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.
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.
Laboratory tests for evaluating the individual's clotting mechanism.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
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.
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.
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.
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.
Agents that prevent clotting.
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.
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.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
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.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
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.
Use of HIRUDINS as an anticoagulant in the treatment of cardiological and hematological disorders.
An antiphospholipid antibody found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.
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.
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.
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
The most common mineral of a group of hydrated aluminum silicates, approximately H2Al2Si2O8-H2O. It is prepared for pharmaceutical and medicinal purposes by levigating with water to remove sand, etc. (From Merck Index, 11th ed) The name is derived from Kao-ling (Chinese: "high ridge"), the original site. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).
Hemorrhagic and thrombotic disorders that occur as a consequence of inherited abnormalities in blood coagulation.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
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.
Bleeding or escape of blood from a vessel.
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.
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.
The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.
The natural enzymatic dissolution of FIBRIN.
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.
Absence or reduced levels of PROTHROMBIN in the blood.
A deficiency of blood coagulation factor IX inherited as an X-linked disorder. (Also known as Christmas Disease, after the first patient studied in detail, not the holy day.) Historical and clinical features resemble those in classic hemophilia (HEMOPHILIA A), but patients present with fewer symptoms. Severity of bleeding is usually similar in members of a single family. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma. Treatment is similar to that for hemophilia A. (From Cecil Textbook of Medicine, 19th ed, p1008)
Agents that cause clotting.
Stable blood coagulation factor activated by contact with the subendothelial surface of an injured vessel. Along with prekallikrein, it serves as the contact factor that initiates the intrinsic pathway of blood coagulation. Kallikrein activates factor XII to XIIa. Deficiency of factor XII, also called the Hageman trait, leads to increased incidence of thromboembolic disease. Mutations in the gene for factor XII that appear to increase factor XII amidolytic activity are associated with HEREDITARY ANGIOEDEMA TYPE III.
System established by the World Health Organization and the International Committee on Thrombosis and Hemostasis for monitoring and reporting blood coagulation tests. Under this system, results are standardized using the International Sensitivity Index for the particular test reagent/instrument combination used.
Coagulant substances inhibiting the anticoagulant action of heparin.
Formation and development of a thrombus or blood clot in the blood vessel.
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).
Hemorrhagic and thrombotic disorders resulting from abnormalities or deficiencies of coagulation proteins.
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.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
A hereditary deficiency of blood coagulation factor XI (also known as plasma thromboplastin antecedent or PTA or antihemophilic factor C) resulting in a systemic blood-clotting defect called hemophilia C or Rosenthal's syndrome, that may resemble classical hemophilia.
The time required by whole blood to produce a visible clot.
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.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
A nutritional condition produced by a deficiency of VITAMIN K in the diet, characterized by an increased tendency to hemorrhage (HEMORRHAGIC DISORDERS). Such bleeding episodes may be particularly severe in newborn infants. (From Cecil Textbook of Medicine, 19th ed, p1182)
Inflammation of a vein associated with a blood clot (THROMBUS).
Any type of variation in the appearance of energy output of the sun. (NASA Thesaurus, 1994)
The number of LEUKOCYTES and ERYTHROCYTES per unit volume in a sample of venous BLOOD. A complete blood count (CBC) also includes measurement of the HEMOGLOBIN; HEMATOCRIT; and ERYTHROCYTE INDICES.
Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.
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 attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
The residual portion of BLOOD that is left after removal of BLOOD CELLS by CENTRIFUGATION without prior BLOOD COAGULATION.
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.
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.
The presence of antibodies directed against phospholipids (ANTIBODIES, ANTIPHOSPHOLIPID). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (ANTIBODIES, ANTICARDIOLIPIN). Present also are high levels of lupus anticoagulant (LUPUS COAGULATION INHIBITOR).
Hemorrhage following any surgical procedure. It may be immediate or delayed and is not restricted to the surgical wound.
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)
Substances found in many plants, containing the 4-hydroxycoumarin radical. They interfere with vitamin K and the blood clotting mechanism, are tightly protein-bound, inhibit mitochondrial and microsomal enzymes, and are used as oral anticoagulants.
An amino acid formed in vivo by the degradation of dihydrouracil and carnosine. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, the compound may be a false transmitter replacing GAMMA-AMINOBUTYRIC ACID. A rare genetic disorder, hyper-beta-alaninemia, has been reported.
Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.
Control of bleeding during or after surgery.
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.
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.
A plasma protein which is the precursor of kallikrein. Plasma that is deficient in prekallikrein has been found to be abnormal in thromboplastin formation, kinin generation, evolution of a permeability globulin, and plasmin formation. The absence of prekallikrein in plasma leads to Fletcher factor deficiency, a congenital disease.
Activated form of factor XII. In the initial event in the intrinsic pathway of blood coagulation, kallikrein (with cofactor HIGH MOLECULAR WEIGHT KININOGEN) cleaves factor XII to XIIa. Factor XIIa is then further cleaved by kallikrein, plasmin, and trypsin to yield smaller factor XII fragments (Hageman-Factor fragments). These fragments increase the activity of prekallikrein to kallikrein but decrease the procoagulant activity of factor XII.
Laboratory examination used to monitor and evaluate platelet function in a patient's blood.
A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
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.
Blood coagulation disorder usually inherited as an autosomal recessive trait, though it can be acquired. It is characterized by defective activity in both the intrinsic and extrinsic pathways, impaired thromboplastin time, and impaired prothrombin consumption.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.
Injuries resulting in hemorrhage, usually manifested in the skin.
Multicellular marine macroalgae including some members of red (RHODOPHYTA), green (CHLOROPHYTA), and brown (PHAEOPHYTA) algae. They are widely distributed in the ocean, occurring from the tide level to considerable depths, free-floating (planktonic) or anchored to the substratum (benthic). They lack a specialized vascular system but take up fluids, nutrients, and gases directly from the water. They contain CHLOROPHYLL and are photosynthetic, but some also contain other light-absorbing pigments. Many are of economic importance as FOOD, fertilizer, AGAR, potash, or source of IODINE.
Endogenous peptides present in most body fluids. Certain enzymes convert them to active KININS which are involved in inflammation, blood clotting, complement reactions, etc. Kininogens belong to the cystatin superfamily. They are cysteine proteinase inhibitors. HIGH-MOLECULAR-WEIGHT KININOGEN; (HMWK); is split by plasma kallikrein to produce BRADYKININ. LOW-MOLECULAR-WEIGHT KININOGEN; (LMWK); is split by tissue kallikrein to produce KALLIDIN.
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).
Heparin fractions with a molecular weight usually between 4000 and 6000 kD. These low-molecular-weight fractions are effective antithrombotic agents. Their administration reduces the risk of hemorrhage, they have a longer half-life, and their platelet interactions are reduced in comparison to unfractionated heparin. They also provide an effective prophylaxis against postoperative major pulmonary embolism.
A division of predominantly marine EUKARYOTA, commonly known as brown algae, having CHROMATOPHORES containing carotenoid PIGMENTS, BIOLOGICAL. ALGINATES and phlorotannins occur widely in all major orders. They are considered the most highly evolved algae because of their well-developed multicellular organization and structural complexity.
The process of observing, recording, or detecting the effects of a chemical substance administered to an individual therapeutically or diagnostically.
Reduction of blood viscosity usually by the addition of cell free solutions. Used clinically (1) in states of impaired microcirculation, (2) for replacement of intraoperative blood loss without homologous blood transfusion, and (3) in cardiopulmonary bypass and hypothermia.
Low-molecular-weight fragment of heparin, having a 4-enopyranosuronate sodium structure at the non-reducing end of the chain. It is prepared by depolymerization of the benzylic ester of porcine mucosal heparin. Therapeutically, it is used as an antithrombotic agent. (From Merck Index, 11th ed)
Antiphospholipid antibodies found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN.
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.
An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.
A deficiency or absence of FIBRINOGEN in the blood.
Tests used in the analysis of the hemic system.
A subnormal level of BLOOD PLATELETS.
Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. Several endogenous antiplasmins are known. The drugs are used to control massive hemorrhage and in other coagulation disorders.
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)
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Techniques for controlling bleeding.
Starches that have been chemically modified so that a percentage of OH groups are substituted with 2-hydroxyethyl ether groups.
Substances used for the detection, identification, analysis, etc. of chemical, biological, or pathologic processes or conditions. Indicators are substances that change in physical appearance, e.g., color, at or approaching the endpoint of a chemical titration, e.g., on the passage between acidity and alkalinity. Reagents are substances used for the detection or determination of another substance by chemical or microscopical means, especially analysis. Types of reagents are precipitants, solvents, oxidizers, reducers, fluxes, and colorimetric reagents. (From Grant & Hackh's Chemical Dictionary, 5th ed, p301, p499)
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
The relationship between the dose of an administered drug and the response of the organism to the drug.
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals.
Proteins prepared by recombinant DNA technology.
Diseases of the domestic dog (Canis familiaris). This term does not include diseases of wild dogs, WOLVES; FOXES; and other Canidae for which the heading CARNIVORA is used.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.
A single-chain polypeptide derived from bovine tissues consisting of 58 amino-acid residues. It is an inhibitor of proteolytic enzymes including CHYMOTRYPSIN; KALLIKREIN; PLASMIN; and TRYPSIN. It is used in the treatment of HEMORRHAGE associated with raised plasma concentrations of plasmin. It is also used to reduce blood loss and transfusion requirements in patients at high risk of major blood loss during and following open heart surgery with EXTRACORPOREAL CIRCULATION. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
The introduction of whole blood or blood component directly into the blood stream. (Dorland, 27th ed)
Elements of limited time intervals, contributing to particular results or situations.
Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal SYPHILIS SERODIAGNOSIS.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
Injections made into a vein for therapeutic or experimental purposes.
Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both the heart and lungs.
A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.
Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.
The formation or presence of a blood clot (THROMBUS) within a vein.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
The giving of drugs, chemicals, or other substances by mouth.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Compounds with a BENZENE fused to IMIDAZOLES.
Loss of blood during a surgical procedure.
Precordial pain at rest, which may precede a MYOCARDIAL INFARCTION.

Low-molecular-weight heparin in outpatient treatment of DVT. (1/681)

Patients with a diagnosis of acute deep venous thrombosis have traditionally been hospitalized and treated with unfractionated heparin followed by oral anticoagulation therapy. Several clinical trials have shown that low-molecular-weight heparin is at least as safe and effective as unfractionated heparin in the treatment of uncomplicated deep venous thrombosis. The use of low-molecular-weight heparin in an outpatient program for the management of deep venous thrombosis provides a treatment alternative to hospitalization in selected patients. Use of low-molecular-weight heparin on an outpatient basis requires coordination of care, laboratory monitoring, and patient education and participation in treatment. Overlapping the initiation of warfarin permits long-term anticoagulation. Advantages include a decreased incidence of heparin-induced thrombocytopenia and fewer episodes of bleeding complications. Future clinical trials evaluating the safety and efficacy of low-molecular-weight heparin in the treatment of complicated deep venous thrombosis will further define appropriate indications for use and strategies for outpatient management.  (+info)

Structure and anticoagulant activity of sulfated fucans. Comparison between the regular, repetitive, and linear fucans from echinoderms with the more heterogeneous and branched polymers from brown algae. (2/681)

Sulfated fucans are among the most widely studied of all the sulfated polysaccharides of non-mammalian origin that exhibit biological activities in mammalian systems. Examples of these polysaccharides extracted from echinoderms have simple structures, composed of oligosaccharide repeating units within which the residues differ by specific patterns of sulfation among different species. In contrast the algal fucans may have some regular repeating structure but are clearly more heterogeneous when compared with the echinoderm fucans. The structures of the sulfated fucans from brown algae also vary from species to species. We compared the anticoagulant activity of the regular and repetitive fucans from echinoderms with that of the more heterogeneous fucans from three species of brown algae. Our results indicate that different structural features determine not only the anticoagulant potency of the sulfated fucans but also the mechanism by which they exert this activity. Thus, the branched fucans from brown algae are direct inhibitors of thrombin, whereas the linear fucans from echinoderms require the presence of antithrombin or heparin cofactor II for inhibition of thrombin, as reported for mammalian glycosaminoglycans. The linear sulfated fucans from echinoderms have an anticoagulant action resembling that of mammalian dermatan sulfate and a modest action through antithrombin. A single difference of one sulfate ester per tetrasaccharide repeating unit modifies the anticoagulant activity of the polysaccharide markedly. Possibly the spatial arrangements of sulfate esters in the repeating tetrasaccharide unit of the echinoderm fucan mimics the site in dermatan sulfate with high affinity for heparin cofactor II.  (+info)

Antithrombotic efficacy of thrombin inhibitor L-374,087: intravenous activity in a primate model of venous thrombus extension and oral activity in a canine model of primary venous and coronary artery thrombosis. (3/681)

The small molecule direct thrombin inhibitor L-374,087 was characterized across species in an in vitro activated partial thromboplastin clotting time (aPTT) assay and in vivo in rhesus monkey and dog thrombosis models. In vitro in rhesus, dog, and human plasma, L-374,087 concentrations eliciting 2-fold increases in aPTT were 0.25, 1.9, and 0.28 microM, respectively. In anesthetized rhesus monkeys, 300 microgram/kg bolus plus 12 microgram/kg/min and 300 microgram/kg bolus plus 30 microgram/kg/min L-374,087 i.v. infusions significantly reduced jugular vein thrombus extension, with both regimens limiting venous thrombus extension to 2-fold that of baseline thrombus mass compared with a 5-fold extension observed in the vehicle control group. Antithrombotic efficacy in the rhesus with the lower-dose regimen was achieved with 2.3- to 2.4-fold increases in aPTT and prothrombin time. In a conscious instrumented dog model of electrolytic vessel injury, the oral administration of two 10 mg/kg L-374,087 doses 12 h apart significantly reduced jugular vein thrombus mass, reduced the incidence of and delayed time to occlusive coronary artery thrombosis, and significantly reduced coronary artery thrombus mass and ensuing posterolateral myocardial infarct size. Antithrombotic efficacy in the dog was achieved with 1.6- to 2.0-fold increases in aPTT at 1 to 6 h after oral dosing with L-374,087. These results indicate significant antithrombotic efficacy against both venous and coronary arterial thrombosis with L-374,087 with only moderate elevations in aPTT or prothrombin time. The oral efficacy of L-374,087 characterizes this compound as a prototype for the further development of orally active direct thrombin inhibitors.  (+info)

Factor VIII and other hemostasis variables are related to incident diabetes in adults. The Atherosclerosis Risk in Communities (ARIC) Study. (4/681)

OBJECTIVE: Our objective was to evaluate whether selected hemostasis variables, some of which may reflect inflammation or endothelial dysfunction, are independently associated with the development of diabetes. RESEARCH DESIGN AND METHODS: We studied a biethnic cohort of 12,330 men and women, 45-64 years of age, of the Atherosclerosis Risk in Communities Study. New cases of diabetes were diagnosed by a reported physician diagnosis, hypoglycemic medication use, or a casual or fasting serum glucose level of > or = 11.1 or > or = 7 mmol/l, respectively. RESULTS: Over an average follow-up of 7 years, 1,335 new cases of diabetes were detected. The odds ratios (4th versus 1st quartile) of developing diabetes, adjusted by logistic regression for age, sex, race, study center, family history of diabetes, fasting glucose, physical activity, and smoking, were 1.2 (95% CI 1.0-1.5) for fibrinogen and 1.4 (1.1-1.6) for factor VII. Associations for factor VIII, von Willebrand factor, and activated partial thromboplastin time were found to be 1.8 (1.3-2.3), 1.4 (1.1-1.8), and 0.63 (0.49-0.82), respectively, in women. Although further adjustment for BMI and waist-to-hip ratio diminished the relationships, a highly statistically significant association (P = 0.001) remained for factor VIII (1.6 [1.2-2.1]) in women. CONCLUSIONS: Factor VIII and other hemostasis variables are associated with the development of diabetes in middle-aged adults. These findings support a role for inflammation and, particularly in women, endothelial dysfunction in the pathogenesis of type 2 diabetes.  (+info)

The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease. (5/681)

AIM: This study evaluated a novel specific thrombin inhibitor, inogatran, in comparison with unfractionated heparin, with regard to markers for coagulation activity in patients with unstable coronary artery disease. METHODS AND RESULTS: In the Thrombin Inhibition In Myocardial Ischaemia (TRIM) study patients were randomized to one of three different doses of inogatran or to unfractionated heparin, given intravenously over 72 h. In a subpopulation of 320 patients, markers for coagulation activity were measured at baseline, during and after the study infusion. Prothrombin fragment 1 + 2, indicating thrombin generation, decreased in the low, medium and high dose inogatran groups and in the heparin group during the first 6 h of treatment by 12%, 15%, 21% and 26%, respectively. From 6 h to 72 h after the start of infusion the levels changed by -7%, -6%, -4% and +34%, respectively. The increase in the heparin group continued after the infusion was stopped. Thrombin-antithrombin complex, also indicating thrombin generation, decreased by 0%, 2%, 18% and 22%, respectively, during the first 6 h of treatment. During the same period soluble fibrin, an intermediate in fibrin formation, increased both in the low and medium inogatran group by 9%, while a decrease by 4% and 18%, respectively, was seen in the high dose inogatran group and in the heparin group. Fibrin dissolution, as measured by fibrin D-dimer, decreased during the first 24 h of treatment by 20%, 18%, 18% and 20%, respectively. The first 24 h after discontinuation of infusion, fibrin D-dimer increased by 6%, 23%, 25% and 44%, respectively. After 72 h, at the end of infusion, patients treated with inogatran, to a larger extent than those given heparin, had suffered from death, myocardial infarction or refractory angina pectoris. After 7 days this trend was less marked. CONCLUSION: The more pronounced decrease in thrombin generation and fibrin turnover during the first 6 h of infusion, and the later increase in thrombin generation and fibrin turnover, in the heparin group, as compared to the inogatran groups, may be related to the lower clinical event rate during infusion with heparin compared with inogatran and the recurrence of ischaemic events, early after cessation of heparin infusion.  (+info)

Adenovirus-mediated local expression of human tissue factor pathway inhibitor eliminates shear stress-induced recurrent thrombosis in the injured carotid artery of the rabbit. (6/681)

The main cause of acute coronary syndrome may be recurrent thrombosis, which is initiated by the activation of the extrinsic coagulation pathway. Tissue factor (TF) pathway inhibitor (TFPI) efficiently inhibits an early step in this pathway by the formation of a complex with factor VIIa, TF, and factor Xa. We determined whether local TFPI gene transfer can inhibit thrombosis in an injured artery without inducing systemic side effects. Balloon-injured rabbit carotid arteries were infected with an adenoviral vector that expressed either human TFPI (AdCATFPI) or bacterial beta-galactosidase (AdCALacZ). Two to 6 days after gene transfer, thrombosis was induced by the production of constant stenosis of the artery, and blood flow was measured continuously with an electromagnetic flow probe. A cyclic flow variation, which is thought to reflect the recurrent formation and dislodgment of mural thrombi, was observed in all AdCALacZ-infected arteries as well as in saline-infused arteries. In contrast, no cyclic flow variation was detectable in AdCATFPI-transfected arteries, even in the presence of epinephrine (1 microg. kg-1. min-1 infusion). Prothrombin time, activated partial thromboplastin time, and the ex vivo platelet aggregation induced by either adenosine diphosphate or collagen were unaltered in AdCATFPI-infected rabbits. We found that in vivo TFPI gene transfer into an injured artery completely inhibits the recurrent thrombosis induced by shear stress even in the presence of catecholamine, without affecting systemic coagulation status. Adenovirus-mediated local expression of TFPI may have the potential for the treatment of human thrombosis.  (+info)

Impaired anticoagulant response to infusion of thrombin in atherosclerotic monkeys associated with acquired defects in the protein C system. (7/681)

To examine the effects of atherosclerosis on the protein C anticoagulant pathway in vivo, we measured anticoagulant responses to intravenous administration of human alpha-thrombin or activated protein C (APC) in cynomolgus monkeys. Two groups of monkeys were fed either a control diet (n=18) or an atherogenic diet (n=12) that produces both hypercholesterolemia and moderate hyperhomocyst(e)inemia. A third group (n=8) was fed an atherogenic diet for 15 months, and then fed the atherogenic diet supplemented with B vitamins for 6 months to correct the hyperhomocyst(e)inemia. The plasma homocyst(e)ine level was higher in monkeys fed the atherogenic diet (9.6+/-1.0 micromol/L) than in monkeys fed the control diet (3.7+/-0.2 micromol/L) or the atherogenic diet with B vitamins (3.6+/-0.2 micromol/L) (P<0.001). Infusion of thrombin produced a much greater prolongation of the activated partial thromboplastin time in monkeys fed the control diet (52+/-10 seconds) than in monkeys fed the atherogenic diet either with (24+/-4 seconds) or without (27+/-5 seconds) supplemental B vitamins (P<0.02). Thrombin-dependent generation of circulating APC was higher in control (294+/-17 U/mL) than in atherosclerotic (240+/-14 U/mL) monkeys (P<0.05), although levels of fibrinogen, plasminogen, D-dimer, and thrombin-antithrombin complexes were similar in each group. Injection of human APC produced a similar prolongation of the activated partial thromboplastin time in control (31+/-3 seconds) and atherosclerotic (29+/-2 seconds) monkeys. These findings provide evidence for impaired anticoagulation, due partly to decreased formation of APC, in atherosclerosis. The blunted anticoagulant response to thrombin in hypercholesterolemic monkeys was not corrected by supplementation with B vitamins.  (+info)

Large amounts of vascular endothelial growth factor at the site of hemostatic plug formation in vivo. (8/681)

Vascular endothelial growth factor (VEGF) is important for the proliferation, differentiation, and survival of microvascular endothelial cells. It is a potent angiogenic factor and a specific endothelial cell mitogen that increases fenestration and extravasation of plasma macromolecules. Recently, large quantities of VEGF were detected in human megakaryocytes. Incubation of human platelets with thrombin in vitro resulted in the release of large amounts of VEGF. To investigate whether VEGF is released from platelets during coagulation activation in vivo, we measured in human subjects VEGF at the site of plug formation, ie, in blood emerging from a standardized injury made to determine bleeding time (shed blood). VEGF was also determined in the same volunteers after treatment with the specific thrombin inhibitor recombinant hirudin (r-hirudin). In a double-blind, randomized, crossover study, 17 healthy male volunteers (aged 20 to 35 years) were investigated. VEGF concentrations were measured in venous blood and in shed blood by the use of an immunoassay 10 minutes after intravenous administration of r-hirudin (0.35 mg/kg of body weight) or physiological saline. Prothrombin fragment f1.2 (f1.2) and beta-thromboglobulin (beta-TG) were determined as indicators of coagulation and platelet activation, respectively. Concentrations of VEGF, f1.2, and beta-TG in shed blood 4 minutes after injury were significantly higher than in venous blood (VEGF, 55.8+/-9.2 versus <20 pg/mL, P<0.001; f1.2, 71.3+/-10.4 versus 0.78+/-0.03 nmol/L, P<0. 001; beta-TG, 2290+/-170 versus 53.2+/-14.0 ng/mL, P<0.001). Administration of r-hirudin caused a >50% inhibition of the beta-TG and f1.2 levels in shed blood. In a similar manner, much lower amounts of VEGF were detectable at the site of plug formation after r-hirudin treatment (69.0+/-9.5 versus 37.8+/-2.6 pg/mL per minute; P=0.0015). Our data indicate that substantial quantities of VEGF are released from platelets during the interaction with the injured vessel wall in vivo. This finding may be relevant with respect to wound healing and tissue repair, tumor vascularization, or arterial thrombus formation.  (+info)

Background: The concept of developmental hemostasis has been universally accepted. Physiological reference ranges for coagulation tests are available for infants and children of different ages. However, on Oriental children they are rare.. Methods: Results of preoperative activated partial thromboplastin time (APTT) in neonates, infants, children aged 1-18 years and adults with minor elective surgery in a university affiliated hospital were reviewed retrospectively. Plasma activity of factors VIII, IX, XI, XII (FVIII: C, FIX: C, FXI: C, FXII: C) and lupus anticoagulants (LAC) in 47 children with prolonged APTT and 34 adult controls were measured to investigate the causes of prolongation.. Results: Compared with adults, APTT values were prolonged significantly and were age-dependent in children, especially in neonates and infants aged 1-6 months. Mean values for FXII: C and FIX: C in children with prolonged APTT values were significantly lower than those in adults ( ...
INTRODUCTION: Patients on intravenous heparin require regular activated partial thromboplastin time monitoring. Laboratory-based activated partial thromboplastin time assays necessitate a delay between blood sampling and dose adjustment. Point-of-care testing could permit immediate dose adjustments, potentially enabling tighter control of anticoagulation. AIM: To assess equivalence of activated partial thromboplastin time measured by conventional laboratory assay and by a novel proprietary point-of-care testing system (Hemochron Response, ITC, Thoratec Corporation, Edison, NJ) among surgical ward patients on intravenous heparin. METHODS: A total of 39 blood samples from patients on intravenous heparin were tested with both laboratory and point-of-care assays. Assay equivalence was assessed by Bland-Altman analysis. Results. Point-of-care measurements exceeded laboratory activated partial thromboplastin time by a mean of 15 seconds (standard deviation 19). In 19 cases (49%), the point-of-care measurement
The activated partial thromboplastin time (APTT) assay is a very common coagulation test, used for several reasons. The test is conventionally used for assessing the contact factor (intrinsic) pathway of blood coagulation, and thus for screening deficiencies in this pathway, most typically factors VIII, IX, and XI. The APTT is also sensitive to contact factor deficiencies, including factor XII, prekallikrein, and high-molecular-weight kininogen. The APTT may also be elevated in a variety of conditions, including liver disease, vitamin K deficiency, and disseminated intravascular coagulation. The APTT can also be used for monitoring unfractionated heparin (UFH) therapy, as well as for screening lupus anticoagulant (LA) or for assessing thrombosis risk. Which of these separate uses is important to a given laboratory or clinician depends on the laboratory and the clinical context. For example, UFH sensitivity is important in hospital-based laboratories, where UFH therapy is used, but not in ...
TY - JOUR. T1 - Prolonged partial thromboplastin time without bleeding history; Fletcher factor deficiency. AU - Üstün, Celalettin. AU - Jillella, Anand. AU - Hendriks, Linda. AU - Jonah, Mary. AU - Kutlar, Ferdane. AU - Burgess, Russell. AU - Kutlar, Abdullah. PY - 2002/12/1. Y1 - 2002/12/1. N2 - A 67-year-old patient was admitted to the hospital to perform an esophagogastrectomy because a lesion at the lower esophagus was strongly suspicious for cancer. Her medical history and her family history were negative for bleeding tendency or thrombosis. Her activated partial thromboplastin time (aPTT) was prolonged (44 s) whereas her prothrombin time (PT) was normal (11 s) presurgery. Mixing of her plasma with normal plasma corrected her prolonged aPTT (27.9 s). Prolonged incubation shortened the patients aPTT (36.3 s). Fletcher factor activity was found to be 50%. The patient underwent an esophagogastrectomy without bleeding complications under spinal anesthesia. Fletcher factor deficiency, a rare ...
Introduction: The most commonly used test for monitoring heparin therapy is the activated partial thromboplastin time (aPTT). The response of available aPTT reagents to heparin varies significantly. The aim of this study was to highlight the differences between aPTT reagents stored in a dried format to select the most suitable formulations to be used for the development of point-of-care diagnostic devices used for monitoring of unfractionated heparin dose response. Methods: Ten reagents were analysed in terms of their performance in liquid and in dried form after storage for 24 h and 14 days. Performance was assessed by measurement of the clotting time (CT) as evidenced by the onset of thrombin formation using a chromogenic thrombin substrate in plasma samples activated with these formulations. Results: Reagents in all of the three forms tested (liquid, 24 h and 14 days) resulted in significant shortening of CTs in comparison with the nonactivated plasma CT. Liquids returned more rapid CTs in comparison
Do not take a sample for APTT testing from the same limb through which the patient is recieving heparin. If there is no other option, then stop the heparin infusion, flush the line and wait several minutes before taking the APTT sample ...
APS is an acquired hypercoagulable state which presents classically as recurrent arterial and/or venous thrombosis and is a major cause of late first- and second-trimester spontaneous fetal loss. In addition to thrombotic complications, diagnosis of APS requires the presence of ≥ 1 of the following antiphospholipid antibodies on 2 occasions ≥12 weeks apart: 1) anti-ß2-glycoprotein…
Activated partial thromboplastin times (APTT) for monitoring heparin therapy for venous thromboembolism tended to be inappropriately short if blood was collected in commercially available evacuated glass tubes. Five types of evacuated tubes marketed under the trade names Vacutainer and Venoject were examined. The APTT of heparinized blood collected in these tubes correlated poorly (r = 0.04 to 4 = 0.25) with that of blood samples from the same patients collected in plastic tubes. Most of the evacuated tube APTT were shorter than that of blood collected in plastic or siliconised glass tubes, but the results were unpredictable and varied from tube to tube and from batch to batch. This effect on heparin is apparently due to an unidentified substances which is eluted from the rubber stoppers of the tubes. Heparin control according to the APTT blood collected in these evacuated tubes is hazardous.. ...
Order a PT PTT / Prothrombin Time w/INR and Partial Thromboplastin Time Blood Test to diagnose excessive or unexplained bleeding.
Prothrombin Time Activated Partial Thromboplastin Time and Platelets Count among Hypertensive Patients Attending a Tertiary Health Institution in Yenagoa,
Use this page to view the contact information, documents, and history of considerations for the coding analysis for labs (cal) for prothrombin time and partial thromboplastin time (revision of icd-9-cm codes for swelling of limb) (cag-00201n).
BACKGROUND:Coagulation abnormalities are frequently encountered in patients with coronavirus disease 2019 (COVID-19), especially in those with more severe disease. These hematologic abnormalities are suspected to occur in the context of underlying immune dysregulation and endothelial dysfunction. Elevated D-dimer levels, COVID-19-associated coagulopathy (CAC), disseminated intravascular coagulation (DIC), and positive lupus anticoagulants are the most common findings to date. Current guidelines suggest that all patients with COVID-19 should receive pharmacologic thromboprophylaxis. CASE REPORT:An 89-year-old man with a medical history of hypertension, type 2 diabetes, and advanced prostate cancer in remission presented with generalized weakness. At our center, a reverse transcription-polymerase chain reaction test was positive for severe acute respiratory syndrome coronavirus 2, but the patient did not have symptoms of COVID-19. He was also found to have a prolonged activated partial thromboplastin time
A partial thromboplastin time (PTT) test measures how long it takes for a clot to form in a blood sample. A clot is a thick lump of blood that the body produces to seal leaks, wounds, cuts, and scratches and prevent excessive bleeding.. The bloods ability to clot involves platelets (also called thrombocytes) and proteins called clotting factors. Platelets are oval-shaped cells made in the bone marrow. Most clotting factors are made in the liver.. When a blood vessel breaks, platelets are first to the area to help seal off the leak and temporarily stop or slow the bleeding. But for the clot to become strong and stable, the action of clotting factors is required.. The bodys clotting factors are numbered using the Roman numerals I through XII. They work together in a specialized sequence, almost like pieces of a puzzle. When the last piece is in place, the clot develops - but if even one piece is missing or defective, the clot cant form.. The PTT test is used to evaluate the ability of a ...
Simultaneous or sequential haemorrhage and thrombosis in the presence of a prolonged activated partial thromboplastin time (aPTT) is a rare occurrence: we describe the case a 37 year old lady who developed post-delivery deep vein thrombosis treated w
A partial thromboplastin time (PTT) test is used to evaluate bloods ability to clot. It may be done as part of an evaluation for a bleeding disorder or to monitor the effects of blood-thinning medicine.
A partial thromboplastin time (PTT) test is used to evaluate bloods ability to clot. It may be done as part of an evaluation for a bleeding disorder or to monitor the effects of blood-thinning medicine.
Use this page to view the contact information, documents, and history of considerations for the coding analysis for labs (cal) for partial thromboplastin time (addition of icd-9-cm 289.81, primary hypercoagulable state as a covered indication) (cag-00327n).
This study investigated the effect of dabigatran on the activated partial thromboplastin time and activated clotting time in artrial fibrillation patients.
Use of bedside activated partial thromboplastin time monitor to adjust heparin dosing after thrombolysis for acute myocardial infarction: Results of gusto-i ...
The Coagulation Panel is a common set of labs ordered to monitor a patients bleeding status. Lab values are commonly presented in a 3-way diagram, colloquially known as the Mercedes diagram. The top left value is the Prothrombin Time (PT). This lab value evaluates the extrinsic pathway and common pathways of coagulation. PT is primarily affected by the following coagulation factors: I (1), II (2), V (5), VII (7), and X (10). The top right value is the Partial Thromboplastin Time (PTT), sometimes called the activated partial thromboplastin time (aPTT). This lab value evaluates the intrinsic pathway and common pathways of coagulation. PTT is primarily affected by the following coagulation factors: VIII (8), IX (9), XI (11), and XII (12). The bottom value is the International Normalized Ratio (INR). The INR is a ratio calculated from a patients PT value, by dividing it by a normal PT value, or population mean. INR is primarily used in patients taking warfarin (Coumadin), to monitor therapeutic
BACKGROUND: Several hemostatic abnormalities have been described in hypothyroidism, such as modification of coagulation proteins and bleeding tendency. Although thyroid hormone deficiency is considered to be responsible for these changes, the underlying mechanisms have not yet been established. OBJECTIVE: To evaluate the respective influence of peripheral thyroid hormones (free thyroxine) and TSH on blood clotting by assessing coagulation parameters in patients with a history of total thyroidectomy for thyroid cancer, under three different conditions: induced hypothyroidism, euthyroid state, and following recombinant human TSH (rhTSH) administration. METHODS: Coagulation parameters (platelet count, fibrinogen, international normalized ratio, prothrombin time, thrombin time, activated partial thromboplastin time (APTT), factor VIII activity ((FVIII:C), as well as von Willebrand factor antigen (VWF:Ag) and VWF activity using collagen binding assay (VWF:CBA)) were measured in patients with severe ...
TY - JOUR. T1 - Association of postprandial blood sugar with hypercoagulability in comparison to fasting blood sugars in diabetic and healthy patients. T2 - A cross-sectional study. AU - Kadiyala, Sri Ramulu. AU - Rao, Karthik. AU - Rao, N. R.. AU - Bhat, Ram. AU - Rao, Jayaprakash. AU - Navin, P.. AU - Balaji, O.. PY - 2017/1/1. Y1 - 2017/1/1. N2 - Objective: The aim of this study was to find the association of postprandial blood glucose with hypercoagulability in comparison to fasting blood sugars(FBS) in diabetic and healthy patients. Methods: The present study involved a total of 156 patients, of which 78 were taken as cases (diabetics) and other 78 as controls (non-diabetics). Laboratory analysis included prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen assay done along with fasting, and postprandial sugars. Results: Platelets in diabetics and healthy controls were in normal range. Decrease in PT and partial thromboplastin time was noted in diabetics compared ...
TY - JOUR. T1 - The effect of Dabigatran on select specialty coagulation assays. AU - Adcock, Dorothy M.. AU - Gosselin, Robert. AU - Kitchen, Steve. AU - Dwyre, Denis M. PY - 2013/1. Y1 - 2013/1. N2 - Dabigatran etexilate is a new oral anticoagulant that functions as a direct thrombin inhibitor. An inhibitor of thrombin has the potential to interfere with essentially all clot-based coagulation assays and select chromogenic assays, whereas the drug would not be expected to interfere in antigen-based assays. The purpose of this study was to evaluate the effect of dabigatran on various specialized coagulation assays using normal plasma specimens with varying concentrations of dabigatran (the active form of dabigatran etexilate). We have demonstrated that samples containing therapeutic levels of dabigatran may lead to underestimation of intrinsic factor activities with abnormal activated partial thromboplastin time (aPTT) mixing study results and a false-positive factor VIII Bethesda titer; ...
TY - JOUR. T1 - The unwarranted use of replicate analysis in routine coagulation studies. AU - Sage-El, A.. AU - Burns, E.. AU - Wenz, B.. PY - 1985/1/1. Y1 - 1985/1/1. N2 - The need to assure the validity of semiautomated coagulation procedures by performing replicate determinations is assessed. Prothrombin times (PT) and activated partial thromboplastin times (aPTT) were run as duplicate assays using two different photo-optical detection systems. Sixty specimens with a broad range of PT and aPTT results were studied as aliquots of 80, 100, and 140 μL of plasma. A total of 1,440 studies were performed. No statistically significant differences were found among the data for complementary groups of assays. It is concluded that replicate analyses do not enhance the precision nor the accuracy of these coagulation studies. These factors are more controlled adequately by quality assurance procedures, including frequent calibration checks, the use of internal standards, and multilevel commercial ...
At many institutions, clot-based assays such as thrombin time, prothrombin time (PT)/INR, and activated partial thromboplastin time (aPTT) are readily available. Dabigatran has a more marked effect on the clot-based assays of aPTT and thrombin time than on PT. Thrombin time is typically very sensitive to dabigatran therapy. The result often exceeds the upper limit of the assay even with low dabigatran concentrations, according to current clinical data.15 Dabigatran can also cause prolongation of aPTT, although the degree of prolongation does not correlate well with drug concentration and varies with the reagent used for the aPTT test. An aPTT result within the reference range does not rule out the presence of dabigatran because low troughlike concentrations of dabigatran may yield a normal aPTT measurement. The presence of dabigatran may alter the PT/INR, but results may be variable.15,16 The factor Xa inhibitor agents have a more marked effect on PT/INR than on aPTT and have no clinical ...
Coronary artery often reoccludes after therapy of acute myocardial infarction with recombinant tissue plasminogen activator rt-PA, most likely due to in situ thrombin generation during thrombolysis. Previous studies with high molecular weight thrombin inhibitors, such as hirudin, have shown variable improvement in the frequency of sustained thrombolysis. This study was conducted to examine the modulation of thrombolysis, indices of thrombin generation and activated partial thromboplastin time (APTT) by a novel low molecular weight direct thrombin inhibitor, inogatran. A stable occlusive intracoronary thrombus was created in 19 dogs. Nine dogs were given an intravenous bolus of saline (group A), and 5 dogs were given inogatran (group B) followed by rapid infusion of rt-PA (1 mg/kg over 20 min), whereas saline or inogatran was continuously infused for 2 hr. Five other dogs were given inogatran (bolus and continuous infusion) only after thrombolysis by rt-PA was obtained (group C). Time to reflow ...
Activated partial thromboplastin clotting time (aPTT) is one of a handful of diagnostic coagulation tests that provides a measurement for the length of time it takes an individuals blood to form a clot. Blood clotting factors come together in a cascade process when a blood vessel is damaged to form a blood clot and stop bleeding. Clotting factors XII, IX, II, X, XI, VIII, V, fibrinogen, prekallikrein, and high-molecular-weight kininogen are components that make up the intrinsic clotting pathway and the common final pathway. These factors are measured in the aPTT test. The partial thromboplastin time test is performed before the activated partial thromboplastin time. The difference between these two tests is a special activation solution is added to the sample for the aPTT that increases the clotting time to provide a smaller reference range. If both the PTT and aPTT tests yield abnormal results, it is suggested the patient has a deficiency of factor I, V, X, or II. A normal PTT with an abnormal ...
Argatroban or lepirudin anticoagulation therapy in patients with heparin induced thrombocytopenia (HIT) or HIT suspect is typically monitored using the activated partial thromboplastin time (aPTT). Although aPTT correlates well with plasma levels of argatroban and lepirudin in healthy volunteers, it might not be the method of choice in critically ill patients. However, in-vivo data is lacking for this patient population. Therefore, we studied in vivo whether ROTEM or global clotting times would provide an alternative for monitoring the anticoagulant intensity effects in critically ill patients. This study was part of the double-blind randomized trial
Methods: We collected blood samples from 48 random patients, who were referred for routine coagulation testing, into low-volume (1 mL) and conventional (2.7 mL) sodium citrate tubes. We assayed the samples for prothrombin time (PT), activated partial thromboplastin time (aPTT), and D-dimer using the automated coagulation analyzer. Results: There was excellent correlation (r > 0.97) between the results of the two tubes for PT, aPTT, and D-dimer. The PT and aPTT for the low-volume sodium citrate tube were significantly shorter than those of the conventional sodium citrate tube. There was no statistically significant difference in the results for D-dimer. The percent biases calculated with Bland-Altman analysis were 0.8% for PT and 2.0% for aPTT. Both of them were within the desirable specifications for bias with 2.0% for PT and 2.3% for aPTT ...
In order to develop new anticoagulants as potential heparin alternatives, two pullulans with different molecular weight (MW) were used as starting polymers for the partial synthesis of a structurally new class of sulfated polysaccharides. Sulfation of these linear α-1,4-/1,6-glucans was carried out by a method with a SO3-pyridine complex in DMF, which had been optimized for the modification of β-1,3-glucans. Modifications of this methods resulted in pullulan sulfates with degrees of sulfation (DS) ranging from 0.17 to 1.99 and MW between 15 and 250 kDa. More than 50% of the sulfate groups were bound to the secondary C atoms in positions 2, 3 and 4 of the glucose monomers. The anticoagulant activity of the obtained pullulan sulfates was determined in the coagulation assays prothrombin time (PT), activated partial thromboplastin time (APTT), Heptest® and thrombin time (TT). They represent potent anticoagulants reaching the efficacy of heparin. Their activity not only improves with increasing DS ...
BACKGROUND/AIM: Acute myocardial infarction (AMI) is associated with increased coagulation which in the presence of unstable atheroma or endothelial damage leads to occlusive coronary vessel thrombosis. AMI is usually characterized by increased levels of catecholamines. It is possible there may be a link between catecholamines and hypercoagulation, but this still remains to be determined. In the current study we sought to verify whether hypercoagulation is associated with hypersympathetic activity in AMI patients, and whether there is a correlation between increased Methoxyhydroxyphenylglycol (MOPEG) levels (a metabolite of catecholamines) and shorter APTT (a marker of hypercoagulation). RESULTS: Shorter APTT values were detected in the plasma of AMI patients, which had also increased MOPEG levels. A linear correlation between APTT and MOPEG values was observed. High levels of the coagulation marker prothrombin (fragments 1+2) were also found. CONCLUSION: Shortened APTT demonstrates ...
[email protected] The APTT/PT/TT/FIB Reagent Kit is intended to measure the activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT) and quantitatively determine fibrinogen (FIB). Clinically, it is mainly used to screen the in...
Prandoni and colleagues (1) suggest that subcutaneous unfractionated heparin is an attractive approach to treating deep venous thrombosis compared with the use of low-molecular-weight-heparin (LMWH) because of the lower cost of unfractionated heparin. The main problems associated with the use of unfractionated heparin are the high variability of the anticoagulant response and the lack of an accepted method of standardization in the activated partial thromboplastin time, which is used to monitor treatment. Because unfractionated heparin treatment must be monitored (2), each hospital must establish its own therapeutic range based on a calibration curve of activated partial thromboplastin time against heparin levels assessed by anti-Xa activity. This procedure is difficult to perform, and it does not guarantee a full comparison of the anticoagulation regimens in different hospitals ...
TY - JOUR. T1 - Thrombophilia in patients with hypercholesterolemia. AU - Chan, Paul. AU - Tomlinsoin, Brain. AU - Tsai, Chung Wen. AU - Pan, Wen Harn. AU - Lee, Ying Shiung. PY - 1996. Y1 - 1996. N2 - To investigate a possible interrelationship between hypercholesterolemia and the coagulation and fibrinolytic system, the Cardiovascular Disease Risk Factor. Two-Township Study in Taiwan was undertaken as a longitudinal prospective study focusing on the evolution of cardiovascular disease risk factors, with an emphasis on hemostatic factors. Hemostatic parameters measured in this study included prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, factor VIIc, factor VIIIc, antithrombin III, and plasminogen. Subjects of both sexes with hypercholesterolemia (, 6.2 mmol/L) also had significant elevations of diastolic blood pressure, plasma glucose, triglycerides, fibrinogen, and factor VIIc and reduced PT and APTT compared with subjects with lower cholesterol. The ...
TY - JOUR. T1 - Thrombophilia in patients with hypertriglyceridemia. AU - Chan, Paul. AU - Huang, Tsuei Yuan. AU - Shieh, Shyh Ming. AU - Lin, Tz Shing. AU - Tsai, Chung Wen. PY - 1997. Y1 - 1997. N2 - Objectives: To investigate a possible relationship between hypertriglyceridemia and the coagulation system, a Cardiovascular Risk Factor Two-township Study was conducted in Taiwan. Design: A case-control study. This longitudinal, prospective study focused on the evolution of cardiovascular disease risk factors with emphasis on haemostatic factors. Subjects: Hypertriglyceridemic subjects (triglyceride , 2.26 mmoll -1, n = 327) and age-matched normal controls from a population screening program. Main outcome measures: Haemostatic parameters measured in this study included prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, factors VIIc and VIIIc, and antithrombin-III and plasminogen levels. Results: In our male hypertriglyceridemic subjects, aPTT was not significantly ...
Abstract:. Objective: To investigate the blood coagulation function in COVID-19 patients, and the correlation between coagulopathy and disease severity. Methods: We retrospectively collected 147 clinically diagnosed COVID-19 patients at Wuhan Leishenshan Hospital of Hubei, China. We analyzed the coagulation function in COVID-19 patients through the data including thrombin-antithrombin complex (TAT), 2-plasmininhibitor-plasmin Complex (PIC), thrombomodulin (TM), t-PA/PAI-1 Complex (t-PAIC), prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (APTT), fibrinogen (FIB), thrombin time (TT), D-Dimer (DD), and platelet (PLT). Result: The levels of TAT, PIC, TM, t-PAIC, PT, INR, FIB, and DD in COVID-19 patients were higher than health controls ( ...
TY - JOUR. T1 - The incidence and significance of hemostatic abnormalities in patients with head injuries. AU - Olson, J. D.. AU - Kaufman, H. H.. AU - Moake, J.. AU - OGorman, T. W.. AU - Hoots, K.. AU - Wagner, K.. AU - Kice Brown, C.. AU - Gildenberg, P. L.. PY - 1989. Y1 - 1989. N2 - Abnormal coagulation and fibrinolysis is a frequent complication in patients with head injury. This complication can be severe enough to lead to hemorrhage or thrombosis. A study was undertaken to determine if the hemostatic abnormalities are reliable indicators of outcome. Hemostasis in 269 patients with head injuries alone was screened using platelet count (PC), prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin clotting time (TCT), fibrinogen assay (FIB), level of fibrin-fibrinogen degradation products (FDP), and disseminated intravascular coagulation (DIC) score in the first 24 hours after injury. Test restults were compared with the outcome (discharged or dead) in the entire ...
Clinicians may wish to consider use of a stratified, 3-tiered approach of low-intensity anticoagulation, intermediate-intensity anticoagulation, and therapeutic-dose anticoagulation. Patients can be categorized by tier depending on their risk factors for VTE, acuity of illness, and laboratory values such as D-dimer level, according to the article.. The authors said they are offering guidance on anticoagulation consideration and dosing to assist clinicians faced with challenging anticoagulation-related situations in caring for hospitalized COVID patients until formal evidence-based guidelines become available.. The review noted that hematologic abnormalities commonly seen in patients with COVID-19 include elevations in D-dimer and fibrinogen, prolonged prothrombin time and activated partial thromboplastin time (aPTT), as well as changes in levels of inflammatory markers such as C-reactive protein (CRP), interleukin-6, and ferritin.. Understanding of these abnormalities is continually ...
Aim: To analyze the bone mineral density (BMD) changes of type 2 diabetes mellitus (T2DM) after being complicated with osteoporosis (OP) and their correlations with multiple risk factors. Methods: 240 cases of elderly T2DM patients were divided into an OP group and a non-OP group according to the BMD values. The results were subjected to correlation analyses. Thereafter the 120 patients in the OP group were randomly divided into three groups to be treated with alfacalcidol (group A), vitamin K1 (group B) and alfacalcidol plus vitamin K1 (group C) continuously for 12 months. The BMD, FBG levels, fasting insulin (FINS) levels, prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT) and fibrinogen (FIB) levels were measured 0, 6 and 12 months after administration. The heights, weights, BMI and HOMA-insulin resistance (HOMA-IR) of the patients were measured by designated personnel. Results: The patients in the OP group were of older age, longer disease course, lower BMD, and
Demonstrate adequate organ function as defined below, all screening labs should be performed within 10 days of treatment initiation.. Hematological Absolute neutrophil count (ANC) ≥1,500 /mcL Platelets ≥100,000 / mcL Hemoglobin ≥8 g/dL or ≥4.96 mmol/L. Renal Serum creatinine OR Measured or calculated creatinine clearance ≤1.5 X upper limit of normal (ULN) OR ≥60 mL/min for subject with creatinine levels , 1.5 X institutional ULN (GFR can also be used in place of creatinine or CrCl). Hepatic Serum total bilirubin ≤ 1.5 X ULN OR Direct bilirubin ≤ ULN for subjects with total bilirubin levels , 1.5 ULN AST (SGOT) and ALT (SGPT) ≤ 2.5 X ULN OR ≤ 5 X ULN for subjects with liver metastases Albumin ,2.5 mg/dL. Coagulation International Normalized Ratio (INR) or Prothrombin Time (PT) ≤1.5 X ULN unless subject is receiving anticoagulant therapy as long as PT or PTT is within therapeutic range of intended use of anticoagulants. Activated Partial Thromboplastin Time (aPTT) ≤1.5 X ...
Normal Factor Activity. Pooled Normal Plasma (PNP) contains citrated plasma from 30 or more carefully screened normal human donors. Our PNP is platelet poor with no buffers or preservatives making it most like your patient plasma. An approximately equal number of male and female donors are included. A Certificate of Analysis (CofA) accompanies each shipment of PNP. This lot specific CofA certifies the normalcy of this plasma satisfying regulatory guidelines. Assay values are assigned and reported on the CofA for Prothrombin Time (PT) and activated Partial Thromboplastin Time (aPTT). Fibrinogen and Factors II, V, VII, VIII, IX, X, XI and XII are assayed and certified to be within the normal range. No prepackaged amounts, order what you need!. ...
The aim of the present study is to isolate the sulfated polysaccharides from marine macro algae S. wightii. The crude sulfated polysaccharides were fractionated by anionic resin (Amberlite IRA-900) and the separated active fractions were confirmed by agarose gel electrophoresis. The active fractions were pooled, dialyzed and purified by molecular sieve (Sephadex G-100) chromatography. The molecular weight of fractionated as well as purified sulfated polysaccharides was determined through gradient polyacrylamide gel electrophoresis (PAGE) and the disaccharide profile of purified sulfated polysaccharides was also analyzed. The structure of purified sulfated polysaccharides was dogged by 1H-NMR spectrum. The elements such as Carbon, Hydrogen and Nitrogen (CHN) and Activated Partial Thromboplastin Time (APTT) were observed from the purified sulfated polysaccharides. The hexosamine, uronic acid and the CHN content in the purified sulfated polysaccharides were found to be low (except molecular weight) ...
OBJECTIVES: To evaluate whether patients with Cushings syndrome (CS) had i) changes in coagulative and fibrinolytic parameters associated with CS activity and ii) higher prevalence of venous thromboembolic events (VTE). DESIGN: Prospective study conducted on patients with CS evaluated at diagnosis and 12 months after surgery. PATIENTS AND METHODS: Forty patients with active CS (36 with Cushings disease (CD) and 4 with an adrenal adenoma) were evaluated. Forty normal subjects and 70 patients with non-ACTH-secreting pituitary adenomas served as controls. All patients and controls underwent an assessment of coagulation and fibrinolysis indexes before and after surgery. RESULTS: CS patients at baseline had a hypercoagulative phenotype when compared with normal subjects (activated partial thromboplastin time (aPTT), fibrinogen, D-Dimer, von Willebrand factor (VWF), plasminogen activator inhibitor 1 (PAI-1 or SERPINE1), antithrombin III (ATIII or SERPINC1), P,0.0001, α(2) antiplasmin, P=0.0004, ...
There are sufficient organ and bone marrow functions, defined as follows: Blood routine (no blood transfusion within 14 days before treatment, no use of G-CSF, no use of drugs to correct), Neutrophil count (ANC) ≥ 1,500/mm3 (1.5 × 109/L), Platelet count (PLT) ≥ 100,000/mm3 (100 × 109/L), Hemoglobin (Hb) ≥ 9 g/dL (90 g/L); Blood chemistry, Serum creatinine (Cr) ≤ 1.5 × upper limit of normal (ULN) or creatinine clearance (Cockroft-Gault formula) ≥ 60 ml / min, Total bilirubin (TBIL) ≤ 1.5 × ULN; Aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels ≤ 2.5 × ULN, liver metastases should be ≤ 5 × ULN; Coagulation, International normalized ratio (INR) ≤ 1.5, prothrombin time (PT) and activated partial thromboplastin time (APTT) ≤ 1.5 × ULN; Urine routine, Urine protein ,2+; if urine protein ≥ 2+, 24-hour urine protein quantitation shows that the protein must be ≤ 1g; Thyroid function, Thyroid stimulating hormone (TSH) ≤ ULN; if abnormalities should ...
TREATMENT. A- Supportive Care:-Oxygen Therapy. B- Prevention of Recurrent Emboli is the major therapeutic goal.. Anticoagulation: Heparin I/V. A bolus of heparin (80 units/kg) followed by continuous infusion (18 units/kg/hr) titrated individually to achieve an activated partial thromboplastin time (aPTT) between 1½ and 2½ times the control value, continued for 5-10 days. If APTT is not available, clotting time should be monitored with the help of capillary tubes at 2-3 times the baseline level. ...
Cardiovascular collapse is present, liver function tests ast and alt, international normalized ratio inr for prothrombin time, partial thromboplastin time aptt, and tt are normal. This layer is moved or mobilized by the superficial tissues to relax, simultaneously ceasing your counterforce. A good example of this directive was to identify infants at increased risk for little league elbow medial epicondylar physis and sclerosis of arteries and nerves, are important for osteopathic medicine. These symptoms can include osteomyelitis, subperiosteal abscess, sinus thrombosis, bacteremia, meningitis, epidural and subdural collections to areas that could lead to syncope and other studies have shown that bag-mask ventilation to restore patency of the visual eld decits. In one recent study, age was the sole symptom, without wheezing as seen in the chronic strain on lumbar spine flexion disc herniation usually medial to lateral across the profession and on transport to the local treatment of the ...
Initial laboratory studies include an arterial blood gas with pH of 7.03, a Pco2 of 70 mm Hg, calculated bicarbonate of 18 mEq/L, and a base excess of -13; the patients serum lactate level was 6.7 mmol/L. The white blood cell count is 25.6 × 103/μL (25.6 × 109/L) with 41% neutrophils and 38% band forms. The C-reactive protein level is 107 mg/L. The serum total bilirubin is 1.3 mg/dL, alanine aminotransferase is 22 U/L, and aspartate aminotransferase is 88 U/L. Her prothrombin time (PT) is 31.9 seconds (international normalized ratio: 3.1), and activated partial thromboplastin time (aPTT) is 51.9 seconds. The cerebrospinal fluid cell count (CSF) cell count, differential, protein, and glucose are normal. Samples of blood, urine, CSF, and endotracheal tube aspirate were sent for viral and bacterial culture and polymerase chain reaction assays. Quantitative … ...
APTTP : Monitoring heparin therapy (unfractionated heparin)   Screening for certain coagulation factor deficiencies   Detection of coagulation inhibitors such as lupus anticoagulant, specific factor inhibitors, and nonspecific inhibitors
The most commonly used test for monitoring heparin therapy is the activated partial thromboplastin time (aPTT). The response of available aPTT reagents to heparin varies significantly. The aim of this study was to highlight the differences between aPTT reagents stored in a dried format to select the most suitable formulations to be used for the development of point-of-care diagnostic devices used for monitoring of unfractionated heparin dose response. METHODS: Ten reagents were analysed in terms of their performance in liquid and in dried form after storage for 24 h and 14 days. Performance was assessed by measurement of the clotting time (CT) as evidenced by the onset of thrombin formation using a chromogenic thrombin substrate in plasma samples activated with these formulations. RESULTS: Reagents in all of the three forms tested (liquid, 24 h and 14 days) resulted in significant shortening of CTs in comparison with the nonactivated plasma CT. Liquids returned more rapid CTs in comparison with dried
To distinguish the above causes, mixing tests are performed, in which the patients plasma is mixed (initially at a 50:50 dilution) with normal plasma. If the abnormality does not disappear, the sample is said to contain an inhibitor (either heparin, antiphospholipid antibodies or coagulation factor specific inhibitors), while if it does disappear a factor deficiency is more likely. Deficiencies of factors VIII, IX, XI and XII and rarely von Willebrand factor (if causing a low factor VIII level) may lead to a prolonged aPTT correcting on mixing studies. ...
The partial thromboplastin time (PTT), also known as the activated partial thromboplastin time (aPTT or APTT), is a blood test ... Partial thromboplastin time is typically analyzed by a medical technologist or a laboratory technician on an automated ... The blood is mixed, then centrifuged to separate blood cells from plasma (as partial thromboplastin time is most commonly ... "MedlinePlus Medical Encyclopedia: Partial thromboplastin time (PTT)". Retrieved 2009-01-01. Korte, Wolfgang; Clarke, Susan; ...
... or activated partial thromboplastin time. It was not until much later that the subcomponents of thromboplastin and partial ... a derivative could be created called partial thromboplastin. Partial thromboplastin was used to measure the intrinsic pathway. ... Historically, thromboplastin was a lab reagent, usually derived from placental sources, used to assay prothrombin times (PT). ... However, partial thromboplastin is just phospholipids, and not tissue factor. Therefore, the coagulation cascade is triggered ...
Blood tests: Prothrombin time Partial thromboplastin time "hemostasis". Merriam-Webster Dictionary. Retrieved 2016-01-21. " ... Doctors of this time realized if these were plugged, blood could not continue to flow out of the body. Nevertheless, it took ... At this time many more advances in the general medical field were developed through the study of Egyptian mummification ... Putting pressure and/or dressing to a bleeding wound slows the process of blood loss, allowing for more time to get to an ...
Specifically Activated Partial Thromboplastin Time (aptt) is prolonged. The diagnosis is confirmed by an assay detecting very ...
Prolonged prothrombin and activated partial thromboplastin times are typical. Urinalysis can show bilirubinuria, proteinuria, ... RHD caused by RHDVa was reported for the first time in the United Kingdom in 1992. This initial epidemic was brought under ... Had the disease been introduced at a better time, control of the population would have been more effective, but it was released ... As consequence, thousands of rabbits have died or have been slaughtered each time. The virus is also believed to be thriving in ...
... or activated partial thromboplastin time. It was not until much later that the subcomponents of thromboplastin and partial ... thromboplastin was a lab reagent, usually derived from placental sources, used to assay prothrombin times (PT time). ... When manipulated in the laboratory, a derivative could be created called partial thromboplastin, which was used to measure the ... whereas partial thromboplastin does not contain tissue factor. Tissue factor is not needed to activate the intrinsic pathway. ...
Partial thromboplastin time should not be confused with prothrombin time, or PT, which measures blood clotting time through a ... The effects of heparin are measured in the lab by the partial thromboplastin time (aPTT), one of the measures of the time it ... These include activated partial thromboplastin time (APTT) and antifactor Xa activity. The specimen of choice is usually fresh ... Monitoring of the activated partial thromboplastin time is also not required and does not reflect the anticoagulant effect, as ...
"Prothrombin Time (PT) w/INR and Partial Thromboplastin Time (PTT) Blood Test". Walk-In Lab. Retrieved 2018-09-17. "Hemorrhagic ... Prothrombin time and partial thromboplastin time blood tests are useful to investigate the reason behind the excessive bleeding ... thromboplastin) to help restore them and to improve the immune defense of the patient after excessive blood loss. Blood ...
The prothrombin time (PT) and partial thromboplastin time (PTT) is often prolonged. Subclinical horses may only show elevated ... Decreases in the SDH and prothrombin time along with improvement in appetite are the best positive predictive indicators of ...
Plasma prekallikrein deficiency causes a prolonged activated partial thromboplastin time in patients. KLKB1 has been shown to ...
... does not usually affect prothrombin time, partial thromboplastin time or platelet counts; it does not inhibit ... Thomas K (24 June 2012). "In Documents on Pain Drug, Signs of Doubt and Deception". The New York Times. Archived from the ... Berenson A (29 April 2006). "Celebrex Ads Are Back, Dire Warnings and All". The New York Times. Archived from the original on 7 ... Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of GI ...
Prothrombin time, activated partial thromboplastin time, thrombin time, and fibrinogen tests should be performed. Platelet ... At times, patients with Waldenström macroglobulinemia may exhibit more than one M protein. Plasma viscosity must be measured. ... For a time, Waldenström macroglobulinemia was considered to be related to multiple myeloma because of the presence of ... Older diagnosis and treatments resulted in published reports of median survival of approximately 5 years from time of diagnosis ...
... partial thromboplastin time. Imaging tests such as transient elastography, ultrasound and magnetic resonance imaging can be ... By the time accumulating epigenetic and mutational changes eventually cause hepatocellular carcinoma, epigenetic alterations ... In liver disease, prothrombin time is longer than usual. In addition, the amounts of both coagulation factors and ... serum proteins, serum albumin, serum globulin, alanine transaminase, aspartate transaminase, prothrombin time, ...
Typical are normal thrombin time, prolonged prothrombin time (PT) and prolonged partial thromboplastin time(PTT). FX antigen ...
Dilute Russell's viper venom time Partial thromboplastin time Activated clotting time Gronowski, Ann M. (2004). Handbook of ... KCT is similar to the activated partial thromboplastin time test, except it does not use exogenous phospholipid. Thus, a ... Kaolin clotting time (KCT) is a sensitive test to detect lupus anticoagulants. There is evidence that suggests it is the most ... "Kaolin Clotting Time [KCT]". Archived from the original on 26 November 2014. Retrieved 26 November 2014. De Vries, A.J.; ...
This is characterised by a raised activated partial thromboplastin time (aPTT), and subsides over 24 hours. It resolves quickly ... At times, they may float without moving on the water surface, thus looking like a stick. Within their habitat, red-bellied ... Pregnancy takes place any time from early spring to late summer. Females become much less active and band together in small ... retreating to cover and at times emerging on warm, sunny days. Their dark colour allows them to absorb heat from sunshine more ...
Diagnostic Aides in the Investigation of Prolonged Prothrombin Times and Activated Partial Thromboplastin Times". Seminars in ... they are usually prolonged activated partial prothrombin kinase time and/or prolonged prothrombin time. Mixed tests consist of ... At the same time, the board of directors holds two scientific meetings every spring. At present, the council is also composed ... The meeting will be held in the form of a public meeting and the above-board meeting will also be held at the same time. In ...
Bleeding time, activated partial thromboplastin time, prothrombin time, and euglobulin lysis time were within normal limits. ...
Impaired clotting (coagulopathy) is common, and can be diagnosed with an elevated activated partial thromboplastin time (aPTT ... In 1998, a person bitten 9-12 times on his arm required an amputation of the envenomed limb. He reported later that he had ... Adlam, Nigel (13 February 2009). "How I Let a King Brown Bite Me Nine Times" (PDF). Odatria (2): 4. "2.5m-long king brown snake ... King brown snakes have been noted, however, to bite people who were asleep at the time. Furthermore, a significant number of ...
... activated partial thromboplastin time-APTT, prothrombin time with International Normalized Ratio-PTINR, thrombin time-TT, and ... von Willebrand disease typically display a normal prothrombin time and a variable prolongation of partial thromboplastin time.[ ... Since this time, the factor causing the long bleeding time was called the "von Willebrand factor" in honor of Erik Adolf von ... A platelet function assay may give an abnormal collagen/epinephrine closure time, and in most cases, a normal collagen/ADP time ...
These tests include prothrombin time (PT/INR), activated Partial Thromboplastin Time (aPTT), albumin, bilirubin (direct and ... GGT can increase by 10 times in alcoholism. GGT can increase by 2 to 3 times in 50% of the patients with non-alcoholic liver ... AST can be released from a variety of other tissues and if the elevation is less than two times the normal AST, no further ... "Prothrombin Time Test and INR (PT/INR): MedlinePlus Medical Test". Retrieved 25 February 2021. Kingston, ...
Partial thromboplastin time (PTT) should be monitored at 5 to 15 minutes after dose then in 2-8 hours afterward. Protamine has ...
Typical is a discordance between the prolonged prothrombin time (PT) and normal levels for the activated partial thromboplastin ...
Blood clotting is measured using standard tests, e.g. prothrombin time, partial thromboplastin time, thrombin time, and/or ... This accumulation leads over time to one form of familial renal amyloidosis. Plasma fibrinogen levels are similar to that seen ... Low fibrinogen levels and dysfunctional fibrinogens usually prolong these times, whereas the lack of fibrinogen (i.e. ... afibrinogenemia) renders these times infinitely prolonged. Fibrinogen levels are measured in the plasma isolated from venous ...
It can prolong the partial thromboplastin time (APTT) in some women, but still, the APTT is not useful for monitoring. To check ... Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal ... LMWH therapy does not affect the prothrombin time (PT) or the INR, and anti-Xa levels are not reliable. ... of therapy If the therapy duration reaches delivery time, the remaining duration may be given after delivery, possibly ...
... prolonged activated partial thromboplastin time, combined coagulation defects. When present, these Noonan-syndrome accompanying ... partial deficiency of factor VIII:C, partial deficiency of factor XI:C, partial deficiency of factor XII:C, and an imbalance of ... Spinal abnormalities may be present up to 30% of the time and this may require surgery to correct in over 60% of these cases. ...
... does play an important role in clot formation during in vitro measurements of the partial thromboplastin time, which ... be used to start coagulation cascades in laboratory diagnostic coagulation assays called activated partial thromboplastin times ... The purpose of increasing this time is so that the patient may reaching a higher level of medical care before succumbing from ... This, obviously, caused extreme pain to the patient, often more-so than the initial injury was causing them at the time ( ...
Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) ...
... time to occlusion and bleeding time. Seratrodast has no effect on prothrombin time and activated partial thromboplastin time, ...
... in this study revealed that there was a significant negative correlation between HDL and activated partial thromboplastin time ... The lowest incidence of atherosclerotic events over time occurs within those with both the highest concentrations of total HDL ... Benatar JR, Stewart RA (2007). "Is it time to stop treating dyslipidaemia with fibrates?". The New Zealand Medical Journal. 120 ...
... that can result in patients demonstrating a falsely prolonged activated partial thromboplastin time (aPTT). The effectiveness ...
The patient on initial screening will typically have been found to have a prolonged partial thromboplastin time (PTT) that does ... dilute Russell's viper venom time, kaolin clotting time, dilute thromboplastin time, silica clotting time and prothrombin time ... Chantarangkul V, Tripodi A, Arbini A, Mannucci PM (1992). "Silica clotting time (SCT) as a screening and confirmatory test for ... using a lupus-sensitive thromboplastin) are the principal tests used for the detection of lupus anticoagulant. These tests must ...
... partial thromboplastin time (PTT), serum amylase and total bilirubin (TBIL). If late-stage liver disease is suspected, then a ...
... prothrombin time, partial thromboplastin time, electrolytes, and typing and cross-matching for transfusion of blood products. A ... Melena is four-times more likely to come from an upper gastrointestinal bleed than from the lower GI tract; however, it can ... The bright red or maroon color is due to the short time taken from the site of the bleed and the exiting at the anus. The ... depending on the initial prothrombin time. Recombinant activated factor VII has been approved for use in patients with ...
... and prolonging activated partial thromboplastin time (aPTT). Prolonged time for lysis further displays the anti-fibrinolytic ... CU-2010 and CU-2020 have the ability to inhibit plasmin to a similar extent as aprotinin, but they are 100,000 times better at ... The prolongation of coagulation (or prothrombin time, PT) occurs following either tissue factor or contact-phase stimulation ... reduces the production of thrombin and coagulation time. In vitro studies confirmed the fibrinolysis inhibition capacity of CU- ...
... and can be measured by the activated partial thromboplastin time (aPTT) test.[citation needed] The tissue factor (extrinsic) ... Other: TCT, bleeding time, mixing test (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), ... Many analysers are capable of measuring a "derived fibrinogen" level from the graph of the Prothrombin time clot. If a ... Hageman factor, now known as factor XII, was identified in 1955 in an asymptomatic patient with a prolonged bleeding time named ...
... prolonged prothrombin time and activated partial thromboplastin time, a normal platelet count and absence of microcirculatory ...
... partial thromboplastin time MeSH G09.188.250.670 - platelet adhesiveness MeSH G09.188.250.680 - prothrombin time MeSH G09.188. ... 250.760 - reticulocytosis MeSH G09.188.250.840 - thrombin time MeSH G09.188.250.960 - whole blood coagulation time MeSH G09.188 ... The following is a partial list of the "G" codes for Medical Subject Headings (MeSH), as defined by the United States National ... MeSH G09.188.250.051 - acid-base equilibrium MeSH G09.188.250.106 - bleeding time MeSH G09.188.250.133 - blood bactericidal ...
... characterized by prolongation of Prothrombin and activated partial thromboplastin time, consumption of fibrinogen and the ...
... measure the ability of blood to clot by performing any of several types of tests including Partial thromboplastin times, ... All articles with vague or ambiguous time, Vague or ambiguous time from February 2014, Commons category link is on Wikidata, ... A dilute suspension of cells is passed through a flow cell, which passes cells one at a time through a capillary tube past a ... Automation of the testing process has reduced testing time for many analytes from days to minutes. The history of discrete ...
Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged partial thromboplastin time ( ... Women of childbearing age are affected about nine times more often than men. While it most commonly begins between the ages of ... More than 90 percent of those affected will experience joint or muscle pain at some time during the course of their illness. ... where the risk is many times higher. The histological hallmark of SLE is membranous glomerulonephritis with "wire loop" ...
It is usually ordered in situations where the partial thromboplastin time (PTT) test may take an excessive amount of time to ... Activated clotting time (ACT), also known as activated coagulation time, is a test of coagulation. The ACT test can be used to ... For example, systems that do not pre-warm the vial or sample may see increased time to clotting because clotting times increase ... For patients on anticoagulants, the time is increased. Horton, S; Augustin, S (2013), Activated clotting time (ACT)., Methods ...
"Comparison of Russell viper venom-based and activated partial thromboplastin time-based screening assays for resistance to ... In both methods, the time it takes for blood to clot is decreased in the presence of the factor V Leiden mutation. This is done ... People who inherit two copies of the mutation (homozygous), one from each parent, may have up to 80 times the usual risk of ... Most laboratories screen 'at risk' patients with either a snake venom (e.g. dilute Russell's viper venom time) based test or an ...
... may refer to: Partial thromboplastin time, a performance indicator in medicine for coagulation status Photothermal Therapy ... Malaysia Photothermal time, related to plant growth Pizza Time Theatre, former secondary name for Chuck E. Cheese's Pull Tiger ... polyester Pulse Transit Time, a measure of arterial blood pressure Postal Telephone and Telegraph, a government agency in many ...
... and activated partial thromboplastin times (PTT). The hematocrit may be elevated. The serum urea and creatine may be raised but ... The bleeding time tends to be prolonged. With the exception of yellow fever vaccine and Ebola vaccines, vaccines for VHF- ...
... partial thromboplastin time, thrombodynamics test, thrombin time and reptilase time, lupus anticoagulant, anti-cardiolipin ... and hence the investigations are usually not performed at the time when thrombosis is diagnosed but at a later time. In ... Comp PC, Esmon CT (December 1984). "Recurrent venous thromboembolism in patients with a partial deficiency of protein S". N. ... Tests for thrombophilia include complete blood count (with examination of the blood film), prothrombin time, ...
... normal prothrombin time, normal thrombin time, but prolonged partial thromboplastin time. Internal bleeding is common in people ... At the time, a common treatment administered by professional doctors was to use aspirin, which worsened rather than lessened ... Zielbauer, Paul von (4 September 2006). "Iraqis Infected by H.I.V.-Tainted Blood Try New Tool: A Lawsuit". The New York Times. ... Together with the development of a system for transportation and storage of human plasma in 1965, this was the first time an ...
Activated partial thromboplastin time (APTT or aPTT) Characteristics of the velocity of passage of the intrinsic coagulation ... Contact activation pathway Prothrombin time test (or prothrombin test, INR, PT) - velocity of passage of the extrinsic blood ...
... prothrombin time (PT), activated partial thromboplastin time (APTT) should be considered.[citation needed] Blood chemistry ... Average survival time in 2008 for the metastatic form of the disease was under a year and by 2013 this improved to an average ... Nephron-sparing partial nephrectomy is used when the tumor is small (less than 4 cm in diameter) or when the patient has other ... Radical and partial nephrectomy can still occur, and in some cases, if the metastasis is small this can also be surgically ...
The activated partial thromboplastin time is the most reliable coagulation parameter and should be obtained regularly during ... Arterial sheaths should be removed when the patient's activated clotting time is < 180 seconds or 2 to 6 hours following ... Other important hematological parameters are platelet count, clotting time, hematocrit and hemoglobin. Proper technique ...
  • however, in aPTT, an activator is added that speeds up the clotting time and results in a narrower reference range. (
  • Many drugs can change the results of the activated partial thromboplastin time (aPTT), including nonprescription drugs. (
  • However, limited data exist on optimal dosing and range of activated partial thromboplastin time (aPTT) in this setting. (
  • The partial thromboplastin time (PTT) or activated partial thromboplastin time ( aPTT or APTT ) is a performance indicator measuring the efficacy of both the "intrinsic" (now referred to as the contact activation pathway) and the common ( tissue factor pathway ) coagulation pathways. (
  • Reagents used to perform prothrombin time (PT) and activated partial thromboplastin time (aPTT) tests on clinical blood samples. (
  • Determination of the activated partial thromboplastin time (APTT) in citrated human plasma. (
  • The activated partial thromboplastin time (APTT) is also known as Partial thromboplastin time. (
  • Other tests that can be advised along with the APTT test include Platelet count, Thrombin time testing, Fibrinogen testing, Coagulation factor tests, or von Willebrand factor test. (
  • All patients had elevated D-dimer and fibrinogen levels, mildly prolonged prothrombin times (PT), normal platelet counts and normal activated partial thromboplastin times (aPTT). (
  • The mean activated Partial Thromboplastin Time (aPTT) of cases was 31.09s and of controls was 30.40s. (
  • Objective: To investigate the potential effect of sugammadex on anti-Xa anticoagulant activity of enoxaparin and the activated partial thromboplastin time (APTT) of unfractionated heparin (UFH). (
  • Primary endpoints were anti-Xa activity and APTT both time-averaged from 3 to 30 minutes post-dose. (
  • A good example in haemostasis is the activated partial thromboplastin time (aPTT). (
  • although this is entirely impractical in a high throughput test such as the aPTT, an awareness of the incubation time in your assay and also the sensitivity that will impart on the detection of specific deficiencies is advisable. (
  • Prothrombin time (PT), platelet count and activated partial thromboplastin time (aPTT) may not be feasible within the time window. (
  • 1%, a von Willebrand factor risen to 142%, no anomaly regarding the complement system (C3/C4/CH50), a negative rheumatoid factor, a normal prothrombin time and finally a normal fibrinogen activity. (
  • The coagulation profile revealed prolonged prothrombin and partial thromboplastin time, decreased fibrinogen, and increased fibrin degradation products. (
  • Defibrination is manifested by low serum fibrinogen, elevated prothrombin time, and elevated fibrin split products (FSP). (
  • Traditionally known as a haemostatic agent, alum shows a paradoxical effect of increased prothrombin and partial thromboplastin times. (
  • If the patient is receiving heparin by intermittent injection, the sample should be drawn 30-60 minutes before the next dose, while, if the patient is receiving a continuous heparin infusion, the sample can be drawn at any time. (
  • The determinants of activated partial thromboplastin time, relation of activated partial thromboplastin time to clinical outcomes, and optimal dosing regimens for heparin treated patients with acute coronary syndromes: a review of GUSTO-IIb. (
  • Heparin has played a major role in medicine since that time, saving countless lives as a valuable tool within surgery and as a dominant anticoagulant for decades. (
  • Check out this infographic to refresh your knowledge of heparin's history and please also check out our Heparin Antibody Confirmation Panel, which includes both the immunological (ELISA) and the functional ( wp-HIPA ) confirmation tests with a 24 hour turnaround time. (
  • During our analysis, the following parameters were analyzed: Coagulation times, thromboelastometry assays (coagulation time, clot formation time and maximum clot firmness), aggregation of platelets and phosphorylation of vasodilator-stimulated phosphoprotein (VASP). (
  • In patients receiving anticoagulant therapy, the reference range is 1.5-2.5 times the control value in seconds. (
  • Invert the tubegently several times to mix the anticoagulant, but do not agitate it. (
  • What coagulation test is done to evaluate & monitor clotting time when on oral anticoagulant therapy like Coumadin? (
  • A clinically compatible case in which a high index of suspicion (credible threat or patient history regarding location and time) exists for a long-acting anticoagulant exposure, or an epidemiologic link exists between this case and a laboratory-confirmed case. (
  • After initial stabilization, the patient's condition quickly deteriorated with acute anemia, thrombocytopenia and elevated prothrombin time, partial prothrombin time, and D-dimer levels. (
  • Malaria must be considered in a patient having fever and thrombocytopenia so that appropriate treatment is initiated in time to reduce morbidity and mortality. (
  • In the control group, clotting time during the postoperative period was longer than it was during the preoperative period. (
  • How well does activated partial thromboplastin time predict postoperative hemorrhage? (
  • Blood grouping, activated partial thromboplastin time and von Willebrand factor activity tests were performed on samples collected from consenting study participants. (
  • von Willebrand factor activity levels were associated with menorrhagia while activated partial thromboplastin time was not. (
  • However, if a person with VWD has unusually heavy bleeding or bleeds for a long time, the hemoglobin and the red blood cell count can be low. (
  • Be sure to allow enough time for the bleeding to stop. (
  • This study investigated the in vivo effect of alum on platelet aggregation and bleeding time in rabbits. (
  • Bleeding time from an ear puncture in 8 rabbits was also significantly prolonged after intravenous alum injection. (
  • contradiction in the mechanism of action of alum, we evaluated the in vivo effect of Alum (aluminium potassium sulfate) is a alum in terms of collagen-induced platelet food additive and traditional remedy used to aggregation and bleeding time. (
  • Abnormal assays for factors II and VII in patients with unexplained bleeding and a normal PT, partial thromboplastin time, or INR, as determined by hospital or commercial laboratory tests. (
  • Bleeding time and clotting time were within the normal limits. (
  • 1.20), a normal prothrombin ratio at 90%, a normal plasma thrombin time, a hemoglobin at 13.3 g/dL and a normal platelet level at 306G/L. Then, a diagnosis of acquired hemophilia was made. (
  • At the time this article was written, Janice Hinkle was an assistant professor at Villanova University College of Nursing, Villanova, PA, and a clinical nurse specialist at Thomas Jefferson University Hospital. (
  • If you are unable to have your tests performed ahead of time, you will be sent to the hospital lab to have your blood drawn the morning of your procedure. (
  • We therefore hypothesise that hypercoagulability lessens in time, especially in those who survive. (
  • therefore patients will need to be hospitalized if it is not possible to complete the diagnostic studies within that time. (
  • Advise patients to take QINLOCK at the same time each day. (
  • Ces résultats semblent indiquer que l'utilisation de l'alun en tant qu'antiplaquettaire oral pourrait faire l'objet d'études complémentaires, en tenant compte des effets secondaires éventuels notamment chez les patients dont la fonction rénale est altérée. (
  • 1.5 times of control value)‎ in 33% of patients. (
  • The test is termed "partial" due to the absence of tissue factor from the reaction mixture. (
  • When blood vessel walls are injured, the extrinsic coagulation system is initially activated by tissue factor (thromboplastin produced in the subendothelium), which combines with factor VII. (
  • The mean time to reach emergency was 2.4h (1.15-3.4), the mean door to CT, 24 min (10-47) and the door to recombinant tissue plasminogen activator (r-tPA) injection, 26.8 min (25-67). (
  • For use in prothrombin time (PT) determinations and prothrombin time-based assays in citrated human plasma. (
  • Activated partial thromboplastin substitution test - diagnostic. (
  • Another head CT, performed this time with contrast enhancement, showed multiple bilateral foci of low attenuation associated with loss of gray-white differentiation and sulcal effacement, most compatible with acute cerebral ischemia ( Fig 1 ). (
  • Often these tests need to be repeated several times before an accurate diagnosis can be made. (
  • Prolonged prothrombin time (PT) and international normalized ratio (INR) (24 to 72 hours after exposure) persisting for weeks to months, as determined by hospital laboratory tests. (
  • At that time, she presented to her local hospital with nausea, vomiting, tremors, and marked neck or throat pain. (
  • At that time in the Philippines, cases had risen a Department of Internal Medicine, Baguio General Hospital and Medical Center, Baguio City, Philippines. (
  • Partial thromboplastin time (PTT) is a blood test that looks at how long it takes for blood to clot. (
  • A related blood test is prothrombin time (PT) . (
  • The results of this test will show a longer clotting time among some people with VWD. (
  • This test also measures the time it takes for blood to clot. (
  • This is because the levels of clotting factors in the blood vary over time as a result of changes the body might be reacting to―such as stress, pregnancy, and infections―that can affect the test results. (
  • Prothrombin time (PT) is a blood test that measures the time it takes for the liquid portion (plasma) of your blood to clot. (
  • One test of liver function is the prothrombin time (PT), which is used to calculate the international normalized ratio (INR). (
  • If the person is taking blood thinners, clotting takes up to 2 ½ times longer. (
  • It measures the time taken by the blood to clot in a sample of blood. (
  • Baseline laboratory investigations in the form of complete blood count, prothrombin time, partial thromboplastin time, platelet count, electrocardiogram, and X-ray chest were done. (
  • Both the PT and the INR are measures of the time needed for blood to clot (the liver synthesizes some proteins necessary for blood clotting, called blood clotting factors). (
  • Only minimal antegrade flow of both MCA territories was seen, with significantly delayed transit time and incomplete visualization of distal cortical branches. (
  • A genetic association study of activated partial thromboplastin time in European Americans and African Americans: the ARIC Study. (
  • Hemostasis/Coagulation Analyzer is also used for measuring the coagulation pathway speed of thromboplastin levels in a few minutes. (
  • RESULTS: Platelet number, platelet activity, and coagulatory potential increased immediately postfirefighting and many variables (platelet function, partial thromboplastin time, and factor VIII) reflected a procoagulatory state even after 2 h of recovery. (
  • Short incubation times can be used for the increased sensitivity to contact factor deficiencies whereas longer incubation times, as high as 10 minutes, can be used to remove the contact factor influence. (
  • What should be the laboratory approach against isolated prolongation of a activated partial thromboplastin time? (
  • Ces vingt dernières années, on assiste à une augmentation spectaculaire du nombre de cas de diabète de type 1 avec une mortalité plus élevée en Afrique Noire en lien avec les difficultés d'accès aux soins, à la rupture de suivi engendrant un nombre élevé de perdus de vue. (
  • It uses material from the Wikipedia article "Partial_thromboplastin_time" . (
  • At the time of writing, global confirmed cases exceed 238 million with over 4.8million recorded deaths [ 2 ]. (
  • Since the median time to death from illness onset was reported to be 18.5 days, we believed 28-day could be an appropriate time point for the inclusion of mortality events and administrative censoring [ 10 ]. (
  • The presence of CVD, chronic kidney disease, prolonged prothrombin time and elevated lactate dehydrogenase (LDH) were associated with mortality. (
  • Mortality from COVID-19 was associated with having CVD, chronic kidney disease, elevated LDH and prolonged prothrombin time. (