coagulation factors

Also found in: Dictionary, Thesaurus, Legal, Financial, Encyclopedia.


1. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation or hotocoagulation.
2. in colloid chemistry, solidification of a sol into a gelatinous mass.
blood coagulation clotting.
diffuse intravascular coagulation (disseminated intravascular coagulation (DIC)) see disseminated intravascular coagulation.
coagulation factors factors essential to normal blood clotting, whose absence, diminution, or excess may lead to abnormality of the clotting. Twelve factors, commonly designated by Roman numerals, have been described (I–V and VII–XIII; VI is no longer considered to have a clotting function). (See table 6.)

Factor I is a high-molecular-weight plasma protein that is converted to fibrin through the action of thrombin; deficiency conditions are called afibrinogenemia and hypofibrinogenemia. Called also fibrinogen. Factor II is a glycoprotein present in the plasma that is converted into thrombin in the common pathway of coagulation; deficiency is called hypoprothrombinemia. Called also prothrombin. Factor III is involved in the extrinsic pathway of coagulation, activating factor X; called also tissue thromboplastin or factor.

Factor IV is calcium, required in many stages of blood clotting. Factor V is a heat- and storage-labile material, present in plasma and not in serum and is involved in the intrinsic and extrinsic pathways of coagulation, causing the cleavage of prothrombin to the active thrombin. Deficiency causes parahemophilia. Called also accelerator globulin or factor and proaccelerin. Factor VI is no longer considered in the scheme of hemostasis, and hence is assigned neither a name nor a function.

Factor VII is a heat- and storage-stable material, present in serum and in plasma and participating in the extrinsic pathway of coagulation, acting with factor III to activate factor X. Deficiency, either hereditary or acquired (vitamin k deficiency), leads to hemorrhagic tendency. Called also proconvertin and serum prothrombin conversion accelerator (SPCA). Factor VIII is a relatively storage-labile material that participates in the intrinsic pathway of coagulation, acting as a cofactor in the activation of factor X. Deficiency, an X-linked recessive trait, results in hemophilia a (classical hemophilia). Called also antihemophilic factor (AHF) and antihemophilic globulin (AHG). Factor IX is a relatively storage-stable substance involved in the intrinsic pathway of coagulation, acting to activate factor X. Deficiency of this factor results in a hemorrhagic syndrome called hemophilia b (or Christmas disease), which is similar to classical hemophilia A. It is treated with purified preparations of the factor, derived from human plasma or recombinant, or with factor IX complex. Called also plasma thromboplastin component (PTC) and antihemophilic factor B.

Factor X is a heat-labile material with some storage stability, which is involved in both intrinsic and extrinsic pathways of coagulation, uniting them to begin the common pathway. Once activated, it complexes with calcium, phospholipid, and activated factor V to form prothrombinase, which cleaves and activates prothrombin to thrombin. Called also Stuart or Stuart-Prower factor. Factor XI is a stable factor involved in the intrinsic pathway of coagulation, activating factor IX. Deficiency results in hemophilia c. Called also plasma thromboplastin antecedent (PTA) and antihemophilic factor C. Factor XII is a stable factor activated by contact with glass or other foreign substances, which initiates coagulation through the intrinsic pathway by activating factor XI; called also Hageman factor. Factor XIII is a factor that polymerizes fibrin monomers, enabling fibrin to form a firm blood clot. Deficiency causes a clinical hemorrhagic diathesis. Called also fibrin-stabilizing factor.
Enlarge picture

Coagulation Factors

Synonym/acronym: See table.

Common use

To detect factor deficiencies and related coagulopathies such as found in disseminated intravascular coagulation (DIC).


Whole blood collected in a completely filled blue-top (3.2% sodium citrate) tube. If the patient’s hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted.

Normal findings

(Method: Photo-optical clot detection) Activity from 50% to 150%.
Preferred NameSynonymRole in Modern Coagulation Cascade ModelCoagulation Test Responses in the Presence of Factor Deficiency
Factor IFibrinogenAssists in the formation of the fibrin clotPT prolonged, aPTT prolonged
Factor IIProthrombinPrethrombinAssists factor Xa in formation of trace thrombin in the initiation phase and assists factors VIIIa, IXa, Xa, and Va to form thrombin in the propagation phase of hemostasisPT prolonged, aPTT prolonged
Tissue factor (formerly known as factor III)Tissue factorTissue thromboplastinAssists factor VII and Ca2+ in the activation of factors IX and X during the initiation phase of hemostasisPT prolonged, aPTT prolonged
Calcium (formerly known as factor IV)CalciumCa2+Essential to the activation of multiple clotting factorsN/A
Factor VProaccelerinLabile factor, accelerator globulin (AcG)Assists factors VIIIa, IXa, Xa, and II in the formation of thrombin during the amplification and propagation phases of hemostasisPT prolonged, aPTT prolonged
Factor VIIProconvertinStabile factor, serum prothrombin conversion accelerator, autoprothrombin IAssists tissue factor and Ca2+ in the activation of factors IX and XPT prolonged, aPTT normal
Factor VIIIAntihemophilic factor (AHF)Antihemophilic globulin (AHG), antihemophilic factor A, platelet cofactor 1Activated by trace thrombin during the initiation phase of hemostasis to amplify formation of additional thrombinPT normal, aPTT prolonged
Factor IXPlasma thromboplastin component (PTC)Christmas factor, antihemophilic factor B, platelet cofactor 2Assists factors Va and VIIIa in the amplification phase and factors VIIIa, Xa, Va, and II to form thrombin in the propagation phasePT normal, aPTT prolonged
Factor XStuart-Prower factorAutoprothrombin III, thrombokinaseAssists with formation of trace thrombin in the initiation phase and acts with factors VIIIa, IXa, Va, and II to form thrombin in the propagation phasePT prolonged, aPTT prolonged
Factor XIPlasma thromboplastin antecedent (PTA)Antihemophilic factor CActivated by thrombin produced in the extrinsic path-way to enhance production of additional thrombin inside the fibrin clot via the intrinsic path-way; this factor also participates in slowing down the process of fibrinolysisPT normal, aPTT prolonged
Factor XIIHageman factorGlass factor, contact factorContact activator of the kinin system (e.g., prekallikrein, and high-molecular-weight kininogen)PT normal, aPTT prolonged
Factor XIIIFibrin-stabilizing factor (FSF)Laki-Lorand factor (LLF), fibrinase, plasma transglutaminaseActivated by thrombin and assists in formation of bonds between fibrin strands to complete secondary hemostasisPT normal, aPTT normal
von Willebrand factorvon Willebrand factorvWFAssists in platelet adhesion and thrombus formationRistocetin cofactor decreased


Hemostasis involves three components: blood vessel walls, platelets, and plasma coagulation proteins. Primary hemostasis has three major stages involving platelet adhesion, platelet activation, and platelet aggregation. Platelet adhesion is initiated by exposure of the endothelium as a result of damage to blood vessels. Exposed tissue factor–bearing cells trigger the simultaneous binding of von Willebrand factor to exposed collagen and circulating platelets. Activated platelets release a number of procoagulant factors, including thromboxane, a very potent platelet activator, from storage granules. These factors enter the circulation and activate other platelets, and the cycle continues. The activated platelets aggregate at the site of vessel injury, and at this stage of hemostasis, the glycoprotein IIb/IIIa receptors on the activated platelets bind fibrinogen, causing the platelets to stick together and form a plug. There is a balance in health between the prothrombotic or clot formation process and the antithrombotic or clot disintegration process. Simultaneously, the coagulation process or secondary hemostasis occurs. In secondary hemostasis, the coagulation proteins respond to blood vessel injury in an overlapping chain of events. The contact activation (formerly known as the intrinsic pathway) and tissue factor (formerly known as the extrinsic pathway) pathways of secondary hemostasis are a series of reactions involving the substrate protein fibrinogen, the coagulation factors (also known as enzyme precursors or zymogens), nonenzymatic cofactors (Ca2+), and phospholipids. The factors were assigned Roman numerals in the order of their discovery, not their place in the coagulation sequence. Factor VI was originally thought to be a separate clotting factor. It was subsequently proved to be the same as a modified form of factor Va, and therefore, the number is no longer used.

The antithrombotic process includes tissue factor pathway inhibitor (TFPI), antithrombin, protein C, and fibrinolysis.

The coagulation factors are formed in the liver. They can be divided into three groups based on their common properties:

  • The contact group is activated in vitro by a surface such as glass and is activated in vivo by collagen. The contact group includes factor XI, factor XII, prekallikrein, and high-molecular-weight kininogen.
  • The prothrombin or vitamin K–dependent group includes factors II, VII, IX, and X.
  • The fibrinogen group includes factors I, V, VIII, and XIII. They are the most labile of the factors and are consumed during the coagulation process. The factors listed in the table are the ones most commonly measured.
For many years it was believed that the intrinsic and extrinsic pathways operated equally, in parallel. A more modern concept of the coagulation process has replaced the traditional model (formerly called the coagulation cascade) and is presented on the next page. The cellular-based model includes four overlapping phases in the formation of thrombin: initiation, amplification, propagation, and termination. It is now known that the tissue factor pathway is the primary pathway for the initiation of blood coagulation. Tissue factor (TF)–bearing cells (e.g., endothelial cells, smooth muscle cells, monocytes) can be induced to express TF and are the primary initiators of the coagulation cascade either by contact activation or trauma. The contact activation pathway is more related to inflammation, and although it plays an important role in the body’s reaction to damaged endothelial surfaces, a deficiency in factor XII does not result in development of a bleeding disorder, which demonstrates the minor role of the intrinsic pathway in the process of blood coagulation. Substances such as endotoxins, tumor necrosis factor alpha, and lipoproteins can also stimulate expression of TF. TF, in combination with factor VII and calcium, forms a complex that then activates factors IX and X in the initiation phase. Activated factor X in the presence of factor II (prothrombin) leads to the formation of thrombin. TFPI quickly inactivates this stage of the pathway so that limited or trace amounts of thrombin are produced, which results in the activation of factors VIII and V. Activated factor IX, assisted by activated factors V and VIII, initiate amplification and propagation of thrombin in the cascade. Thrombin activates factor XIII and begins converting fibrinogen into fibrin monomers, which spontaneously polymerize and then become cross-linked into a stable clot by activated factor XIII.

Qualitative and quantitative factor deficiencies can affect the function of the coagulation pathways. Factor V and factor II (prothrombin) mutations are examples of qualitative deficiencies and are the most common inherited predisposing factors for blood clots. Approximately 5% to 7% of Caucasians, 2% of Hispanics, 1% of African Americans and Native American, and 0.5% of Asians have the factor V Leiden mutation, and 2% to 3% of Caucasians and 0.3% of African Americans have a prothrombin mutation. Hemophilia A is an inherited deficiency of factor VIII and occurs at a prevalence of about 1 in 5,000 to 10,000 male births. Hemophilia B is an inherited deficiency of factor IX and occurs at a prevalence of about 1 in about 20,000 to 34,000 male births. Genetic testing is available for inherited mutations associated with inherited coagulopathies. The tests are performed on samples of whole blood. Counseling and informed written consent are generally required for genetic testing.

The PT/INR measures the function of the tissue factor pathway of coagulation and is used to monitor patients receiving warfarin or coumarin-derivative anticoagulant therapy. The aPTT measures the function of the contact activation pathway of coagulation and is used to monitor patients receiving heparin anticoagulant therapy.

This procedure is contraindicated for



  • Identify the presence of inherited bleeding disorders
  • Identify the presence of qualitative or quantitative factor deficiency

Potential diagnosis

Increased in


Decreased in

    Congenital deficiency Disseminated intravascular coagulation (related to consumption of factors as part of the coagulation cascade) Liver disease (related to inability of damaged liver to synthesize coagulation factors)

Critical findings

    Fibrinogen: Less than 80 mg/dL (SI: Less than 2.4 micromol/L).
  • Note and immediately report to the health-care provider (HCP) any critically decreased values and related symptoms.

  • It is essential that a critical finding be communicated immediately to the requesting health-care provider (HCP). A listing of these findings varies among facilities.

  • Timely notification of a critical finding for lab or diagnostic studies is a role expectation of the professional nurse. Notification processes will vary among facilities. Upon receipt of the critical value the information should be read back to the caller to verify accuracy. Most policies require immediate notification of the primary HCP, Hospitalist, or on-call HCP. Reported information includes the patient’s name, unique identifiers, critical value, name of the person giving the report, and name of the person receiving the report. Documentation of notification should be made in the medical record with the name of the HCP notified, time and date of notification, and any orders received. Any delay in a timely report of a critical finding may require completion of a notification form with review by Risk Management.

  • Signs and symptoms of microvascular thrombosis include cyanosis, ischemic tissue necrosis, hemorrhagic necrosis, tachypnea, dyspnea, pulmonary emboli, venous distention, abdominal pain, and oliguria. Possible interventions include identification and treatment of the underlying cause, support through administration of required blood products (cryoprecipitate or fresh frozen plasma), and administration of heparin. Cryoprecipitate may be a more effective product than fresh frozen plasma in cases where the fibrinogen level is less than 100 mg/dL, the minimum level required for adequate hemostasis, because it delivers a concentrated amount of fibrinogen without as much plasma volume.

Interfering factors

  • Drugs that may increase factor II levels include fluoxymesterone, methandrostenolone, nandrolone, and oxymetholone.
  • Drugs that may decrease factor II levels include warfarin.
  • Drugs that may increase factor V, VII, and X levels include anabolic steroids, fluoxymesterone, methandrostenolone, nandrolone, oral contraceptives, and oxymetholone.
  • Drugs that may decrease factor V levels include streptokinase.
  • Drugs that may decrease factor VII levels include acetylsalicylic acid, asparaginase, cefamandole, ceftriaxone, dextran, dicumarol, gemfibrozil, oral contraceptives, and warfarin.
  • Drugs that may increase factor VIII levels include chlormadinone.
  • Drugs that may decrease factor VIII levels include asparaginase.
  • Drugs that may increase factor IX levels include chlormadinone and oral contraceptives.
  • Drugs that may decrease factor IX levels include asparaginase and warfarin.
  • Drugs that may decrease factor X levels include chlormadinone, dicumarol, oral contraceptives, and warfarin.
  • Drugs that may decrease factor XI levels include asparaginase and captopril.
  • Drugs that may decrease factor XII levels include captopril.
  • Test results of patients on anticoagulant therapy are unreliable.
  • Placement of tourniquet for longer than 1 min can result in venous stasis and changes in the concentration of plasma proteins to be measured. Platelet activation may also occur under these conditions, causing erroneous results.
  • Vascular injury during phlebotomy can activate platelets and coagulation factors, causing erroneous results.
  • Hemolyzed specimens must be rejected because hemolysis is an indication of platelet and coagulation factor activation.
  • Icteric or lipemic specimens interfere with optical testing methods, producing erroneous results.
  • Incompletely filled collection tubes, specimens contaminated with heparin, clotted specimens, or unprocessed specimens not delivered to the laboratory within 1 to 2 hr of collection should be rejected.

Nursing Implications and Procedure

Potential nursing problems

ProblemSigns & SymptomsInterventions
Bleeding (Related to alerted clotting factors secondary to heparin use or depleted clotting factors)Altered level of consciousness; hypotension; increased heart rate; decreased HGB and HCT; capillary refill greater than 3 sec; cool extremities Increase frequency of vital sign assessment with variances in results; monitor for vital sign trends; administer blood or blood products as ordered; administer stool softeners as needed; monitor stool for blood; encourage intake of foods rich in vitamin K; monitor and trend HGB/HCT; assess skin for petechiae, purpura, hematoma; monitor for blood in emesis, or sputum; institute bleeding precautions (prevent unnecessary venipuncture; avoid IM injections; prevent trauma; be gentle with oral care, suctioning; avoid use of a sharp razor); administer prescribed medications (recombinant human activated protein C; epsilon aminocaproic acid)
Gas exchange (Related to deficient oxygen capacity of the blood)Irregular breathing pattern, use of accessory muscles; altered chest excursion; adventitious breath sounds (crackles, rhonchi, wheezes, diminished breath sounds); copious secretions; signs of hypoxia; altered blood gas results; confusion; lethargy; cyanosis Monitor respiratory rate and effort based on assessment of patient condition; assess lung sounds frequently; monitor for secretions, bloody sputum; suction as necessary; use pulse oximetry to monitor oxygen saturation; collaborate with physician to administer oxygen as needed; elevate the head of the bed 30 degrees or higher; monitor IV fluids and avoid aggressive fluid resuscitation; assess level of consciousness; anticipate the need for possible intubation
Tissue perfusion (Related to compromised clotting factor; blood loss; deficient oxygen-carrying capacity of the blood)Hypotension; dizziness; cool extremities; capillary refill greater than 3 sec; weak pedal pulses; altered level of consciousness Monitor blood pressure; assess for dizziness; check skin temperature for warmth; assess capillary refill; assess pedal pulses; monitor level of consciousness; administer prescribed vasodilators and inotropic drugs; use oxygen as required
Confusion (Related to an alteration in the oxygen-carrying capacity of the blood; blood loss; compromised clotting factor)Disorganized thinking, restless, irritable, altered concentration and attention span, changeable mental function over the day, hallucinations; altered attention span; inability to follow directions; disorientation to person, place, time, and purpose; inappropriate affectTreat the medical condition; correlate confusion with the need to reverse altered electrolytes; evaluate medications; prevent falls and injury through appropriate use of postural support, bed alarm, or restraints; consider pharmacological interventions; record accurate intake and output to assess fluid status; administer blood or blood products; monitor and trend HGB/HCT


  • Positively identify the patient using at least two unique identifiers before providing care, treatment, or services.
  • Patient Teaching: Inform the patient this test can assist in evaluating the effectiveness of blood clotting and identify deficiencies in blood factor levels.
  • Obtain a history of the patient’s complaints, including a list of known allergens, especially allergies or sensitivities to latex.
  • Obtain a history of the patient’s hematopoietic and hepatobiliary systems, any bleeding disorders, and results of previously performed laboratory tests and diagnostic and surgical procedures.
  • Obtain a list of the patient’s current medications. Include anticoagulants, aspirin and other salicylates, herbs, nutritional supplements, and nutraceuticals (see Effects of Natural Products on Laboratory Values online at DavisPlus). Such products should be discontinued by medical direction for the appropriate number of days prior to a surgical procedure.
  • Review the procedure with the patient. Inform the patient that specimen collection takes approximately 5 to 10 min. Address concerns about pain and explain that there may be some discomfort during the venipuncture.
  • Sensitivity to social and cultural issues, as well as concern for modesty, is important in providing psychological support before, during, and after the procedure.
  • Note that there are no food, fluid, or medication restrictions unless by medical direction.


  • Potential complications: N/A
  • Avoid the use of equipment containing latex if the patient has a history of allergic reaction to latex.
  • Instruct the patient to cooperate fully and to follow directions. Direct the patient to breathe normally and to avoid unnecessary movement.
  • Observe standard precautions, and follow the general guidelines in Patient Preparation and Specimen Collection. Positively identify the patient, and label the appropriate specimen container with the corresponding patient demographics, initials of the person collecting the specimen, date, and time of collection. Perform a venipuncture. When multiple specimens are drawn, the blue-top tube should be collected after sterile (i.e., blood culture) tubes. Otherwise, when using a standard vacutainer system, the blue top is the first tube collected. When a butterfly is used and due to the added tubing, an extra red-top tube should be collected before the blue-top tube to ensure complete filling of the blue top tube.
  • Remove the needle and apply direct pressure with dry gauze to stop bleeding. Observe/assess venipuncture site for bleeding or hematoma formation and secure gauze with adhesive bandage.
  • Promptly transport the specimen to the laboratory for processing and analysis. The Clinical Laboratory Standards Institute (CLSI) recommendation for processed and unprocessed samples stored in unopened tubes is that testing should be completed within 1 to 4 hr of collection.


  • Inform the patient that a report of the results will be made available to the requesting health-care provider (HCP), who will discuss the results with the patient.
  • Depending on the results of this procedure, additional testing may be performed to evaluate or monitor progression of the disease process and determine the need for a change in therapy. Evaluate test results in relation to the patient’s symptoms and other tests performed.
  • Patient Education

    • Instruct the patient to report immediately any signs of unusual bleeding or bruising.
    • Inform the patient with decreased factor levels of the importance of taking precautions against bruising and bleeding.
    • Reinforce information given by the patient’s HCP regarding further testing, treatment, or referral to another HCP.
    • Answer any questions or address any concerns voiced by the patient or family.
  • Expected Patient Outcomes

    • Knowledge
    • States bleeding precautions that include the use of a soft bristle toothbrush, use of an electric razor, avoidance of constipation, avoidance of acetylsalicylic acid and similar products, and avoidance of intramuscular injections
    • States importance of monitoring stool, sputum, and urine for blood
    • Skills
    • Demonstrates proficiency in self-administering prescribed medications
    • Demonstrates proficiency in adequately elevating the head of the bed to facilitate adequate gas exchange
    • Attitude
    • Complies with the recommendation to refrain from risky behavior that could result in trauma and bleeding
    • Adheres to the recommendation to report any new bleeding to the HCP

Related Monographs

  • Related tests include aPTT, ALT, ALP, AT-IIII, AST, clot retraction, CBC platelet count, copper, fibrinogen, FDP, plasminogen, procalcitonin, protein C, protein S, PT/INR, and vitamin K.
  • Refer to the Hematopoietic and Hepatobiliary systems tables at the end of the book for related tests by body system.

coagulation factors

; clotting factors approximately 20 soluble plasma factors, including fibrinogen (factor [F] I), prothrombin (FII), thromboplastin (FIII) and calcium ions (FIV), which on activation initiate a biochemical cascade that converts soluble plasma fibrinogen into insoluble fibrin (into which platelets enmesh, forming a clot); factor deficiency (e.g. FVIII; FXII) causes bleeding disorders (haemophilia; Christmas disease and von Willebrand's disease)


1. formation of a clot.
2. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation.

activated coagulation time (ACT)
a test of the intrinsic or common pathway of coagulation, using diatomaceous earth as an activating agent to hasten coagulation of whole blood, the time being measured. More sensitive than Lee-White or capillary tube tests. See also clotting time.
biterminal coagulation
see monopolar electrocoagulation.
coagulation cascade
the sequence of enzymatic reactions leading to the formation of a blood clot. Each is initiated by the preceding and, in turn, produces the enzyme that catalyzes the next with an amplification of the process as it progresses.
cerebrospinal coagulation
normal CSF does not coagulate. Inflammation of the meninges or contamination of the fluid by blood, possibly during collection, can cause coagulation in a sample.
coagulation defects
disseminated intravascular coagulation (DIC)
widespread formation of thromboses in the microcirculation, mainly within the capillaries. It is a secondary complication of a wide variety of disorders all of which activate in some way the intrinsic coagulation sequence. Paradoxically, the intravascular clotting ultimately produces hemorrhage because of rapid consumption of fibrinogen, platelets, prothrombin, and clotting factors V, VIII and X. Because of this pathology, DIC is sometimes called defibrination syndrome or consumption coagulopathy. Called also diffuse intravascular coagulation. Called also consumption coagulopathy, defibrination syndrome, defibrinogenation syndrome.
coagulation factors
see clotting factors. platelet factors also play a role in coagulation. They are designated by Arabic numerals from 1 to 4.
coagulation inhibitors
these systems prevent widescale intravascular coagulation as a result of minor injury. The important systems are c1-inactivator, antithrombin III, alpha1-antitrypsin, α2-macroglobulin, factor XIa inhibitor, lipoprotein factor Xa inhibitor.
coagulation necrosis
coagulation pathways
the coagulation cascade can follow alternative routes depending on the initiating factor. The extrinsic pathway is initiated by tissue thromboplastin (factor III) and involves calcium ions and factor VII. In the intrinsic pathway, factors XII, XI, IX and VIII are activated by exposure to subendothelial collagen or foreign surfaces. Both pathways lead to the activation of factor X and proceed along the common pathway, involving factors V, II, I and XIII, to the formation of a fibrin clot.
coagulation proteins
see clotting factors.
synovial coagulation
normal synovial fluid does not clot, but gels on standing (thixotropism). It contains no fibrinogen, nor any of the coagulation factors. Clotting is an indication of damage to the synovial membrane.
coagulation tests
are used to determine the integrity of the coagulation pathways, and platelet function. In general, the common tests for the intrinsic or common pathways are the activated partial thromboplastin time (APTT) and activated coagulation time (ACT). One-stage prothrombin time (OSPT) is usually used to evaluate the extrinsic or common pathways, and platelet count, clot retraction, bleeding time and activated coagulation time reflect platelet numbers and function.
coagulation time
see clotting time.
unipolar coagulation
see bipolar electrocoagulation.
References in periodicals archive ?
Factor V is a structurally unique coagulation factor (24) composed of a heavy chain and a light chain, joined by a connecting region (Figure 2).
Among other coagulation factor deficiencies factor IX deficiency was the second most common after factor VIII deficiency.
In addition, there were occasional specimens with the activity levels of vitamin K-dependent coagulation factors that when associated with an inherited deficiency would be expected to be associated with significant bleeding.
Apart from recombinant products, plasma-derived coagulation factors still play a considerable role, albeit bovine derived products are considerably being challenged by human recombinant and plasma-derived products.
Procurement Supply Drugs for Hospital and Er, and Related Medications National Cancer Program and the National Hemophilia Program - 8 Batches Lot 1-Bupivacainum Heavy Sp; Lot 2 Carboxymaltosum Ferri; Lot 3-Thiaminum; Lot 4 Complex Combined Protrombina- Coagulation Factors (Factor Ii, Vii and X Protein C and S); Lot 5-Fluorouracilum; Lot 6-Rituximabum; Lot 7- Coagulation Factor Viii and Human Von Willebrand Factor; Lot 8 Octocog Alfa 500 Iu;
The report Coagulation Factors 2010 - The Portfolio Aspect as Decisive Force: A Competitive Landscape and R&D Pipeline Analysis of Hemostasis Proteins provides a description, evaluation and assessment of the recombinant and plasma-derived coagulation factor pipelines as of September 2010.
Replacement of plasma-derived coagulation factors by marketed recombinant molecules is ongoing and will further increase by new recombinant coagulation factors in development.
The authors analyze and assess the target pipeline for each of the coagulation factors used for systemic and topical administration.
ProGenetics is developing production of the human coagulation factors IX and VIII in the milk of transgenic pigs and has patents that cover the transgenic production of human fibrinogen.
The first program of the collaboration will be to develop recombinant human factor VIIa as a potential treatment for hemophilia in patients with antibodies to other coagulation factors.