase in affinity as compared to Fondaparinux. Idraparinux ... Factor Xa is inhibited by the antithrombin III/heparin system, which also acts to inhibit thrombin. Deficiencies of either ...

https://en.wikipedia.org/wiki/Prothrombinase

Kiehl R, Hellstern P, Wenzel E (January 1987). "Hereditary antithrombin III (AT III) deficiency and atypical localization of a ... and antithrombin III deficiency. Although the above hypothesis is the most commonly accepted, others believe that it is a ... Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of ... which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in ...

https://en.wikipedia.org/wiki/Warfarin_necrosis

... (TAT) is a protein complex of thrombin and antithrombin. It is a marker of net activation of ... Since thrombin is rapidly bound by antithrombin, TAT is a useful measure for thrombin level in the blood. Thrombin can pass the ... "Analysis of thrombin-antithrombin complex contents in plasma and hematoma fluid of hypertensive intracerebral hemorrhage ... 90 (3): 642-72. doi:10.1016/j.fertnstert.2007.07.1298. PMID 17923128. Wu, C. -H.; Yang, R. -L.; Huang, S. -Y.; Li, H. -Z.; Wang ...

https://en.wikipedia.org/wiki/Thrombin–antithrombin_complex

Instead, three guanines (G5, G7 and G16) adopt syn conformation, and only one guanine (G12) adopts anti conformation. ... Anti-thrombin aptamers are G-quadruplex-bearing oligonucleotides, which recognizes the exosites of human thrombin. The first ... 352 (3): 812-817. doi:10.1016/j.bbrc.2006.11.088. PMID 17150180. Chi, Chun-Wei; Lao, Yeh-Hsing; Li, Yi-Shan; Chen, Lin-Chi ( ... anti-thrombin aptamer, TBA, was generated through via SELEX (Systematic Evolution of Ligands by Exponential Enrichment) ...

https://en.wikipedia.org/wiki/Anti-thrombin_aptamers

"Enzymatic modification of heparan sulfate on a biochip promotes its interaction with antithrombin III". Biochemical and ... Heparan sulfate glucosamine 3-O-sulfotransferase 1 is an enzyme that in humans is encoded by the HS3ST1 gene. Heparan sulfate ... The D-glucosaminyl 3-O-sulfotransferase reaction: target and inhibitor saccharides". The Journal of Biological Chemistry. 270 ( ... Liu J, Shworak NW, Fritze LM, Edelberg JM, Rosenberg RD (October 1996). "Purification of heparan sulfate D-glucosaminyl 3-O- ...

https://en.wikipedia.org/wiki/HS3ST1

The main ones are antithrombin III deficiency, protein C deficiency and protein S deficiency. Milder rare congenital ... Antithrombin deficiency is present in 0.2% of the general population and 0.5-7.5% of people with venous thrombosis. Protein C ... 13 (2): iii, ix-x, 1-91. doi:10.3310/hta13020. PMID 19080721. Wu O, Greer IA (September 2007). "Is screening for thrombophilia ... Even small perturbances of proteins, such as the reduction of antithrombin to only 70-80% of the normal level, can increase the ...

https://en.wikipedia.org/wiki/Thrombophilia

The structure is similar to antithrombin III (ATIII), which was known to effectively inhibit thrombin as well as coagulation ... This protein shares homology with antithrombin III and other members of the alpha-1 antitrypsin superfamily. Mutations in this ... Pizzo SV (1989). "Serpin receptor 1: a hepatic receptor that mediates the clearance of antithrombin III-proteinase complexes". ... heparin cofactor activities in a family with hereditary antithrombin III deficiency: evidence for a second heparin cofactor in ...

https://en.wikipedia.org/wiki/Heparin_cofactor_II

Koide T, Odani S, Ono T (November 1985). "Human histidine-rich glycoprotein: simultaneous purification with antithrombin III ... 31 (3): 239-46. doi:10.1203/00006450-199203000-00009. PMID 1561009. van den Berg EA, le Clercq E, Kluft C, Koide T, van der Zee ... 34 (3): 307-12. doi:10.1007/s12016-007-8058-6. PMID 18219588. S2CID 37799666. Hennis BC, van Boheemen PA, Wakabayashi S, Koide ... 412 (3): 559-62. doi:10.1016/S0014-5793(97)00827-2. PMID 9276466. S2CID 46534395. Shigekiyo T, Yoshida H, Matsumoto K, Azuma H ...

https://en.wikipedia.org/wiki/Histidine-rich_glycoprotein

... reverses effect of all anticoagulants that act directly through FXa or by binding antithrombin III. The drug is ... the amount of available factor Xa for coagulation It was approved in the United States in 2018 based on data from two phase III ... 19 (3): 251. doi:10.1038/nm0313-251. PMID 23467222. S2CID 13340319. Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens ...

https://en.wikipedia.org/wiki/Andexanet_alfa

The HS-binding properties of a number of other proteins are also being studied: Antithrombin III Fibroblast Growth Factors ... The 3OSTs are divided into two functional subcategories, those that generate an antithrombin III binding site (HS3ST1 and ... Three glucosaminyl 6-O-transferases (6OSTs) have been identified that result in the formation of GlcNS(6S) adjacent to sulfated ... It occurs as a proteoglycan (HSPG, i.e. Heparan Sulfate ProteoGlycan) in which two or three HS chains are attached in close ...

https://en.wikipedia.org/wiki/Heparan_sulfate

Dalteparin acts by potentiating the activity of antithrombin III, inhibiting formation of both Factor Xa and thrombin. It is ...

https://en.wikipedia.org/wiki/Dalteparin_sodium

MedlinePlus Encyclopedia: 003652 Antithrombin III at eMedicine Antithrombin CO000300 in Coagulation Test Handbook at ... 18 (3): 228-37. doi:10.1016/j.ghir.2007.09.005. PMID 17997337. Taken from the assay method giving the lowest and highest ... 80 (3): 752-58. doi:10.1093/ajcn/80.3.752. PMID 15321818. Reusch J, Ackermann H, Badenhoop K (May 2009). "Cyclic changes of ... 25 (3): 274-75. doi:10.1097/00043426-200303000-00019. PMID 12621252. Derived from mass values using molar mass of 44324.5 g/mol ...

https://en.wikipedia.org/wiki/Reference_ranges_for_blood_tests

Use in antithrombin III deficiency: FFP can be used as a source of antithrombin III in patients who are deficient of this ... There are purified, human derived, as well as recombinant forms of antithrombin III available in the US. Treatment of ... 31 (3): 149-338. doi:10.1002/jca.21470. ISSN 0733-2459. PMID 27322218. S2CID 866923. Sikka, Paul K.; Beaman, Shawn T.; Street, ... 154 (3): 311-324. doi:10.1111/j.1365-2141.2011.08753.x. ISSN 1365-2141. PMID 21671894. S2CID 14749058. "Society for the ...

https://en.wikipedia.org/wiki/Fresh_frozen_plasma

A small percentage of patients, such as those with an antithrombin III deficiency, may exhibit resistance to heparin. In these ... or other blood products such as recombinant anti-thrombin III to achieve adequate anticoagulation. A persistent left superior ... For type III reactions, heparin is redosed and the patient may need to go back on bypass. CPB may contribute to immediate ... There are three types of protamine reactions, and each may cause life-threatening hypotension (type I), anaphylaxis (type II), ...

https://en.wikipedia.org/wiki/Cardiopulmonary_bypass

O-sulfation of the antithrombin-binding region". J. Biol. Chem. 263 (30): 15474-84. PMID 3139669. Shworak NW, Fritze LM, Liu J ... In enzymology, a [heparan sulfate]-glucosamine 3-sulfotransferase 1 (EC 2.8.2.23) is an enzyme that catalyzes the chemical ... Liu J, Shworak NW, Fritze LM, Edelberg JM, Rosenberg RD (1996). "Purification of heparan sulfate D-glucosaminyl 3-O- ... Other names in common use include heparin-glucosamine 3-O-sulfotransferase, 3'-phosphoadenylyl-sulfate:heparin-glucosamine 3-O- ...

https://en.wikipedia.org/wiki/(heparan_sulfate)-glucosamine_3-sulfotransferase_1

... acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates". Intensive Care Med. 16 (2): 121 ... resulting in decreased synthesis of the regulatory proteins antithrombin, protein C and protein S, with increased synthesis of ... 16 (3): 233-237. doi:10.1080/088800199277281. PMID 10326221. Levin M, Eley BS, Louis J, Cohen H, Young L, Heyderman RS (1995 ... 42 (3): 572-581. doi:10.1016/j.yjmcc.2006.11.018. PMC 1983066. PMID 17276456. Goldenberg NA, Manco-Johnson MJ (2008). "Protein ...

https://en.wikipedia.org/wiki/Purpura_fulminans

... capillary electrophoresis for the determination of binding affinities for low molecular weight heparins and antithrombin-III: ... CEC offers the highest separation efficacy of all three ACE techniques as non-matrixed sample components are washed away and ... Affinity capillary electrophoresis can be divided into three distinct techniques: non-equilibrium electrophoresis of ... 3 (1): 42-55. doi:10.3390/proteomes3010042. PMC 5302491. PMID 28248262. Chu, Yen-Ho; Avila, Luis Z.; Gao, Jinming; Whitesides, ...

https://en.wikipedia.org/wiki/Affinity_electrophoresis

The antithrombin III gene's coding region is an example of an imperfect inverted repeat as shown in the figure on the right. ... The three main repeats which are largely found in particular DNA constructs include the closely precise homopurine- ... Specifically, the missense mutation would lead to a defective gene and a deficiency in antithrombin which could result in the ... Sets 1 and 2 are the stem of stem-loop A and are part of the loop for stem-loop B. Similarly, sets 3 and 4 are the stem for ...

https://en.wikipedia.org/wiki/Inverted_repeat

Congenital alopecia X linked Congenital amputation Congenital aneurysms of the great vessels Congenital antithrombin III ... X-linked type 3, recessive Charcot-Marie-Tooth peroneal muscular atrophy, X-linked CHARGE syndrome Charles' disease Charlie M ... monosomy 3q27 Chromosome 3, trisomy 3p Chromosome 3, trisomy 3p25 Chromosome 3, trisomy 3q Chromosome 3, trisomy 3q13 2 q25 ... monosomy 3p Chromosome 3, monosomy 3p14 p11 Chromosome 3, monosomy 3p2 Chromosome 3, monosomy 3p25 Chromosome 3, monosomy 3q13 ...

https://en.wikipedia.org/wiki/List_of_diseases_(C)

... antithrombin and TFPI are the most relevant proteolytic inhibitors of the active factor XIIIa. α2-macroglobulin is a ... It has a 5' UTR of 84 bp and a 3' UTR of 1.6 kbp. F13A1 exon(s) 1 code 5' UTR 2 code activation peptide 2-4 code β-sandwich 4- ... 91 (3): 931-72. doi:10.1152/physrev.00016.2010. PMID 21742792. S2CID 24703788. Laki K, Lóránd L (September 1948). "On the ... Seminars in thrombosis and hemostasis". 41 (3): 323-29. {{cite journal}}: Cite journal requires ,journal= (help) Muszbek L, ...

https://en.wikipedia.org/wiki/Factor_XIII

... birth control pills have been found to increase levels of APC-PCI to a similar degree as thrombin-antithrombin complex (TAT) ... 54 (3): 865-78. doi:10.1016/j.jvs.2011.04.010. PMID 21684711. Misra S, Kumar A, Kumar P, Yadav AK, Mohania D, Pandit AK, Prasad ...

https://en.wikipedia.org/wiki/Activated_protein_C–protein_C_inhibitor

The three N-linked glycosylations sites are mainly equipped with so-called diantennary N-glycans. However, one particular site ... An extremely rare form of Pi, termed PiPittsburgh, functions as an antithrombin (a related serpin), due to a mutation ( ... Owen MC, Brennan SO, Lewis JH, Carrell RW (September 1983). "Mutation of antitrypsin to antithrombin. alpha 1-antitrypsin ... 3-19. Guttman O, Baranovski BM, Schuster R, Kaner Z, Freixo-Lima GS, Bahar N, Mizrahi MI, Brami I, Ochayon DE, Lewis EC ( ...

https://en.wikipedia.org/wiki/Alpha-1_antitrypsin

Based on this statement, Definite CAPS diagnosis requires: a) Vascular thrombosis in three or more organs or tissues and b) ... Measuring serum levels of protein C, free and total protein S, factor VIII, antithrombin, plasminogen, tissue plasminogen ... and two positive blood test results spaced at least three months apart that detect lupus anticoagulant, anti-apolipoprotein ... There are 3 distinct APS disease entities: primary (the absence of any comorbidity), secondary (when there is a pre-existing ...

https://en.wikipedia.org/wiki/Antiphospholipid_syndrome

The three major mechanisms for such an imbalance are enumerated in Virchow's triad: alterations in normal blood flow, injury to ... protein S or antithrombin, or related problems Nephrotic syndrome, a kidney problem causing protein loss in the urine Chronic ... If the thrombosis developed under temporary circumstances (e.g. pregnancy), three months are regarded as sufficient. If the ... 4 (3): 419-30. doi:10.1161/01.str.4.3.419. PMID 4713031. Ribes MF (1825). "Des recherches faites sur la phlebite". Rev. Med. Fr ...

https://en.wikipedia.org/wiki/Cerebral_venous_sinus_thrombosis

"Anti-Thrombin, Anti-Adhesive, Anti-Migratory, and Anti-Proliferative Activities of Sulfated Galactans from the Tropical Green ... 345 (3): 179. doi:10.11646/phytotaxa.345.3.1. ISSN 1179-3163. Cummings, Joel (April 2003). "Algaebase2003195Edited by M.D. ...

https://en.wikipedia.org/wiki/Udotea_flabellum

These medications are usually one of three types: Substances that are (nearly) identical to the body's key signaling proteins. ... "European Regulators Curdle Plans for Goat Milk Human Antithrombin" (PDF). Retrieved 2006-06-23. "Go-ahead for 'pharmed' goat ... 31 (1): 3-9. doi:10.1007/s00449-007-0151-y. PMID 17701058. S2CID 4673669. Dove A (October 2000). "Milking the genome for profit ... 26 (3): 145-152. doi:10.1007/bf03262388. S2CID 14604362. Retrieved 2012-06-13. EMA (2008-10-30). "Questions and answers on ...

https://en.wikipedia.org/wiki/Biopharmaceutical

... a plays a key role in all three of these stages. In stage 1, Factor VII binds to the transmembrane protein TF on the ... antithrombin (AT) to inactivate several coagulation factors IIa, Xa, XIa and XIIa. The affinity of unfractionated heparin and ... This model has three stages: 1) initiation of coagulation on TF-bearing cells, 2) amplification of the procoagulant signal by ... The S4 sub-pocket has three ligand binding domains: the "hydrophobic box", the "cationic hole" and the water site. Factor Xa ...

https://en.wikipedia.org/wiki/Factor_X

... and anti-thrombin III, can manifest as iron-resistant microcytic anemia. An example reference range for transferrin is 204-360 ... III) binding sites. The affinity of transferrin for Fe(III) is extremely high (association constant is 1020 M−1 at pH 7.4) but ... Drosophila melanogaster has three transferrin genes and is highly divergent from all other model clades, Ciona intestinalis one ... Each monomer consists of three domains: the protease, the helical, and the apical domains. The shape of a transferrin receptor ...

https://en.wikipedia.org/wiki/Transferrin

... freeze-dried human antithrombin III concentrate Streptase, freeze-dried streptokinase Wound Healing: Beriplast P Combi-Set, ... antithrombin III) Vivaglobin, sub-cutaneous human immune globulin indicated for the treatment of primary immunodeficiency. This ... p. 3 - via Trove. Hobbins, Peter G.; Winkel, Kenneth D. (3 December 2007). "The forgotten successes and sacrifices of Charles ... Global product portfolio CSL Behring, 3 November 2010 "CSL wins equal opportunity award for onsite childcare centre". CSL ...

https://en.wikipedia.org/wiki/CSL_Limited

The three main forms are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency or "Christmas disease") and ... Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases: thrombin, FIXa, FXa, FXIa, and FXIIa. ... Factors III[citation needed] and VI[citation needed] are unassigned, as thromboplastin was never identified, and actually ... At this stage, it was known that thrombokinase/thromboplastin (factor III) is released by damaged tissues, reacting with ...

https://en.wikipedia.org/wiki/Coagulation

It also possesses a minor anti-thrombin activity, mediated equally via AT and Heparin Co-factor II producing a ratio of anti-Xa ... Thromb Haemostas 1987;57/3:286-93] to provide an index of antithrombotic potential, of danaparoid has a half-life of 6.7 hours ... Bone Marrow Transplant 2016;1-3 Doi:10.1038/bmt.2016.270] that occur after haemopoietic stem-cell transplantation in patients ... with haematogenous and solid malignancies.[citation needed] It has also been used in Kasabach-Merritt syndrome in 3 cases. On ...

https://en.wikipedia.org/wiki/Danaparoid

ALDH alkaline phosphatase alpha6-integrin Anti-WNT2B monoclonal antibody antithrombin III (AT) asialo GM1 Bcl-2 Beta- ... 95 (3): 952-8. doi:10.1182/blood.V95.3.952.003k27_952_958. PMID 10648408. Archived from the original on 1 August 2012. Zhou L, ... 9 (3): 196-201. doi:10.1111/j.1087-0024.2004.09313.x. PMID 15369213. Rubin DC, Swietlicki E, Roth KA, Gordon JI (25 July 1992 ... 3 (12): 1481-3. doi:10.4161/cc.3.12.1281. PMID 15539950. Munoz JR, Stoutenger BR, Robinson AP, Spees JL, Prockop DJ (December ...

https://en.wikipedia.org/wiki/Stem_cell_marker

... antithrombin iii MeSH D12.776.377.715.085.214 - ceruloplasmin MeSH D12.776.377.715.085.394 - haptoglobins MeSH D12.776.377.715. ... myosin type iii MeSH D12.776.220.525.475.681 - myosin type iv MeSH D12.776.220.525.475.750 - myosin type v MeSH D12.776.220.525 ... Type III collagen MeSH D12.776.860.300.250.300.400 - Type V collagen MeSH D12.776.860.300.250.300.500 - Type XI collagen MeSH ... electron transport complex iii MeSH D12.776.556.579.374.375.977 - nitrate reductase (nad(p)h) MeSH D12.776.556.579.374.375.988 ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D12.776)

If successful, a red and itchy bump develops at the vaccine site in three or four days. In the first week, the bump becomes a ... is characterized by a decrease in all of the elements of the coagulation cascade and an increase in circulating antithrombin. ... Smallpox vaccination within three days of exposure will prevent or significantly lessen the severity of smallpox symptoms in ... The last naturally occurring case of the more deadly variola major had been detected in October 1975 in a three-year-old ...

https://en.wikipedia.org/wiki/Smallpox

Within the first three hours, someone with sepsis should have received antibiotics and, intravenous fluids if there is evidence ... On the other hand, the use of antithrombin to treat disseminated intravascular coagulation is also not useful. Meanwhile, the ... Within the first three hours of suspected sepsis, diagnostic studies should include white blood cell counts, measuring serum ... The Surviving Sepsis Campaign has recommended 30 mL/kg of fluid to be given in adults in the first three hours followed by ...

https://en.wikipedia.org/wiki/Sepsis

Deficiencies of three proteins that normally prevent blood from clotting-protein C, protein S, and antithrombin-contribute to ... Three compression ultrasound scanning techniques can be used, with two of the three methods requiring a second ultrasound some ... These deficiencies in antithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors. They ... With this prediction rule, three points or less means a person is at low risk for DVT. A result of four or more points ...

https://en.wikipedia.org/wiki/Deep_vein_thrombosis

... including heparan sulfate which acts as a cofactor for activating antithrombin, a protease that inactivates several factors in ... 4 (3): 351-60. doi:10.2217/bmm.10.61. PMC 2911781. PMID 20550469. Lopez-Garcia E, Hu FB (August 2004). "Nutrition and the ... In April 2020, the presence of viral elements in endothelial cells of 3 patients who had died of COVID-19 was reported for the ... 20 (3): 210-2. doi:10.1093/oxfordjournals.bmb.a070333. eISSN 1471-8391. PMID 14209761. Milosevic, V., Edelmann, R.J., Fosse, J. ...

https://en.wikipedia.org/wiki/Endothelium

... thrombin-antithrombin complex (TAT), fragment 1+2, and D-dimer and decreased fibrinogen, factor VII, antithrombin, protein S, ... In a previous review, the increase in breast cancer risk was found to not be significantly different between these three ... Estrogens are one of three types of sex hormone agonists, the others being androgens/anabolic steroids like testosterone and ... doi:10.1007/978-3-0348-0664-0_1. ISBN 978-3-0348-0663-3. ISSN 2296-6056. Turner N, Ro J, André F, Loi S, Verma S, Iwata H, ...

https://en.wikipedia.org/wiki/Estrogen_(medication)

... a Northwestern Iranian language The Three Affiliated Tribes (TAT), a Northern Plains Native American tribe also known as the ... a projective psychological test Thrombin-antithrombin complex, a protein complex Tropine acyltransferase, an enzyme Twin- ...

https://en.wikipedia.org/wiki/Tat

Angiotensin converting enzyme Antithrombin-III Lipoprotein lipase Apolipoproteins Growth factors Chemokines The enzymes and ... 3. p. 345-359 Ebong, Eno; Macaluso FP; Spray DC; Tarbell JM (August 2011). "Imaging the Endothelial Glycocalyx In Vitro By ... 80 (3): 389-402. doi:10.1111/bcp.12629. PMC 4574825. PMID 25778676. Gouverneur, Mirella. Dissertation. "Fluid shear stress ...

https://en.wikipedia.org/wiki/Glycocalyx

... antithrombin iii MeSH D12.776.124.790.106.214 - ceruloplasmin MeSH D12.776.124.790.106.394 - haptoglobins MeSH D12.776.124.790. ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D12.776.124)

Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. ... The abnormal gene leads to a low level of the antithrombin III protein. This low level of antithrombin III can cause abnormal ... Antithrombin III is a protein in the blood that blocks abnormal blood clots from forming. It helps the body keep a healthy ... Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of the ...

https://medlineplus.gov/ency/article/000558.htm

AT III) is a protein that helps control blood clotting. A blood test can determine the amount of AT III present in your body. ... Functional antithrombin III; Clotting disorder - AT III; DVT - AT III; Deep vein thrombosis - AT III ... Antithrombin III (AT III) is a protein that helps control blood clotting. A blood test can determine the amount of AT III ... Antithrombin III (AT-III) test - diagnostic. In: Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 6th ...

https://medlineplus.gov/ency/article/003661.htm

... antithrombin III), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & lactation ... encoded search term (antithrombin III (Thrombate III)) and antithrombin III (Thrombate III) What to Read Next on Medscape ... Base on pre-therapy plasma antithrombin III (AT-III) level. In order to increase plasma AT-III levels to that found in normal ... antithrombin III increases levels of ethotoin by unknown mechanism. Use Caution/Monitor.. ethotoin, antithrombin III. Other ( ...

http://reference.medscape.com/drug/342868

It has been suggested that Antithrombin III (AT III) might have an anti-inflammatory effect in addition to its well known anti- ... Cobas Meyer, M., Vangerow, B., Ahrens, J. et al. Effects of Antithrombin III on body cavity effusions, fluid balance, colloid ... Effects of Antithrombin III on body cavity effusions, fluid balance, colloid osmotic pressure and hemodynamics in porcine ... Effects of Antithrombin III on body cavity effusions, fluid balance, colloid osmotic pressure and hemodynamics in porcine ...

https://ccforum.biomedcentral.com/articles/10.1186/cc744

AT III) inhibits thrombin and activated clotting factors like factor Xa, IXa and VIIa. AT III deficiency increases risk for ... Abstract: Antithrombin III (AT III) inhibits thrombin and activated clotting factors like factor Xa, IXa and VIIa. AT III ... Dhruvin Shah, Hetal Pandya, Siraj Vadhvaniya, "Multiple Arterial Thrombosis in Anti Thrombin III Deficiency", International ... Inherited deficiency of AT III is relatively rare with prevalence in general population between 1500 to 150001. AT III ...

https://www.ijsr.net/get_abstract.php?paper_id=ART2016597

Christmas day, three weeks later, I was being rushed by ambulance to the nearest CCU with a life threatening saddle clot. ... I woke up only three times in the trauma unit that I remember. Each was after unsuccessful attempts at putting my hip into ... This entry was posted on June 11, 2014, in Survivor and tagged American Heart Association, Antithrombin Deficiency, blood, ... This entry was posted on April 18, 2014, in Survivor and tagged American Heart Association, Antithrombin Deficiency, blood, ...

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... G. Bertelli;P. Pronzato;D ... Mean values of total, HDL and LDL cholesterol, triglycerides, glucose, uric acid, and antithrombin III were evaluated in 55 ... Mean values of total, HDL and LDL cholesterol, triglycerides, glucose, uric acid, and antithrombin III were evaluated in 55 ... The possible estrogenic effects of tamoxifen on plasma lipids and antithrombin III levels were investigated in 91 breast cancer ...

https://iris.unimore.it/handle/11380/738328

Antithrombin III activity is markedly potentiated by heparin, the principle mechanism by which both heparin and low molecular ... Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by lysing thrombin and factor Xa. ... encoded search term (Antithrombin III Deficiency) and Antithrombin III Deficiency What to Read Next on Medscape ... In these patients, replacement of antithrombin III using antithrombin III concentrates or fresh frozen plasma is recommended. ...

https://www.staging.medscape.com/answers/954688-119851/what-are-the-sexual-predilections-of-antithrombin-iii-atiii-deficiency

Antithrombin III activity is markedly potentiated by heparin, the principle mechanism by which both heparin and low molecular ... Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by lysing thrombin and factor Xa. ... Antithrombin-III concentrates. Class Summary. Antithrombin III concentrate (Thrombate III [Bayer Corporation]) is used for ... Antithrombin III (ATIII) deficiency may be quickly corrected with infusions of antithrombin III concentrates. Long-term therapy ...

https://emedicine.staging.medscape.com/article/954688-medication

Antithrombin III activity in cerebrovascular accidents.. Authors: Singh, V P. Singh, M K. Kumar, V. Sinha, M K. Dwivedi, R C. ... CONCLUSION: Decrease of antithrombin III in occlusive and increase in haemorrhagic stroke indicates that these changes have at ... Singh VP, Singh MK, Kumar V, Sinha MK, Dwivedi RC, Rai M, Dube B. Antithrombin III activity in cerebrovascular accidents. ... METHOD: Biological activity of antithrombin III was done by the method as described by Innerfield et al (1976). Immunological ...

https://imsear.searo.who.int/handle/123456789/94231

Treatment and prophylaxis of thrombosis in patients with hereditary antithrombin-III deficiency. ...

https://medschool.co/drug-guide/antithrombin-iii

Diseases [C] » Hemic and Lymphatic Diseases [C15] » Hematologic Diseases » Thrombophilia » Antithrombin III Deficiency ... Diseases [C] » Hemic and Lymphatic Diseases [C15] » Hematologic Diseases » Blood Protein Disorders » Antithrombin III ... An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis. MeSH ...

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Protein C, Protein S, Antithrombin III, and Factor V Leiden Deficiencies. Deficiencies of antithrombin III, protein C, and ... 94] Currently, however, these agents (eg, antithrombin recombinant, antithrombin III) are approved only for use in patients ... Activated antithrombin III is a major inhibitor of thrombin and factor Xa, with smaller effects on factors IX, XI, and XII. ... Antithrombin III, protein C, and protein S are all essential components of the coagulation process. All are synthesized by the ...

https://www.medscape.com/answers/210467-178088/what-is-the-role-of-antithrombin-iii-in-the-etiology-of-nonplatelet-hemostatic-disorders

THROMBATE III is FDA approved for treatment of thromboembolism and prevention of perioperative and peripartum thromboembolism, ... THROMBATE III® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and ... Pregnancy in women with congenital antithrombin III deficiency: experience of treatment with heparin and antithrombin. Gynecol ... 11. Ranucci M. Antithrombin III: key factor in extracorporeal circulation. Minerva Anestesiol. 2002;68(5):454-457. 12. Foy P, ...

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Thrombosis in Antithrombin-III-deficient Persons Academic Article ...

https://experts.mcmaster.ca/display/publication486123

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Order Antithrombin III antibody biotin 01012566903 at Gentaur Antithrombin III ... antithrombin-III; Antithrombin-III; antithrombin-III; serpin C1; antithrombin III; serine-cysteine proteinase inhibitor clade C ... member 1; serine (or cysteine) proteinase inhibitor, clade C (antithrombin), member 1; serpin peptidase inhibitor, clade C ( ...

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Anti-thrombin III, %. 83-128. 56. 47. Protein C activity, %. 70-130. 58. 52. ... Leukocyte count, × 103 cells/μL. 3.5−10.0. 12.2. 14.7. 11.7. 28.4. 26.5. 31.9. 58.9. 24.3. 17.4. 29.1. 31.5. 14.2. 19.0. 16.0. ... Absolute lymphocyte count, × 103 cells/μL. 1.0−3.9. 0.7. 0.5. 0.8. 0.9. 0.8. 0.6. 2.5. 1.4. 1.4. 2.0. 0.8. 1.2. 2.3. 1.9. 2.6. ... Absolute neutrophil count, × 103/μL. 1.9−7.4. 11.1. 13.0. 10.3. 27.1. 24.8. 31.4. 54.3. 22.42. 14.7. 26.6. 19.2. 12.1. 15.7. ...

https://wwwnc.cdc.gov/eid/article/28/2/21-1938-t1

3 months. HTTP. _fbp. Facebook. Registers a unique ID that is used to generate statistical data on how the visitor uses the ... 3 months. HTTP. IDE. Google. Used by Google DoubleClick to register and report the website users actions after viewing or ...

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Hereditary deficiency of antithrombin (AT), previously called AT III, is a hereditary thrombophilia of low prevalence (0.02%- ... Thrombosis of an aortic porcine xenobioprosthesis associated with familial antithrombin III deficiency. ... January 2021 Antithrombin deficiency as a cause of aortic valve thrombosis in a bicuspid aortic... ... Antithrombin deficiency as a cause of aortic valve thrombosis in a bicuspid aortic valve ...

https://www.revespcardiol.org/en-antithrombin-deficiency-as-cause-aortic-articulo-S1885585720303066

Antithrombin III Human * Apixaban * Apomorphine * Aprindine * Ardeparin * Argatroban * Aripiprazole * Aripiprazole Lauroxil * ...

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TABLE III: ANNUAL NUMBER OF BIRTH-RELATED OR METHOD-RELATED DEATHS ASSOCIATED WITH CONTROL OF FERTILITY PER 100,000 NONSTERILE ... a. Increased prothrombin and factors VII, VIII, IX, and X; decreased antithrombin 3; increased norepinephrine-induced platelet ... You should consult your health-care provider about stopping oral contraceptives three to four weeks before surgery and not ... These side effects, especially nausea and vomiting, may subside within the first three months of use. ...

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You should consult your doctor about stopping oral contraceptives three to four weeks before surgery and not taking oral ... Increased prothrombin and factors VII, VIII, IX, and X; decreased antithrombin 3; increased norepinephrine-induced platelet ... These side effects, especially nausea and vomiting, may subside within the first three months of use. ... spotting or light bleeding or gastric distress during the first one to three cycles, (c) missing pills can also cause spotting ...

https://www.rxlist.com/vyfemla-drug.htm

Deficiencies of protein C, protein S, or antithrombin III account for approximately 5-10% of all cases of DVT. [74] ... Deep venous thrombosis (DVT). This chart depicts perioperative antithrombin III levels and DVT formation. View Media Gallery ... These include the heparin-antithrombin III (ATIII), protein C and thrombomodulin protein S, and the tissue factor inhibition ... Deep venous thrombosis (DVT). This chart shows postoperative antithrombin III levels. View Media Gallery ...

https://emedicine.medscape.com/article/1911303-overview

DEFICIÊNCIA DE ANTITROMBINA III. ANTITHROMBIN III DEFICIENCY. DEFICIENCIA DE ANTITROMBINA III. DEFICIÊNCIA DE PROTEÍNA C. ... 3 UNTRANSLATED REGIONS. REGIONES NO TRADUCIDAS 3. REGIÕES 5 NÃO TRADUZIDAS. 5 UNTRANSLATED REGIONS. REGIONES NO TRADUCIDAS ...

https://decs.bvs.br/P/decswebpage2p.htm

Acquired antithrombin III deficiency is a deficiency of antithrombin primarily due to consumption or decreased production. (medscape.com)
Common conditions that result in acquired antithrombin III deficiency include disseminated intravascular coagulation (DIC) , microangiopathic hemolytic anemias due to endothelial damage (ie, hemolytic-uremic syndrome ), veno-occlusive disease (VOD) (in patients undergoing bone marrow transplantation ), sepsis, liver disease, and nephrotic syndrome. (medscape.com)

Once a patient with congenital antithrombin III deficiency has developed thrombosis, anticoagulation is more strongly indicated. (medscape.com)
Treatment and prophylaxis of thrombosis in patients with hereditary antithrombin-III deficiency. (medschool.co)
An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis. (liu.edu)
Clinical outcomes of antithrombin III-based therapy for patients with portal vein thrombosis: A retrospective, multicenter study. (bvsalud.org)
Bicuspid aortic valve is the most common congenital heart disease (1%-2%) and carries a higher risk of complications such as valvular dysfunction, aortic dissection, and even aortic valve thrombosis, which is commonly related to hypercoagulable states such as protein S deficiency 2 and antiphospholipid syndrome, 3 and may even occur spontaneously. (revespcardiol.org)
In this review, we focus on contributions of blood composition, vascular cells, and blood flow to hemostasis and thrombosis, and suggest that cross-talk among the 3 components of Virchow's triad is necessary for hemostasis and determines propensity for thrombosis or bleeding. (lww.com)
Arterial thrombosis is directly related to atherosclerosis and represents the leading cause of mortality in the world, commonly manifesting as acute myo- cardial infarction (AMI), cerebrovascular accident (CVA)/transient ischemic attack (TIA), and peripheral arterial obstructive disease(1,3). (bvsalud.org)

The anticoagulant effect of heparin is enhanced by concurrent treatment with THROMBATE III in patients with hereditary AT deficiency. (thrombate.com)
Thus, in order to avoid bleeding, the dosage of heparin (or low molecular weight heparin) may need to be reduced during treatment with THROMBATE III. (thrombate.com)
THROMBATE III ® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and prevention of thromboembolism and for prevention of perioperative and peripartum thromboembolism. (thrombate.com)
Because THROMBATE III is made from human blood, it may carry a risk of transmitting infectious agents, eg, viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. (thrombate.com)
Please see full Prescribing Information for THROMBATE III. (thrombate.com)
1. THROMBATE III [Prescribing Information]. (thrombate.com)

Once a person is diagnosed with antithrombin III deficiency, all close family members should be screened for this disorder. (medlineplus.gov)

Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa, IXa, Xa). (medscape.com)
This recombinant protein (r-Antidote, PRT064445) is catalytically inactive and lacks the membrane-binding γ-carboxyglutamic acid domain of native fXa but retains the ability of native fXa to bind direct fXa inhibitors as well as low molecular weight heparin-activated antithrombin III (ATIII). (nih.gov)
Moreover, we noticed that antithrombin III (ATIII) was activated at 3h after reperfusion, which preceded the alleviation of renal injury. (oncotarget.com)

Antithrombin III (AT III) inhibits thrombin and activated clotting factors like factor Xa, IXa and VIIa. (ijsr.net)
Antithrombin: the principal inhibitor of thrombin. (medscape.com)
CusabioRat thrombin-antithrombin complex, TAT ELISA Kit is Available at Gentaur Genprice with the fastest delivery.Online Order. (joplink.net)

amobarbital decreases effects of antithrombin III by increasing metabolism. (medscape.com)
azithromycin increases effects of antithrombin III by decreasing metabolism. (medscape.com)
bazedoxifene/conjugated estrogens decreases effects of antithrombin III by pharmacodynamic antagonism. (medscape.com)
cefamandole increases effects of antithrombin III by pharmacodynamic synergism. (medscape.com)
cefazolin increases effects of antithrombin III by pharmacodynamic synergism. (medscape.com)
clarithromycin increases effects of antithrombin III by decreasing metabolism. (medscape.com)
Inhibitory effects of antithrombin III against leukocyte rolling and infiltration during endotoxin-induced uveitis in rats. (medscape.com)

[ 3 ] Platelets localize coagulation to the hemostatic thrombus and protect coagulation enzymes from inhibition by plasma and platelet inhibitors, thus preventing disseminated intravascular coagulation (DIC). (medscape.com)

Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. (medlineplus.gov)
Congenital antithrombin III deficiency is an inherited disease. (medlineplus.gov)
Congenital antithrombin III deficiency is an autosomal dominant disorder in which an individual inherits one copy of the SERPINC1 (also called AT3 ) gene on chromosome 1q25.1, which encodes antithrombin III. (medscape.com)
Severe congenital antithrombin III deficiency, in which the individual inherits two defective genes, is a rare autosomal recessive condition associated with increased thrombogenesis, typically noted in the neonatal period or early infancy. (medscape.com)
The primary outcome was the occurrence of congenital thrombophilia diagnosed through tests for congenital anticoagulants activity (including protein C, protein S, and antithrombin III), factor V Leiden and prothrombin G20210A sequence variants. (bvsalud.org)

Hereditary deficiency of antithrombin (AT), previously called AT III, is a hereditary thrombophilia of low prevalence (0.02%-0.2%) that was first described in 1965 and has autosomal dominant inheritance and variable penetrance. (revespcardiol.org)
Genotype for patients with thrombophilia revealed that 10 (76.9%) protein C deficiency patients were PROC sequence variant carriers, 4 (21.1%) protein S deficiency were PROS1 sequence variant carriers, and 2 (50.0%) antithrombin III deficiency were SERPINC1 sequence variant carriers. (bvsalud.org)
Egeberg O. Inherited antithrombin deficiency causing thrombophilia. (medscape.com)

viscosity, reduced red cell deformability, The main objectives of this study were abnormal red cell adhesive properties, en- to assess platelet aggregation patterns and dothelial intimal proliferation, bone marrow levels of PC, PS and AT III in SCA patients or fat embolism and a chronic hypercoagula- in the steady state and in vaso-occlusive ble state [6]. (who.int)
Three days later, warfarin was stopped and because of low activity of Antithrombin III and elevation of FDP and D-dimer and decrease in platelet count, heparin infusion was stopped and enoxaparin (a low- molecular-weight heparin (LMWH), was started at a dose of 1 mg/kg/day. (ispub.com)
The patients' levels of protein C, antithrombin III and in vitro platelet aggregation in response to collagen were compared with those of 20 controls. (who.int)
The study suggests that thrombocytosis, increased platelet aggregation and decreased natural coagulation inhibitors [‎protein C and antithrombin III]‎ in splenectomized thalassaemic children may be significant in thrombotic complications in such patients. (who.int)
Fibrinogen, platelet count, antithrombin III and prothrombin time did not differ with the different dialysis procedures. (elsevier.com)

Hereditary and acquired antithrombin deficiency: epidemiology, pathogenesis, and treatment options. (thrombate.com)
Prevention and treatment of venous thromboembolism in pregnancy and patients with hereditary antithrombin deficiency. (thrombate.com)
10. Pabinger I, Schneider B. Thrombotic risk in hereditary antithrombin III protein C, or protein S deficiency. (thrombate.com)

A typical lab can meet 91% of its Hemostasis testing needs with HemosIL liquid, ready-to-use assays, including PT, APTT, D-Dimer and Antithrombin. (werfen.com)

La DEFICIENCIA EN ANTITROMBINA III, hereditaria o adquirida, da lugar a tromboembolias. (bvsalud.org)
Algunos autores utilizan el término antitrombina para referirse a la antitrombina III. (bvsalud.org)

antithrombin alfa and antithrombin III both increase anticoagulation. (medscape.com)
antithrombin III and bemiparin both increase anticoagulation. (medscape.com)
antithrombin alfa and reteplase both increase anticoagulation. (medscape.com)

It has been suggested that Antithrombin III (AT III) might have an anti-inflammatory effect in addition to its well known anti-thrombotic properties. (biomedcentral.com)
He was diagnosed as having AT III deficiency as a cause for these multiple arterial thrombotic events. (ijsr.net)
A group of 40 thalassaemic patients [‎20 splenectomized and 20 nonsplenectomized]‎ from the Haematology Unit of Tanta University Hospital [‎age range: 3-14 years]‎ were studied to identify the mechanisms by which haemorrhagic and thrombotic complications occur in thalassaemic patients. (who.int)

AT III deficiency is transmitted in autosomal dominant manner. (ijsr.net)

Antithrombin III activity is markedly potentiated by heparin, the principal mechanism by which both heparin and low-molecular-weight heparin result in anticoagulation. (medscape.com)
Anticoagulation is continued throughout pregnancy and for approximately 3 months postpartum. (health.am)

antithrombin III, anagrelide. (medscape.com)

Rosenberg JS, McKenna PW, Rosenberg RD. Inhibition of human factor IXa by human antithrombin. (medscape.com)
Stead N, Kaplan AP, Rosenberg RD. Inhibition of activated factor XII by antithrombin-heparin cofactor. (medscape.com)
Mechanism of antithrombin III inhibition of factor VIIa/tissue factor activity on cell surfaces. (medscape.com)
Enhances the inhibition rate of clotting proteases by antithrombin III. (bcas.ca)

Detection and characterisation of large SERPINC1 deletions in type I inherited antithrombin deficiency. (medscape.com)

Protein C was deficient and Antithrombin III was low. (ispub.com)

Because the antithrombin III level was low, enoxaparin was started and her symptoms improved in a week. (ispub.com)
Comparative Pharmacokinetic Profile Of 3 Batches Of Ovine Low Molecular Weight Heparin And 1 Batch Of Branded Enoxaparin. (luc.edu)

Some patients with dysfibrinogenemia have additional hemostasis defects, including factor V Leiden and deficiencies in antithrombin, protein C, and protein S. (medscape.com)
Other rare conditions, such as protein C, protein S , and antithrombin III deficiencies . (adam.com)

AT III deficiency increases risk for thromboembolic diseases. (ijsr.net)

CONCLUSION: Decrease of antithrombin III in occlusive and increase in haemorrhagic stroke indicates that these changes have at least an additive role in the pathogenesis of stroke. (who.int)

A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. (bvsalud.org)

[3] [4] When activated into factor IXa , in the presence of Ca 2+ , membrane phospholipids, and a Factor VIII cofactor, it hydrolyses one arginine - isoleucine bond in factor X to form factor Xa. (wikidoc.org)

The hypercoagulable state that can occur in some nephrotic states is likely due to loss of antithrombin III in urine. (unboundmedicine.com)

2(3): 235-243, 2022 Jun. (bvsalud.org)
2(3): 247-255, 2022 Jun. (bvsalud.org)

It occurs when a person receives one abnormal copy of the antithrombin III gene from a parent with the disease. (medlineplus.gov)
The abnormal gene leads to a low level of the antithrombin III protein. (medlineplus.gov)

METHOD: Biological activity of antithrombin III was done by the method as described by Innerfield et al (1976). (who.int)

Antithrombin III antibody (biotin) was purified by affinity chromatography. (thrombrin.com)

Antithrombin III is a protein in the blood that blocks abnormal blood clots from forming. (medlineplus.gov)
This low level of antithrombin III can cause abnormal blood clots (thrombi) that can block blood flow and damage organs. (medlineplus.gov)

The possible estrogenic effects of tamoxifen on plasma lipids and antithrombin III levels were investigated in 91 breast cancer patients. (unimore.it)
Mean values of total, HDL and LDL cholesterol, triglycerides, glucose, uric acid, and antithrombin III were evaluated in 55 patients on adjuvant tamoxifen for at least 3 months and compared with those found in 36 patients on no therapy. (unimore.it)
Total cholesterol, LDL cholesterol, and antithrombin III levels were significantly lower in treated patients (p less than 0.05). (unimore.it)
In these patients, replacement of antithrombin III using antithrombin III concentrates or fresh frozen plasma is recommended. (medscape.com)
The study involved 58 VTE patients under age 45 years, 45 of whom had at least one inherited risk factor, including 14 with antithrombin III deficiency. (medscape.com)
RESULTS: The biological and immunological activity of antithrombin III was measured in 98 patient of occlusive and 56 patients of haemorrhagic strokes. (who.int)
This study aimed to evaluate the outcome in patients with PVT who received antithrombin III-based therapy . (bvsalud.org)
Skin necrosis is a rare adverse effect of warfarin, occurring in about one of every 5000 or more patients treated with warfarin, and in about 3% of subjects affected by protein C deficiency. (ispub.com)

Sulodexide is a potent antithrombin agent, however, whether it has beneficial effects on renal ischemia-reperfusion injury (IRI) remains unknown. (oncotarget.com)

Okajima K, Uchiba M. The anti-inflammatory properties of antithrombin III: new therapeutic implications. (medscape.com)
A sensitivity analysis was applied using 3% and 5% discount rates for YLG and by modifying the patterns of health care, intensive care unit costs, and life expectancy by initial co-morbidity and therapeutic efficacy of drotrecogin alpha (activated). (scielo.org)

In this study, we reported a case of cryptogenic recurrent spontaneous EDH (three times) in a 22-year-old woman who received three surgical procedures and finally achieved satisfactory outcomes. (researchsquare.com)

IGF-I circulates primarily in a high molecular weight tertiary complex with IGF-binding protein-3 (IGFBP-3) and acid-labile subunit. (unitslab.com)

. 3 - 5 units of FFP (10-15 mL/kg IV) are necessary to increase plasma coagulation factors by ∼15% to 25% [7]. (iemig.it)

3 In view of these findings, when estrogens are used for the treatment of menopausal symptoms, the lowest dose that will control symptoms should be utilized and medication should be discontinued as soon as possible. (nih.gov)

In antithrombin III deficiency, however, the activity of LMWH is not as reliable as in an otherwise healthy person. (medscape.com)
IMSEAR at SEARO: Antithrombin III activity in cerebrovascular accidents. (who.int)

3. Localization of fibrin clot formation to site of injury. (vin.com)

Inherited deficiency of AT III is relatively rare with prevalence in general population between 1500 to 150001. (ijsr.net)

Bleeding complications range from about 2% to 3% with direct oral anticoagulants (DOACs) [3]. (iemig.it)

The syndrome usually develops 3-8 weeks after the start of warfarin therapy. (ispub.com)
3 ] Skin necrosis usually develops 3 and 8 days after the start of warfarin and the occurrence is characterized by a painful maculo-papular rash in those parts of the body rich in adipose panniculus, quickly changing into hemorrhagic and then necrotizing blebs. (ispub.com)
It usually develops 3-8 weeks after the start of warfarin therapy and is characterized by development of painful purple lesions on the toes. (ispub.com)

The health care provider can also order a blood test to check if you have a low level of antithrombin III. (medlineplus.gov)
Antithrombin III (AT III) is a protein that helps control blood clotting. (medlineplus.gov)
A blood test can determine the amount of AT III present in your body. (medlineplus.gov)
Lower-than-normal AT III may mean you have an increased risk for blood clotting. (medlineplus.gov)
This can occur when there is not enough AT III in your blood, or when there is enough AT III in your blood, but the AT III does not function properly and is less active. (medlineplus.gov)
Blood Rev. 2007;21(3):131-142. (thrombate.com)
Extract normalizes prostate function and contributes to the antithrombotic action of the blood serum due to the increased production of antithrombin. (hotpolkadot.com)

Organisms2

Diseases11

Chemicals and Drugs55

Analytical, Diagnostic and Therapeutic Techniques and Equipment7

Phenomena and Processes13

Information Science2

Sperm chemotaxis. (1/874)

Age-related changes in blood coagulation and fibrinolysis in mice fed on a high-cholesterol diet. (2/874)

Single and combined prothrombotic factors in patients with idiopathic venous thromboembolism: prevalence and risk assessment. (3/874)

Oxidation of methionine residues in antithrombin. Effects on biological activity and heparin binding. (4/874)

Dose response of intravenous heparin on markers of thrombosis during primary total hip replacement. (5/874)

Effect of thrombin inhibition in vascular dementia and silent cerebrovascular disease. An MR spectroscopy study. (6/874)

Comparison of the antithrombotic effect of PEG-hirudin and heparin in a human ex vivo model of arterial thrombosis. (7/874)

Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction. (8/874)

Antithrombin III

Antithrombin III Deficiency

Antithrombins

Heparin

Antithrombin Proteins

Thrombin

Factor Xa

Factor X

Blood Coagulation

Heparin Cofactor II

Prothrombin

Serine Proteinase Inhibitors

Protein C

Blood Coagulation Tests

Disseminated Intravascular Coagulation

Anticoagulants

Blood Coagulation Factors

Thrombophlebitis

Hemostasis

Fibrinogen

Protein C Deficiency

Blood Coagulation Disorders

Thrombophilia

Protein S Deficiency

Thiohydantoins

Hirudins

p-Dimethylaminoazobenzene

Protein S

Factor IXa

Thrombosis

Thrombin Time

Kinetics

Heparin Lyase

alpha 1-Antitrypsin

Immunoelectrophoresis, Two-Dimensional

Chromogenic Compounds

Pentosan Sulfuric Polyester

Partial Thromboplastin Time

Dermatan Sulfate

Factor V

Heparin Antagonists

Fibrinopeptide A

Chromatography, Affinity

Oligosaccharides

alpha-2-Antiplasmin

Factor XIa

Binding Sites

Complement C1 Inactivator Proteins

alpha-Macroglobulins

Heparitin Sulfate

Protein Binding

Fibrinolysis

Protease Inhibitors

Cetacea

Amino Acid Sequence

Fibrinopeptide B

Protease Nexins

Serpins

Glycosaminoglycans

Factor XI

Factor IX

Factor VIIa

Heparinoids

Phlebitis

Benzamidines

Umbelliferones

Molecular Sequence Data

Electrophoresis, Polyacrylamide Gel

Fibrin Fibrinogen Degradation Products

Swine

Fibrin

Pipecolic Acids

Activated Protein C Resistance

Protein Conformation

Molecular Weight

Thromboembolism

Dansyl Compounds

Receptors, Thrombin

Prothrombin Time

Polysaccharides

$Gentaur Molecular :Molecular Innovations \ Human antithrombin \ HATIII-I$ Gentaur Molecular :Molecular Innovations \ Human antithrombin \ HATIII-I