Antithrombin III Deficiency: An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis.Antithrombin III: 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.Protein S Deficiency: An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.Antithrombins: 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.Methionine Adenosyltransferase: An enzyme that catalyzes the synthesis of S-adenosylmethionine from methionine and ATP. EC 2.5.1.6.Cytochromes b: Cytochromes of the b group that have alpha-band absorption of 563-564 nm. They occur as subunits in MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III.Heparin: 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.Electron Transport Complex III: A multisubunit enzyme complex that contains CYTOCHROME B GROUP; CYTOCHROME C1; and iron-sulfur centers. It catalyzes the oxidation of ubiquinol to UBIQUINONE, and transfers the electrons to CYTOCHROME C. In MITOCHONDRIA the redox reaction is coupled to the transport of PROTONS across the inner mitochondrial membrane.Thrombophlebitis: Inflammation of a vein associated with a blood clot (THROMBUS).Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Thrombin: An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.Antithrombin Proteins: An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance.Venous Thrombosis: The formation or presence of a blood clot (THROMBUS) within a vein.Ultrasonography, Doppler: Ultrasonography applying the Doppler effect, with frequency-shifted ultrasound reflections produced by moving targets (usually red blood cells) in the bloodstream along the ultrasound axis in direct proportion to the velocity of movement of the targets, to determine both direction and velocity of blood flow. (Stedman, 25th ed)Ultrasonography, Doppler, Color: Ultrasonography applying the Doppler effect, with the superposition of flow information as colors on a gray scale in a real-time image. This type of ultrasonography is well-suited to identifying the location of high-velocity flow (such as in a stenosis) or of mapping the extent of flow in a certain region.Coronary Thrombosis: Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.Ultrasonography: The visualization of deep structures of the body by recording the reflections or echoes of ultrasonic pulses directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz.Ultrasonography, Doppler, Pulsed: Ultrasonography applying the Doppler effect, with velocity detection combined with range discrimination. Short bursts of ultrasound are transmitted at regular intervals and the echoes are demodulated as they return.Dictionaries, MedicalDictionaries as Topic: Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.Heart Defects, Congenital: Developmental abnormalities involving structures of the heart. These defects are present at birth but may be discovered later in life.Cardiopulmonary Bypass: 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.Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.Cardiac Surgical Procedures: Surgery performed on the heart.Fibrinolysis: The natural enzymatic dissolution of FIBRIN.Dithioerythritol: A compound that, along with its isomer, Cleland's reagent (DITHIOTHREITOL), is used for the protection of sulfhydryl groups against oxidation to disulfides and for the reduction of disulfides to sulfhydryl groups.Cerebrospinal Fluid: A watery fluid that is continuously produced in the CHOROID PLEXUS and circulates around the surface of the BRAIN; SPINAL CORD; and in the CEREBRAL VENTRICLES.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Antiphospholipid Syndrome: 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).Antibodies, Antiphospholipid: 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.Antibodies, Anticardiolipin: 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.beta 2-Glycoprotein I: 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.Lupus Coagulation Inhibitor: 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.Lupus Erythematosus, Systemic: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.Cardiolipins: 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.von Willebrand Diseases: Group of hemorrhagic disorders in which the VON WILLEBRAND FACTOR is either quantitatively or qualitatively abnormal. They are usually inherited as an autosomal dominant trait though rare kindreds are autosomal recessive. Symptoms vary depending on severity and disease type but may include prolonged bleeding time, deficiency of factor VIII, and impaired platelet adhesion.Blood Coagulation Disorders: 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.Hemophilia A: 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.Factor VIII: 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.von Willebrand Factor: 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.Pulmonary Embolism: Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS.Fibrin: A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.Sinus Thrombosis, Intracranial: Formation or presence of a blood clot (THROMBUS) in the CRANIAL SINUSES, large endothelium-lined venous channels situated within the SKULL. Intracranial sinuses, also called cranial venous sinuses, include the superior sagittal, cavernous, lateral, petrous sinuses, and many others. Cranial sinus thrombosis can lead to severe HEADACHE; SEIZURE; and other neurological defects.Disseminated Intravascular Coagulation: 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.Frostbite: Damage to tissues as the result of low environmental temperatures.Snake Bites: Bites by snakes. Bite by a venomous snake is characterized by stinging pain at the wound puncture. The venom injected at the site of the bite is capable of producing a deleterious effect on the blood or on the nervous system. (Webster's 3d ed; from Dorland, 27th ed, at snake, venomous)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.Fibrin Fibrinogen Degradation Products: 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.Multimedia: Materials, frequently computer applications, that combine some or all of text, sound, graphics, animation, and video into integrated packages. (Thesaurus of ERIC Descriptors, 1994)Clot Retraction: Retraction of a clot resulting from contraction of PLATELET pseudopods attached to FIBRIN strands. The retraction is dependent on the contractile protein thrombosthenin. Clot retraction is used as a measure of platelet function.Thrombelastography: Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.

Familial overexpression of beta antithrombin caused by an Asn135Thr substitution. (1/74)

We have investigated the basis of antithrombin deficiency in an asymptomatic individual (and family) with borderline levels (approximately 70% antigen and activity) of antithrombin. Direct sequencing of amplified DNA showed a mutation in codon 135, AAC to ACC, predicting a heterozygous Asn135Thr substitution. This substitution alters the predicted consensus sequence for glycosylation, Asn-X-Ser, adjacent to the heparin interaction site of antithrombin. The antithrombin isolated from plasma of the proband by heparin-Sepharose chromatography contained amounts of beta antithrombin (the very high affinity fraction) greatly increased (approximately 20% to 30% of total) above the trace levels found in normals. Expression of the residue 135 variant in both a cell-free system and COS-7 cells confirmed altered glycosylation arising as a consequence of the mutation. Wild-type and variant protein were translated and exported from COS-7 cells with apparently equal efficiency, in contrast to the reduced level of variant observed in plasma of the affected individual. This case represents a novel cause of antithrombin deficiency, removal of glycosylation concensus sequence, and highlights the potentially important role of beta antithrombin in regulating coagulation.  (+info)

Plasma antithrombin III deficiency in ischaemic stroke in the young. (2/74)

A deficiency of plasma antithrombin III has been identified as a potential risk factor for thrombosis. In a pilot study of 56 patients aged less than 40 years who presented with ischaemic stroke of unknown etiology, we detected only one case of plasma antithrombin III deficiency. Antithrombin III activity was estimated by a chromogenic assay. Hence, antithrombin III deficiency, though rare, should be considered while evaluating young patients with stroke of unknown etiology.  (+info)

Enhancement of heparin cofactor II anticoagulant activity. (3/74)

Heparin cofactor II (HCII) is a serpin whose thrombin inhibition activity is accelerated by glycosaminoglycans. We describe the novel properties of a carboxyl-terminal histidine-tagged recombinant HCII (rHCII-CHis(6)). Thrombin inhibition by rHCII-CHis(6) was increased >2-fold at approximately 5 microgram/ml heparin compared with wild-type recombinant HCII (wt-rHCII) at 50-100 microgram/ml heparin. Enhanced activity of rHCII-CHis(6) was reversed by treatment with carboxypeptidase A. We assessed the role of the HCII acidic domain by constructing amino-terminal deletion mutants (Delta1-52, Delta1-68, and Delta1-75) in wt-rHCII and rHCII-CHis(6). Without glycosaminoglycan, unlike wt-rHCII deletion mutants, the rHCII-CHis(6) deletion mutants were less active compared with full-length rHCII-CHis(6). With glycosaminoglycans, Delta1-68 and Delta1-75 rHCIIs were all less active. We assessed the character of the tag by comparing rHCII-CHis(6), rHCII-CAla(6), and rHCII-CLys(6) to wt-rHCII. Only rHCII-CHis(6) had increased activity with heparin, whereas all three mutants have increased heparin binding. We generated a carboxyl-terminal histidine-tagged recombinant antithrombin III to study the tag on another serpin. Interestingly, this mutant antithrombin III had reduced heparin cofactor activity compared with wild-type protein. In a plasma-based assay, the glycosaminoglycan-dependent inhibition of thrombin by rHCII-CHis(6) was significantly greater compared with wt-rHCII. Thus, HCII variants with increased function, such as rHCII-CHis(6), may offer novel reagents for clinical application.  (+info)

The prevalence of hereditary thrombophilia in the Trakya region of Turkey. (4/74)

The prevalences of deficiencies in antithrombin III (AT III), protein C (PC), protein S (PS) and in the activated protein C (APC) resistance in the thrombotic population of the Trakya region, Turkey were investigated. 37 patients with venous thrombosis (VT) and 17 patients with arterial thrombosis (ArT) were included in this study. The mean ages of the patients with VT and ArT were 46 years (range 20-70) and 38 years (range 32-40), respectively. The activity of AT III was measured by commercially available immuno-turbidimetric assay. The activities of PC and PS were determined by coagulometric assay. The APC resistance was measured using a modified APTT-based clotting assay. Among the VT patients, there were 2 cases (5.4%) with AT III, 5 (13.51%) with PC deficiency, 5 (13.51%) with PS deficiency and 2 (5.4%) with APC resistance. In the ArT patient group, there was 1 patient (5.88%) with AT III, 3 (17.64%) with PC deficiency, 1 (5.88%) with PS deficiency and no APC resistant patients, while there was one (2.08%) with PC deficiency and one (2.08%) with APC resistance in the control group (49 persons, mean age 41 years). The relative risk of thrombosis (odds ratio) was 1.7 in the deficiency of PC and 5.6 in the deficiency of PS. The data presented suggests that the prevalences of AT III, PC and PS deficiencies causing thrombophilia in the Trakya region of Turkey are higher than in other reported studies while the APC resistance is lower than in others. Further studies including more patients would be required to clarify these discrepancies.  (+info)

Complete antithrombin deficiency in mice results in embryonic lethality. (5/74)

Antithrombin is a plasma protease inhibitor that inhibits thrombin and contributes to the maintenance of blood fluidity. Using targeted gene disruption, we investigated the role of antithrombin in embryogenesis. Mating mice heterozygous for antithrombin gene (ATIII) disruption, ATIII(+/-), yielded the expected Mendelian distribution of genotypes until 14.5 gestational days (gd). However, approximately 70% of the ATIII(-/-) embryos at 15.5 gd and 100% at 16.5 gd had died and showed extensive subcutaneous hemorrhage. Histological examination of those embryos revealed extensive fibrin(ogen) deposition in the myocardium and liver, but not in the brain or lung. Furthermore, no apparent fibrin(ogen) deposition was detected in the extensive hemorrhagic region, suggesting that fibrinogen might be decreased due to consumptive coagulopathy and/or liver dysfunction. These findings suggest that antithrombin is essential for embryonic survival and that it plays an important role in regulation of blood coagulation in the myocardium and liver.  (+info)

Inherited thrombophilia in ischemic stroke and its pathogenic subtypes. (6/74)

BACKGROUND AND PURPOSE: One or more of the inherited thrombophilias may be causal risk factor for a proportion of ischemic strokes, but few studies have addressed this association or the association between thrombophilia and pathogenic subtypes of stroke. METHODS: We conducted a case-control study of 219 hospital cases with a first-ever ischemic stroke and 205 randomly selected community control subjects stratified by age, sex, and postal code. With the use of established criteria, cases of stroke were classified by pathogenic subtype in a blinded fashion. The prevalence of conventional vascular risk factors; fasting plasma levels of protein C, protein S, antithrombin III; and genetic tests for the factor V Leiden and the prothrombin 20210A mutation were determined in cases and control subjects. RESULTS: The prevalence of any thrombophilia was 14.7% (95% CI, 9.9% to 19.5%) among cases and 11.7% (95% CI, 7.4% to 17.0%) among control subjects (OR, 1.3; 95% CI, 0.7% to 2.3%). The prevalence of individual thrombophilias among cases ranged from 0.9% (95% CI, 0.1% to 3.4%) for protein S deficiency to 5.2% (95% CI, 0.3% to 9.1%) for antithrombin III deficiency; among control subjects, the prevalence ranged from 1.0% (95% CI, 0.1% to 3.6%) for protein S deficiency to 4.1% (95% CI, 0.2% to 7.8%) for antithrombin III deficiency. There were no significant differences in the prevalence of thrombophilia between cases and control subjects or between pathogenic subtypes of ischemic stroke. CONCLUSIONS: One in 7 patients with first-ever acute ischemic stroke will test positive for one of the inherited thrombophilias, but the relation is likely to be coincidental rather than causal in almost all cases, irrespective of the pathogenic subtype of the ischemic stroke. These results suggest that routine testing for thrombophilia in most patients with acute ischemic stroke may be unnecessary. Whether the thrombophilias may still be important in younger patients with ischemic stroke or in predicting complications (eg, venous thrombosis) and stroke outcome remains uncertain.  (+info)

Mesenteric venous thrombosis: a changing clinical entity. (7/74)

OBJECTIVE: Mesenteric venous thrombosis (MVT) and its clinical spectrum have become better defined following improvements in diagnostic imaging. Historically, MVT has been described as a morbid clinical entity, but this may not necessarily be true. Often, an underlying disease process that predisposes a patient to MVT can be found and potentially treated. This study was designed to evaluate the diagnostics and management of MVT and to review long-term results of treatment. PATIENTS: Thirty-one patients in whom MVT was diagnosed between 1985 and 1999 were retrospectively reviewed. Survivors were contacted for follow-up. There were 15 men and 16 women. Ages ranged from 22 to 80 years (mean, 49.1 years). Thirteen patients had documented hypercoagulability, 10 had a history of previous abdominal surgery, 6 had a prior thrombotic episode, and 4 had a history of cancer. MVT presented as abdominal pain (84%), diarrhea (42%), and nausea/vomiting (32%). Computed tomography (CT) was considered diagnostic in 18 (90%) of 20 patients who underwent the test. CT diagnosed MVT in 15 (100%) of 15 patients presenting with vague abdominal pain or diarrhea. Angiography demonstrated MVT in only five (55.5%) of nine patients. RESULTS: Seven of 31 patients died within 30 days (< 30-day mortality rate, 23%). Twenty-two patients (72%) were initially treated with heparin. Nine patients were not heparinized: four of them died, and two were later given warfarin sodium (Coumadin). Of the 31 patients, only one received lytic therapy. Three patients became symptom free without anticoagulation. Ten patients (32%) underwent bowel resection. Overall, 19 (79%) of 24 survivors were treated with long-term warfarin therapy. Long-term follow-up was obtained in 24 patients (mean, 57.7 months). Twenty-one (88%) of 24 survived in follow-up. CONCLUSION: The diagnosis of MVT should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes or a documented coagulopathy. CT scanning appears to be the primary diagnostic test of choice. Anticoagulation is recommended. If diagnosed and treated early, MVT is not likely to progress to gangrenous bowel. Recent mortality rates for MVT are lower than previously published, perhaps because of earlier diagnosis and aggressive treatment or possibly because we now readily diagnose a more benign form of the disease, which is due to widespread use of CT scanning.  (+info)

Recombinant human transgenic antithrombin in cardiac surgery: a dose-finding study. (8/74)

BACKGROUND: Acquired antithrombin III (AT) deficiency may render heparin less effective during cardiac surgery and cardiopulmonary bypass (CPB). The authors examined the pharmacodynamics and optimal dose of recombinant human AT (rh-AT) needed to maintain normal AT activity during CPB, optimize the anticoagulant response to heparin, and attenuate excessive activation of the hemostatic system in patients undergoing coronary artery bypass grafting. METHODS: Thirty-six patients scheduled to undergo elective primary coronary artery bypass grafting and who had received heparin for 12 h or more before surgery were enrolled in the study. Ten cohorts of three patients each received rh-AT in doses of 10, 25, 50, 75, 100, 125, 175, or 200 U/kg, a cohort of six patients received 150 U/kg of rh-AT, and a control group of six patients received placebo. RESULTS: Antithrombin III activity exceeded 600 U/dl before CPB at the highest dose (200 U/kg). Doses of 75 U/kg rh-AT normalized AT activity to 100 U/dl during CPB. Activated clotting times during CPB were significantly (P < 0.0001) greater in patients who received rh-AT (844 +/- 191 s) compared with placebo patients (531 +/- 180 s). Significant (P = 0.001) inverse relations were observed between rh-AT dose and both fibrin monomer (r = -0.51) and D-dimer (r = -0.51) concentrations. No appreciable adverse events were observed with any rh-AT doses used in the study. CONCLUSIONS: Supplementation of native AT with transgenically produced protein (rh-AT) in cardiac surgical patients was well tolerated and resulted in higher activated clotting times during CPB and decreased levels of fibrin monomer and D-dimer.  (+info)

Looking for online definition of antithrombin III deficiency in the Medical Dictionary? antithrombin III deficiency explanation free. What is antithrombin III deficiency? Meaning of antithrombin III deficiency medical term. What does antithrombin III deficiency mean?
Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism, and repetitive intrauterine fetal death (IUFD). Inheritance is usually autosomal dominant, though a few recessive cases have been noted. The disorder was first described by Egeberg in 1965. The patients are treated with anticoagulants or, more rarely, with antithrombin concentrate. In kidney failure, especially nephrotic syndrome, antithrombin is lost in the urine, leading to a higher activity of Factor II and Factor X and in increased tendency to thrombosis. Heparin enhances ATIII activity and neutralizes "activated serine protease coagulation factors." Patients with ATIII deficiency requiring anticoagulant therapy with heparin will need higher doses of heparin. ATIII binds to thrombin and then forms the thrombin-anti thrombin complex or TAT complex. This is a ...
No sex-related difference is noted in terms of the prevalence of congenital antithrombin III deficiency. Women of childbearing age present special risk factors. Antithrombin III deficiency, like other... more
This should be performed in all patients with antithrombin III deficiency, especially if they have evidence of arterial thrombus. Arterial thrombosis due to antithrombin III deficiency is uncommon. Ve... more
During attempted cannulation of the right internal jugular vein, you puncture the carotid artery in a patient who is to be heparinized intraoperatively.. 1. What is your management?. 2. Would you proceed with the case?. 3. How does heparin anticoagulate?. Heparin binds to antithrombin III and the activated forms of factors II, X, XI, XII, and XIII, having an anticoagulant effect of about ninety minutes. It may produce qualitative or quantitative platelet abnormalities.. 4. The patient is resistant to heparinization. What is the defect?. Antithrombin III deficiency. 5. What is the treatment? Fresh frozen plasma.. 5. What tests measure the intrinsic and common pathways? For the intrinsic pathway, phospholipid is added to the patients plasma, and the time taken for clot formation is taken. Decreased fibrinogen and dysfibrinogenemias prolong both intrinsic and extrinsic pathways. The partial thromboplastin time, or PTT, measures all factors of the intrinsic and common paths, except factor XIII. A ...
Abscess excision Acute myelogenous leukemia (AML) Additional / adjuvant therapy ALCL Anal cancer anaplastic large-cell lymphoma Anemia and iron deficiency Anticardiolipin antibodies Antiphospholipid antibodies Antithrombin III deficiency aplastic anemia Aromatase Inhibitors B12 deficiency Bladder cancer blood diseases blood transfusions Bone density testing bone marrow aspiration bone marrow biopsy Breast cancer cancer care Chemoprevention Chemotherapy Chemotherapy clinical trials Chemotherapy side effect support Chronic lymphocytic leukemia (CLL) Chronic myelogenous leukemia (CML) CMML Colon cancer complete blood count cooleys anemia CT cutaneous ALCL Cyst excision Deep vein thrombosis (DVT) Diffuse large B-cell lymphoma Duodenal cancer Esophageal cancer Esophageal tumors ET extreme fatigue Factor 5 Leiden Follicular lymphoma frequent bruising frequent fever frequent nosebleed Gallbladder cancer / carcinoma Gastric cancer Head and neck cancer Hemachromatosis hemoglobin H disease hemophilia ...
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The results for both activity and antigen tests are given as percentages. Different labs use slightly different normal ranges, but in general, 80% to 120% is considered normal for adults. Newborns usually have about half as much antithrombin as adults. Thrombin levels in infants rise to adult levels by about 6 months of age.. People with genetically inherited antithrombin deficiency typically have test results between 40% and 60%.. In both type 1 and type 2 AT deficiency, the antithrombin activity test shows a low result because you dont have as much working antithrombin as you should have. When the AT activity test shows that levels are low, the antithrombin antigen test can then be used to find out whether the deficiency is type 1 or type 2.. If the follow-up ...
Throughout this stage im you will also start to note that your breasts changing into extra tender and sore and some ladies report that they observed an increase in the dimension of their breasts at the moment. On inherited thrombophilias in pregnancy other hand, you in all probability dont need to skimp out on a being pregnant test - its a thing the place youll wish to inherited thrombophilias in pregnancy in its results. Her urine being yellow is probably because she is dehydrated and needs to drink more water. Imagine going about your everyday business and having someone say you should inherjted hung upside down with your ovaries set on fire. It is going to turn out to be tougher to thrombopbilias a comfy sleeping position throughout the closing weeks of being pregnant, so ladies could also be extremely drained, Burch said. Its possible youll no symptoms of pregnancy at 3 weeks have enough iron resulting from menstrual bleeding and a poor food regimen. Nevertheless, if it adjustments in ...
Our two youngest boys have been diagnosed with Mitchondrial Disease. Our youngest had serum testing in 2009 which showed elevated lactate and pyruvate. This along with his other muscle problems and developing swallowing difficulty (aspirating liquids into his lungs and choking), led one of their doctors to order a muscle biopsy. The biopsy results took several months to complete. They showed a Complex I & III deficiency, a Complex III deficiency, an abnormal coupling ratio and sarcoplasmic masses. While the diagnosis was devestating, it did answer all of our extra questions and alowed us to start the proper supplements. There is no cure for Mitochondrial Disease. The only treatment is a high dose mixture of vitamins and supplements known to help mitochondrial function. Weve found an excellent place to order some of their supplements. Swanson Vitamins. Their Ubiquinol (most bioavailable form of CoQ10) is $5 cheaper per bottle and when they have a sale, it can be $7 cheaper per bottle! They use ...
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Patient Presentation A 6-month-old female came to clinic for her health maintenance visit. She was growing well physically. Her mother had several questions regarding her normal development which were easily answered. The mother was most concerned because the family history was now positive for her sister (patients maternal aunt) having a recent deep venous thrombosis…
Information provided on this site is provided for informational purposes only and is not meant to substitute for the advice provided by your own physician or other medical professional. You should not use the information contained herein for diagnosing or treating a health problem or disorder, or prescribing any medication. The Preeclampsia Foundation presents all data as is, without any warranty of any kind, express or implied, and is not liable for its accuracy, for mistakes or omissions of any kind, nor for any loss or damage caused by a users reliance on information obtained on the site. Professional opinions on this condition vary greatly. The Preeclampsia Foundation endorses no one course of treatment or "cure ...
Abstract. We have investigated the basis of antithrombin deficiency in an asymptomatic individual (and family) with borderline levels (≈70% antigen and activit
Mutations in the assembly chaperone BCS1L constitute a major cause of mitochondrial complex III deficiency. We studied the presence of BCS1L mutations in a complex III-deficient patient with metabolic acidosis, liver failure, and tubulopathy. A previously reported mutation, p.R56X, was identified in one BCS1L allele, and two novel heterozygous mutations, g.1181A|G and g.1164C|G, were detected in the second allele. The g.1181A|G mutation generated an alternative splicing site in the BCS1L transcript, causing a 19-nucleotides deletion in its 5UTR region. Decreased BCS1L mRNA and protein levels, and a respiratory chain complex III assembly impairment, determine a pathogenic role for the novel BCS1L mutations.
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These studies provide convincing evidence that testing for the inherited thrombophilias should not be performed routinely in patients with ischemic stroke, even in the young. No case-control studies of PC, PS, or AT showed an association of these deficiencies and stoke. Multiple case-control studies have demonstrated no association between FVL or PTM and ischemic stroke in patients older than age 60. Case-control studies of FVL and PTM performed in unselected younger patients do not support an association of these disorders and stroke, and meta-analyses are unconvincing because of the inclusion of suboptimal data. Patients who do not have a white ancestor should not be tested for FVL or PTM, and the levels of PC and PS should be interpreted with caution because they may have ethnic variability that could lead to an erroneous diagnosis in patients of African descent. It is unclear if PFO in association with an inherited thrombophilia in the absence of an identified deep venous thrombosis should ...
How can this seemingly disparate evidence be integrated with what was known before? Older data, upon which the guidelines were based, had established that thrombophilia testing was predictive of the relative risk for initial VTE. The situation is completely different for patients who have already had a spontaneous VTE. Why? It has long been known that patients with spontaneous VTE are hypercoagulable, (untreated recurrence rates of 2% to 5% per year) no matter the result of thrombophilia testing. In part this is because comprehensive laboratory testing of clinically thrombophilic patients will yield negative results---no "laboratory lesion"--- in about 30%-40% of cases. The thinking is that those patients have a thrombophilic state that hasnt been discovered yet. To keep it in perspective, remember that the concept of hereditary thrombophilia has been around since the discovery, in 1963, of antithrombin deficiency (Egeberg O: Inherited antithrombin deficiency causing thrombophilia. Thrombosis ...
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The results for both activity and antigen tests are given as percentages. Different labs use slightly different normal ranges, but in general, 80% to 120% is considered normal for adults. Newborns usually have about half as much antithrombin as adults. Thrombin levels in infants rise to adult levels by about 6 months of age. People with genetically inherited antithrombin deficiency typically have test results between 40% and 60%. In both type 1 and type 2 AT deficiency, the antithrombin activity test shows a low result because you dont have as much working antithrombin as you should have. When the AT activity test shows that levels are low, the antithrombin antigen test can then be used to find out whether the deficiency is type 1 or type 2. If the follow-up ...
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... is a protein in the blood that helps regulate blood clot formation. Antithrombin testing is used to investigate the cause of recurrent blood clot formation (such as DVT) and to identify an antithrombin deficiency.
Abcams Antithrombin III ELISA Kit suitable for Cell culture supernatant, Saliva, Milk, Urine, Serum, Plasma, Cell culture media, Cerebral Spinal Fluid in…
This study will be a prospective, unblinded, non-randomized, open-label, multi-center Phase II/III study with 2 segments, i.e. a PK evaluation (Segment I), and an assessment of prophylaxis in surgical interventions and pregnancy/delivery, (Segment II). During the PK segment, the subjects would remain on their current anticoagulation therapy except for subjects on heparin therapy where a wash-out period of at least 5 half lives would be required. In total, 15 subjects with congenital ATIII Deficiency will be enrolled for the PK assessment (Segment I).. For Segment II, fifteen episodes will be treated. Recruitment of individual subjects with high risk for venous thrombosis for Segment II of this study is necessary because of the rarity of Antithrombin deficiency in the population. ...
antithrombin III Glasgow: abnormal antithrombin with increased heparin affinity & reduced ability to inactivate thrombin; associated with familial thrombosis; tryptic peptides Ala(371)-Arg(393) & Ser(394)-Arg(399) present in reduced amounts; Asp(187) replaced by Lys
On one hand, the license to use the new department for filling and lyophilization of the coagulation inhibitor antithrombin (treatment of patients suffering from congenital and acquired antithrombin deficiency) as well as the new department for filling of standard intravenous immunoglobulin (which is also used as a replacement therapy in primary immunodeficiency syndromes, myeloma or chronic lymphocytic leukaemia) ends a process which had begun in 2001 and which involved the opening of the new Plasma Management department, the new Albumin manufacturing plant and the new area for aseptic filling and lyophilization of heat-treated coagulation factors ...
Buy our Antithrombin III 293T transfected lysate (positive control). ab94043 has been validated in western blot. Abcam now offers a 12-month guarantee.
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Antithrombin III for critically ill patients Edited (no change to conclusions) answers are found in the Cochrane Abstracts powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
A quick reference on Thrombophilias in Pregnancy, covering the clinical presentation, investigative approach, and key principles of management
The plasma antithrombin stages, determined as anti-FXa action, experienced a typical distribution in the GAIT study, with a medium worth of 109.05% of the
Shop Antithrombin ELISA Kit, Recombinant Protein and Antithrombin Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
Abstract: 53 patients with lung tuberculosis were divided in 3 groups in accordance with severety of disease. Leukocyte elastase, cationic proteins in neutrophils, activities of a 1-proteinase and a 2-macroglobulin were determined in patients plasma. Thromboelastographic, coagulating, fibrinolytic indices, and antithrombin III activity were also determined in 28 patients of all 3 groups. Results demonstrated the high level of leukocyte elastase (6-fold more than normal) in plasma of patients with acute tuberculosis process. This group of patients demonstrated activation of intravascular coagulation proceeded on the background of significant decrease (up to 60%) of AT III activity. Conclusion: Acuity and severety of tuberculosis process in lung may be characterized by high activity of leukocyte elastase. Degranulating activity of neutrophils and releasing of elastase are the reason of AT III deficiency and increasing of intravascular coagulating activity in tuberculosis ...
Estradiol Progesteron DHEA-s LH FSH SHBG Testosteron IGF-1 APC-R(FactorV Leiden) Protein S deficiency Prothrombin mutation (G20210A) Folic acid deficiency Antithrpombin III deficiency. ...
Inherited thrombophilia is a genetically determined tendency to thrombosis.1 In 1965 the first family with antithrombin deficiency was described, and for many years this was the only identifiable cause of thrombophilia.2 More recently, pedigree and case-control studies have confirmed that the risk of venous thrombosis is increased by deficiencies of antithrombin, protein C, and protein S, and by resistance to activated protein C.3-5 Other candidate genetic factors are included in table 1.J Clin Pathol 2000;53:167-170. The value of obtaining laboratory evidence of thrombophilia is the ability to predict the likelihood of recurrence in symptomatic patients and the risk of thrombosis in their relatives. Thus thrombophilia testing would be used to optimise the benefit/risk ratio of anticoagulant treatment. Therapeutic recommendations would have to be based on a risk-benefit analysis that considers the risk of the disease, the effectiveness of treatment, the risk of treatment, and the predictive ...
This study is the first to evaluate the long-term prognostic significance of hemostatic factor measurements in patients with angina pectoris and known coronary angiographic status. The clinical follow-up spanned 9.5 years, and complete follow-up information was available for 93% of the 225 patients initially recruited to the study. Although the number of patients investigated was comparatively small, the 58 patients with cardiac events, who represented more than a quarter of the original patient sample, allowed meaningful conclusions on risk relationships with hemostatic and angiographic baseline variables. Some earlier cross-sectional studies have indicated lower antithrombin III antigen or activity in patients with CAD compared with individuals without,32 33 34 35 while others have reported higher rather than lower values.36 37 In contrast, more recent investigations in large populations or patient cohorts failed to demonstrate an association of antithrombin III with the prevalence or extent ...
Abstract. Human antithrombin III (ATIII) is a plasma inhibitor of several serine proteases of the blood coagulation system. Previous investigations have report
ATryn® (also known as ATIII) is a recombinant form of human antithrombin. This product demonstrates the high potential for the use of transgenic technology in the production of biotherapeutics. Antithrombin is a plasma protein with anti-coagulative and anti-inflammatory properties that, like many other proteins currently derived from human blood supply, has been difficult to manufacture using conventional recombinant protein production methods.. ...
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肝素經由它的硫化五糖序列與酵素抑制劑抗凝血酶(英语:antithrombin)III結合,使其構形改變而活化[35]。 活化的抗凝血酶III接著抑制凝血酶與凝血因子Xa(英语:factor Xa)以及其他蛋白酶,抑制的效果可因為肝素的加入而上升一千倍[36]。硫化五糖序列如下: GlcNAc/NS(6S)-GlcA-GlcNS(3S,6S)-IdoA(2S)-GlcNS(6S) 抗凝血酶III與肝素結合後導致的構形改變,造成它可抑制凝血因子Xa。至於凝血酶與抗凝血酶III之間的作用,除了酵素以外,還需要同時與肝素結合形成三元複合體(英语:ternary complex)才能達到抑制的效果;這部分肝素的高陰電性擔任了重要的角色[12]。因此,至少要具有十八個糖的肝素才能與凝血酶及抗凝血酶III產生有效的作用;但是與凝血因子Xa的作用只需要硫化五糖序列就可以了[37]。 ...
Background: The incidence of thrombotic complications in patients with malignancy is higher than in the general population. There is little data about..
Patients randomized to the control group will receive a placebo consisting of normal saline in a volume equivalent to the volume of antithrombin the same patient in the treatment group would have received and administered by anesthesia and perfusion in the exact same manner as the AT is administered in the treatment group ...
Opens the Highlight Feature Bar and highlights feature annotations from the FEATURES table of the record. The Highlight Feature Bar can be used to navigate to and highlight other features and provides links to display the highlighted region separately. Links in the FEATURES table will also highlight the corresponding region of the sequence. More... ...
CHAPTER 127 HEREDITARY THROMBOPHILIA Williams Hematology CHAPTER 127 HEREDITARY THROMBOPHILIA SCOTT H. GOODNIGHT JOHN H. GRIFFIN Introduction Major Hereditary Defects Hereditary Resistance to Activated Protein C Prothrombin G20210A Gene Polymorphism Hyperhomocysteinemia Protein C Deficiency Protein S Deficiency Antithrombin Deficiency High Levels of Factor VIII and Other Coagulation Factors Hereditary Thrombotic Dysfibrinogenemia Other Potential Thrombophilic Disorders…
SUMMARY Thrombophilia refers to laboratory abnormalities that increase the risk of venous thromboembolism (VTE). Over the last several decades numerous factors have been identified. The most prevalent examples of hereditary forms of thrombophilia include the factor V Leiden and prothrombin G20210A mutations; deficiencies of the natural anticoagulants antithrombin, protein C, and protein S; persistently elevated levels of coagulation factor VIII; and mild hyperhomocysteinemia. Taken together, some form of hereditary thrombophilia can be identified in more than 50 percent of patients with VTE who are without obvious reasons for VTE, such as trauma or prolonged stasis. Moreover, hereditary thrombophilia has been associated with arterial cardiovascular disease and obstetric complications such as (recurrent) pregnancy loss and preeclampsia. The high yield of thrombophilia testing has led to widespread testing for these abnormalities in patients. Nevertheless, thrombophilia testing remains a topic of ...
List of 6 disease causes of Mesenteric venous thrombosis, patient stories, diagnostic guides. Diagnostic checklist, medical tests, doctor questions, and related signs or symptoms for Mesenteric venous thrombosis.
Thrombophilia (sometimes hypercoagulability or a prothrombotic state) is an abnormality of blood coagulation that increases the risk of thrombosis (blood clots in blood vessels). Such abnormalities can be identified in 50% of people who have an episode of thrombosis (such as deep vein thrombosis in the leg) that was not provoked by other causes. A significant proportion of the population has a detectable abnormality, but most of these only develop thrombosis in the presence of an additional risk factor. There is no specific treatment for most thrombophilias, but recurrent episodes of thrombosis may be an indication for long-term preventative anticoagulation. The first major form of thrombophilia, antithrombin deficiency, was identified in 1965, while the most common abnormalities (including factor V Leiden) were described in the 1990s. The most common conditions associated with thrombophilia are deep vein thrombosis (DVT) and pulmonary embolism (PE), which are referred to collectively as venous ...
From UniProt:. Mitochondrial complex III deficiency, nuclear 4 (MC3DN4): A disorder of the mitochondrial respiratory chain resulting in a highly variable phenotype depending on which tissues are affected. Clinical features include mitochondrial encephalopathy, psychomotor retardation, ataxia, severe failure to thrive, liver dysfunction, renal tubulopathy, muscle weakness and exercise intolerance. [MIM:615159]. ...
Causes of Mesenteric venous thrombosis with diagnosis analysis, related symptoms, patient stories, full-text book chapters, alternative diagnoses, misdiagnosis, treatments, remedies, and much more.
Warfarin exerts its anticoagulant effect by interfering with the synthesis of the vitamin K dependent clotting factors (VII, IX, X, and thrombin). Antithrombin III (ATIII) is a nonvitamin K dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa. Antithrombin III (ATIII) is a nonvitamin K dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa. Top of page Abstract. It also inhibits. Warfarin exerts its anticoagulant effect by interfering with the synthesis of the vitamin K dependent clotting factors (VII, IX, X, and thrombin). It also inhibits. Tensive experimental evidence shows that platelets support tumour metastasis. http://pvessaynjun.edu-essay.com Antithrombin III (ATIII) is a nonvitamin K dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa. E activation of platelets and the coagulation system have a. Antithrombin III (ATIII) is ...
Antithrombin III (AT III) supplementation has proven to be effective in the treatment of disseminated intravascular coagulation. According to the study by the Kumamoto University School of Medicine , administration of AT III is also useful for prevention of organ failure in animals challenged with endotoxin or bacteria and it increases the survival rate of such animals. Since inhibition of coagulation abnormalities failed to prevent organ failure in animals given bacteria, AT III may exert a therapeutic effect independent of its anticoagulant effect. This therapeutic mechanism of AT III has been explored using an animal model of septicemia. AT III prevented pulmonary vascular injury by inhibiting leukocyte activation in rats given endotoxin. This effect is mediated by the promotion of endothelial release of prostacyclin which inhibits leukocyte activation. Interaction of AT III with heparin-like glycosaminoglycans (GAGs) on the endothelial cell surface appears to be important for this effect. ...
TY - JOUR. T1 - Antithrombin III milano 2. T2 - A single base substitution in the thrombin binding domain detected with PCR and direct genomic sequencing. AU - Olds, R. J.. AU - Lane, D.. AU - Caso, R.. AU - Tripodi, A.. AU - Mannucci, P. M.. AU - Thein, S. L.. PY - 1989/12/25. Y1 - 1989/12/25. UR - http://www.scopus.com/inward/record.url?scp=0024844519&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0024844519&partnerID=8YFLogxK. U2 - 10.1093/nar/17.24.10511. DO - 10.1093/nar/17.24.10511. M3 - Article. C2 - 2602168. AN - SCOPUS:0024844519. VL - 17. SP - 10511. JO - Nucleic Acids Research. JF - Nucleic Acids Research. SN - 0305-1048. IS - 24. ER - ...
There are 4 fourteen-letter words containing A, B, 2H and M: ARITHMOPHOBIAS MOUTHBREATHERS RHOMBENCEPHALA & THROMBOPHILIAS. Every word on this site can be used while playing scrabble. Create other lists, that start with or end with letters of your choice.
Specify your expertise for the "Disease/group of diseases" (eg SCT, Molecular diagnosis): All clinical and laboratory aspects. Diseases: Essential thrombocythemia Hereditary thrombocytopenia with early-onset myelofibrosis Gaisböck syndrome Rare coagulation disorder Rare thrombotic disease of hematologic origin Rare thrombotic disorder due to a coagulation factors defect Rare thrombotic disorder due to a constitutional coagulation factors defect Congenital factor XII deficiency Familial thrombomodulin anomalies Hypercoagulability syndrome due to glycosylphosphatidylinositol deficiency Rare hereditary thrombophilia Hereditary thrombophilia due to congenital protein S deficiency Hereditary thrombophilia due to congenital protein C deficiency Hereditary thrombophilia due to congenital antithrombin deficiency Hereditary thrombophilia due to congenital histidine-rich (poly-L) glycoprotein deficiency Rare thrombotic disorder due to an acquired coagulation factors defect Catastrophic antiphospholipid ...
Hereditary thrombophilia is mainly due to antithrombin deficiency, protein C and protein S deficiencies, the activated protein C resistance (mostly due to factor Ⅴ Leiden mutation) or the prothrombin (factor II) mutation. In 1999 Brenner et al. identified thrombophilia as a major cause in more than 40% of women affected by RFL. Following studies confirmed the increased frequency of antithrombin III, protein C, and protein S deficiency in women with RFL. Especially the factor V Leiden gene mutation and the prothrombin A20210G gene mutation play an essential role. Several reports have described an association between early recurrent fetal loss and hyperhomocysteinemia and/or MTHFR C677T gene polymorphism. Acquired thrombophilia has also been associated with RFL ...
A method for the differential determination of plasma antithrombins, antithrombin III and alpha2 macroglobulin, is described. The method is based on the selective inactivation of plasma alpha2 macroglobulin by treatment with 0-1 M methylamine for 10 minutes at 37 degrees C and on the observation that antithrombin III and alpha2 macroglobulin inhibited in defibrinated plasma low concentrations of thrombin without mutual interference and according to pseudo-first order reaction. In healthy subjects antithrombin III was shown to account for about 70% of the total antithrombin activity. But in patients with liver cirrhosis, where low levels of total antithrombin activity were observed, the relative contribution of antithrombin III was found to be noticeably lower.. ...
Antithrombin-III exerts antiinflammatory effects via ligation of heparan sulfate proteoglycans. Here we show in vitro that recombinant human antithrombin-III attenuates CD11b/CD18 expression of activated neutrophils and monocytes in whole blood ex vivo. As leukocyte integrin expression is triggered by extracorporeal circulation, this observation may be of relevance for pharmacological treatment during cardiopulmonary bypass ...
Unfortunately, significant delays often occur between presentation and the diagnosis of MVT because of the nonspecific nature of symptoms. For example, pain resulting from MVT after abdominal surgery is often mistakenly assumed to be postoperative discomfort. Pain in the setting of inflammatory bowel disease is often attributed to disease exacerbation. A high index of suspicion and rapid diagnosis are critical to prevent delays in therapy and adverse outcomes. ...
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NPC313Hu01, AT3; ATIII; SERPINC1; Anti-Thrombin Antibodies; Serpin Peptidase Inhibitor Clade C Member 1; Coding Sequence Signal Peptide Antithrombin Part 1 | Products for research use only!
The majority of serpin diseases are due to protein aggregation and are termed "serpinopathies".[9][63] Serpins are vulnerable to disease-causing mutations that promote formation of misfolded polymers due to their inherently unstable structures.[63] Well-characterised serpinopathies include α1-antitrypsin deficiency (alpha-1), which may cause familial emphysema and sometimes liver cirrhosis, certain familial forms of thrombosis related to antithrombin deficiency, types 1 and 2 hereditary angioedema (HAE) related to deficiency of C1-inhibitor, and familial encephalopathy with neuroserpin inclusion bodies (FENIB; a rare type of dementia caused by neuroserpin polymerisation).[8][9][68]. Each monomer of the serpin aggregate exists in the inactive, relaxed conformation (with the RCL inserted into the A-sheet). The polymers are therefore hyperstable to temperature and unable to inhibit proteases. Serpinopathies therefore cause pathologies similarly to other proteopathies (e.g. prion diseases) via two ...
Background. If a thrombophilia (clotting disorder) has been identified in a patient with blood clots (venous thromboembolism = VTE), the question arises whether other family members should be tested for the same thrombophilia.. My Clinical Approach. My approach in clinical practice to thrombophilia testing in family members is summarized in table 1: Family Member Testing. If the patient has a "strong" inherited thrombophilia (i.e. homozygous factor V Leiden, homozygous prothrombin 20210 mutation, double heterozygous factor V Leiden plus prothrombin 20210 mutation, deficiency of protein C, S or antithrombin) then I consider and discuss testing of other family members. However, if the patient only has heterozygous factor V Leiden or heterozygous prothrombin 20210 mutation, I do not recommend testing of family members, as the finding of one of these "mild" thrombophilias typically has no impact on management of family members also affected by one of those "mild" thrombophilias.. Finding of a ...
... causes substantial disability and death. The incidence of deep venous thrombosis (DVT) is about 1 per 1000 person years. The most serious and potentially preventable complication, pulmonary embolus, kills an estimated 50,000 Americans each year. Venous stasis secondary to chronic valvular incompetence, of- ten a consequence of venous thrombosis, causes varying degrees of pain, edema, and ulceration. The changing demographic patterns, particularly the aging of society, are increasing the risk of venous thromboembolism and the importance of prevention. Recent identificationof inherited defects causing thrombosis (inherited thrombophilias) allows improved prevention through identification of individuals at high risk. The knowledge and tools for effective prevention and treatment are available but currently underused ...
TY - JOUR. T1 - Issues in antithrombin therapy for UA/NSTEMI. AU - Alpert, Joseph S.. AU - Budaj, A. J.. AU - Gurfinkel, E. P.. AU - Henry, T. D.. PY - 2001/8/27. Y1 - 2001/8/27. N2 - In September 2000, participants at the 4th Annual Experts Meeting of the International Cardiology Forum convened to discuss guidelines for the management of unstable angina/non-ST-elevation MI, recently published by North American and European task forces. Discussion of new recommendations for antithrombin therapy focused on the role of low-molecular-weight heparin (LMWH). Although most participants found the new guidelines largely consistent with existing data, and sufficiently adaptable to most clinical settings, there was concern that neither task force specified LMWH as the antithrombin of choice for the medical management of these patients. The new guidelines continue to endorse the use of unfractionated heparin, particularly for high-risk patients, despite the evidence for the efficacy of LMWH in this ...
Fondaparinux (Arixtra) is a synthetic pentasaccharide anticoagulant. Apart from the O-methyl group at the reducing end of the molecule, the identity and sequence of the five monomeric sugar units contained in fondaparinux is identical to a sequence of five monomeric sugar units that can be isolated after either chemical or enzymatic cleavage of the polymeric glycosaminoglycan heparin and heparan sulfate (HS). This monomeric sequence in heparin and HS is thought to form the high affinity binding site for the natural anti-coagulant factor, antithrombin III (ATIII). Binding of heparin/HS to ATIII has been shown to increase the anti-coagulant activity of antithrombin III 1000-fold. Fondaparinux potentiates the neutralizing action of ATIII on activated Factor X 300-fold. Fondaparinux may be used: to prevent venous thromboembolism in patients who have undergone orthopedic surgery of the lower limbs (e.g. hip fracture, hip replacement and knee surgery); to prevent VTE in patients undergoing abdominal ...
The predictive value of inherited thrombophilia screening in those who have a history of venous thromboembolism has been over-estimated in the past, and for family members of affected individuals. Likewise, the association between positive inherited thrombophilia tests and adverse pregnancy outcomes is somewhat controversial. Furthermore, inherited thrombophilia tests are a form of genetic testing. Discussion on an individual patient basis with Haematology may be appropriate in many cases ...
Binds to endothelial cell surfaces and plasma proteins and its activity depends on antithrombin. Heparin binds to antithrombin, causes a conformational change in the inhibitor, exposing its active site for more rapid interaction with proteases. Heparin acts as a co factor for the antithrombin-proteases reaction Antithrombin inhibits proteases espec thrombin 2a, 9a, 10a by forming stable complexes with them and the presence of heparin accelerates this reaction 1000x. The binding of AT Ill and unfractionated heparin t degradation of both factor Xa and thrombin. Pass: Binds to AT III. ...
Laboratory evaluation of A1AT deficiency involves measurement of circulating A1AT protein (quantitation) and characterization of A1AT genetic polymorphisms. In contrast to adult and pediatric populations, there are no reliably documented A1AT serum reference ranges for newborns available. We evaluated blood samples from 145 children collected at 0-7 day after birth within the frame of on-going newborn A1AT deficiency screening program in Central Poland. A1AT and hsCRP serum concentration was measured by nephelometry, A1AT phenotyping performed by isoelectrofocusing. The median A1AT serum concentration for normal newborn population with the MM phenotype (n=135) was 172,0 mg/dL (123-331).Lower concentrations of A1AT correlated with heterozygosity for the S and Z alleles, respectively MS (n=3) 151,0 and MZ (n=3) 125,0 mg/dL. Considerable dynamics in A1AT blood level changes in the first days of life were observed with median A1AT concentration of 155,5 mg/dL at day 0, 158,5 at day1, 183,2 at day2, ...
An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance. . ...
Navarro-Fernandez, J.; Perez-Sanchez, H.; Martinez-Martinez, I.; Meliciani, I.; Guerrero, J.A.; Vicente, V.; Corral, J.; Wenzel, W ...
TY - JOUR. T1 - Bioequivalence of two intravenous formulations of antithrombin III. T2 - A two-way crossover study in healthy Korean subjects. AU - Kim, Kyoung Ah. AU - Lim, Yoon Young. AU - Kim, Sun Ho. AU - Park, Ji-Young. PY - 2013/11/1. Y1 - 2013/11/1. N2 - Background Treatment with antithrombin (AT)-III is indicated for patients with sepsis or hereditary AT deficiency. Objective The purpose of this study was to compare the pharmacokinetic and pharmacodynamic characteristics of 2 AT-III formulations in healthy Korean volunteers to satisfy the regulatory requirements for bioequivalence for marketing purposes. Methods A single-center, single-dose, open-label, randomized, 2-period, 2-sequence crossover study was conducted in healthy Korean volunteers. Blood samples for the drug analysis were collected for up to 216 hours after drug administration. Participants received either the test or reference formulation of AT-III 100 U/kg IV for 20 minutes in the first period and the alternative ...
Schwann cells can form Remak bundles ensheathing multiple, small unmyelinated axons or can form thick or thin myelin sheaths around axons. Generally, the size of the axons correlates with their ensheathment or myelination: the thicker the axon, the thicker the myelin. Taveggia et al. now show that neuregulin-1 (NRG-1) type III serves as a signal to the Schwann cells, with low concentrations of NRG-1 type III in the neuron leading to ensheathment and high concentrations leading to thick myelination. In cultures of rat Schwann cells with dorsal root ganglion (DRG) neurons from wild-type or NRG1 type III -/- mice, the Schwann cells robustly myelinated the wild-type neurites but failed to myelinate the NRG-1 type III-deficient neurites. Forced expression of NRG-1 type III in the deficient DRG cells allowed the Schwann cells to myelinate the neurites, and in some cases the myelin was as much as twice as thick as that surrounding the wild-type neurites. Analysis of the abundance of NRG-1 type III in ...
Introduction. E risk of venous thromboembolism increases significantly during pregnancy, peaks during the postpartum period, and is one of the leading causes of. The past 20 years, knowledge in this field has greatly increased with the identification of a. Acute pulmonary embolism may occur rapidly and unpredictably and may be difficult to diagnose. Venous thromboembolism (VTE) has important heritable components. Number: 0763. Diagnosis and Management of Cerebral Venous Thrombosis A Statement for Healthcare Professionals From the American Heart AssociationAmerican Stroke. Figure 1. This terminology is. Licy. Tna considers homocysteine testing (measurements of plasma homocysteine) medically necessary for the following indications:Protein C deficiency is associated with a small percentage of cases of inherited thrombophilia, as well as the even more uncommon findings of warfarin induced skin. Gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the ...
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterized by airflow limitation that is progressive and associated with an enhanced chronic inflammatory response in the lung to noxious particles or gases. Deficiency of alpha-1 antitrypsin (AAT) is the best-studied genetic risk factor for COPD and one of the most common genetic disorders among Caucasians. The availability of specific therapy for AATD makes it possible to improve outcomes, but however, AATD is underrecognized and undertreated. This program will discuss diagnosis and treatment options for patients with COPD and AATD, with the most recent recommendations from the GOLD 2017 report.. This webcast was recorded live and is being used with the permission of the presenters.. Learning Objective(s): ...
There are some data about genes associated with certain traits of a person in the scientific literature, but these data are often contradictory. It is evident that complexes of genes that affect the manifestation of the trait can be more informative. We have investigated genotypes of 9000 people, using the PCR method, in order to determine their athletic abilities or predisposition to different diseases and pathologies. In particular, we tested about 3000 women with unknown causes of miscarriages for 14 genes associated with the pregnancy development. 1,5 years later we interviewed 700 women and have identified a high genetic risk of pregnancy loss due to hereditary thrombophilia. In most of the cases, doctors took into account our data and applied for these women treatment with anticoagulant drugs such as fragmin in the subsequent pregnancies. So 86.6% of pregnant women have successfully conceived and given birth, and we have received over 500 touching letters of gratitude. Thus, genetic testing
From the hemocyte granules of the horseshoe crabs Limulus and Tachypleus. Factor C is activated by Gram-negative bacterial lipopolysaccharides and chymotrypsin. Inhibited by antithrombin III. In peptidase family S1 (trypsin family ...
Alpha-1 antitrypsin (A1AT) deficiency is a common inherited condition caused by a lack of a protease inhibitor (Pi) normally produced by the liver. The role of A1AT is to protect cells from enzymes such as neutrophil elastase.. ...
Proteins perform their function for adopting a particular 3D structure, referred as native structure, and failure to fold into the native structure has profound deleterious effects, frequently causing diseases
i have been trying for a baby for 2 years, ive unfortunately had 2 miscarriages and found out i have Protein S Deficiency, so when i get to this point i cant help but get mixed emotions...the .... ...
A three panel brochure highlighting the Associations advocacy efforts. It outlines how to make your voice heard as a Diabetes Advocate, how to get help with discrimination concerns, and our work to keep children safe at school ...
Chronic venous ulceration is a major complication of chronic venous disorder with important implications in terms of morbidity and social expenditure. Venous thrombosis and thrombophilia are widespread conditions, often associated with venous ulcers of the lower limbs. This link has not yet been widely described in the literature and aim of this work was to analyze the relationship between these two conditions reviewing the current literature. PubMed, Scopus and ScienceDirect databases were searched for articles using the terms: thrombophilia, venous ulceration, chronic venous disorders and the significant full text were downloaded and analyzed. From the literature review, a description of the most common thrombofilic abnormalities found in literature and the relationship with CVU was given. Conditions such as antithrombin deficiency, protein C deficiency, protein S deficiency, factor V Leiden, hyperhomocystinaemia, prothrombin G20210A mutation, antiphospholipid antibodies, elevated factor VIII ...
Gross deletions-duplications in PROS1 are relatively common in point mutation-negative hereditary protein S deficiency. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
anti-Serine (Or Cysteine) Peptidase Inhibitor, Clade C (Antithrombin), Member 1 (SERPINC1) antibody (Biotin) ABIN770033 from antibodies-online
TY - JOUR. T1 - Antithrombin during extracorporeal membrane oxygenation in adults. T2 - National survey and retrospective analysis. AU - Iapichino, Giacomo E.. AU - Protti, Alessandro. AU - Andreis, Davide T.. AU - Panigada, Mauro. AU - Artoni, Andrea. AU - Novembrino, Cristina. AU - Pesenti, Antonio. AU - Gattinoni, Luciano. PY - 2019/3/1. Y1 - 2019/3/1. N2 - The impact of antithrombin replacement during extracorporeal membrane oxygenation (ECMO) in adults remains unclear. This work comprises a survey, showing that antithrombin is routinely supplemented in many Italian ECMO-Centers, and a retrospective analysis on 66 adults treated with veno-venous ECMO and unfractionated heparin at our Institution. Twenty-four to 72 h after the beginning of ECMO, antithrombin activity was ≤70% in 47/66 subjects and activated partial thromboplastin time (aPTT) ratio was ,1.5 in 20/66 subjects. Activated partial thromboplastin time ratio ,1.5 was associated not with lower antithrombin activity (61 ± 17 vs. 63 ...
BACKGROUND AND OBJECTIVES: The G20210A polymorphism in the prothrombin gene is a common cause of inherited thrombophilia. Scarce information is available about the circumstances of the heralding thrombotic manifestation at different ages. The aim of this study was to determine the risk of spontaneous or secondary venous thromboembolism (VTE) among younger and older carriers of the G20210A prothrombin polymorphism. DESIGN AND METHODS: We performed a case-control study, investigating 650 patients with a first objectively documented deep venous thrombosis of the legs or pulmonary embolism and 703 individuals with no history of vascular disease. In all of them we carried out laboratory screening for antithrombin III, protein C and protein S deficiencies, and for the presence of the factor V Leiden and the G20210A prothrombin polymorphisms. RESULTS. After adjustment for other inherited causes of thrombophilia (deficiency of antithrombin III, protein C or S, factor V Leiden) the overall risk for VTE ...
The team found that 51 patients had mesenteric venous thrombosis, and 6 were diagnosed at autopsy. The highest incidence of 11 per 100, 000 person-years was in the age category 70 to 79 years. The research team noted that activated protein C resistance was present in 13 of 29 patients tested. D-dimer at admission was raised in all 5 patients tested. Multidetector row computed tomography in the portal venous phase was diagnostic in all 20 patients investigated, of whom 19 were managed conservatively. The researchers found that the median length of resected bowel in 12 patients who had surgery was 0.6 m. The overall 30-day mortality rate was 20%.. The team observed that intestinal infarction, treatment on a non-surgical ward, and computed tomography not done were associated with increased mortality. Cancer was independently associated with long-term mortality.. Portal venous phase computed tomography appeared sensitive in diagnosing mesenteric venous thrombosis. Dr Acosta s team concluded, As ...
Novel conjugates of glycosaminoglycans, particularly heparin and dermatan sulfate, and amine containing species and therapeutic uses thereof are described. In particular, mild methods of conjugating heparins to proteins, such as antithrombin III and heparin cofactor II, which provide covalent conjugates which retain maximal biological activity are described. Uses of these conjugates to prevent thrombogenesis, in particular in lung airways, such as found in infant and adult respiratory distress syndrome are also described.
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동물실험에서 페마렐은 뇌와 뼈에서 에스트로겐 수용체에 대한 자극효과를 보였다[3][4]. 이 약물은 홍조 감소[5], 뼈밀도 개선[6] 등의 효과를 보이는 것으로 보고되었으며, 분리된 유방암 세포주[7]나 시궁쥐의 자궁세포주[4][8]에 대해서 안전한 것으로 알려져있다. 페마렐은 조골세포의 활동을 증진시키는 방법으로 뼈 밀도를 증가시키는 것으로 보이며[9], 이 때문에 폐경기 골다공증 증세에 대한 약으로 사용 가능성이 있다. 에스트로겐 수용체를 자극하지만, 페마렐은 혈중 호르몬 수치에 변화를 주지 않는 것으로 보인다[5] 최근의 연구에 따르면 페마렐은 정상인 여성이나 혈전성향증(thrombophilia)을 가진 여성 모두에서 혈전 형성에 영향을 미치지 않는 것으로 나타났다[10].. ...
One of the main objectives of this study was to establish the lifetime risk for VTE in subjects with 1 of the 4 main coagulation defects related to inherited thrombophilia (AT, PC, PS, and APCR) and to compare the clinical features of the different defects. Particular attention was taken to include only families with documented inherited defects and to avoid selection bias, by considering only relatives. Of the 1143 subjects of whom we received data, 746, from 233 kindreds, fulfilled the inclusion criteria. The 513 relatives were included in the study.. The lifetime risk for VTE in the AT group was 4-fold greater than in the APCR group, 3-fold than in the PS group, and 2-fold than in the PC group. It was 2-fold greater in PC than in APCR, whereas no difference was found between the PS and APCR groups. The probability that a subject with APCR will be free of thrombosis at the age of 45 is 0.88, compared with 0.59 for AT, 0.74 for PC, and 0.79 for PS. This finding is in agreement with the study of ...
To the Editor:. The contribution by Troldborg, et al1 is a valuable addition to our understanding of disease, addressing half the question. Serine proteases do not function in isolation, but are also part of an enzyme-inhibitor interaction2. Noting higher enzyme concentrations in their cross-sectional study of patients with systemic lupus erythematosus1, direct correlation with nephritis and titers of anti-dsDNA, and inverse correlation with complement C3, the authors have demonstrated that serine protease levels appear to be markers of disease activity. It may also be worthwhile to assess whether their results reflect disease activity or alteration by the medications used in its treatment, as has been demonstrated for the major serine protease inhibitors, α-1-antitrypsin, α-2-macroglobulin, and antithrombin III2,3,4,5,6. Their implication of a pathophysiologic involvement is an interesting speculation, especially if a moderating component is considered.. Serine protease inhibitor levels are ...
140 ° செல்சியசு வெப்பநிலையில் தங்கம் புரோமினுடன் வினைபுரிந்து தங்கம் (III) சேர்மத்தை உருவாக்குகிறது. ஆனால் அயோடினுடன் மிக மெதுவாக வினைபுரிந்து ஒற்றை அயோடைடை உருவாக்குகிறது. தங்கம் நேரடியாக கந்தகத்துடன் வினைபுரிவதில்லை. ஆனால் குளோரோ ஆரிக் அமிலத்தின் வழியாக அல்லது நீர்த்த தங்கம்(III) குளோரைடு வழியாக ஐதரசன் சல்பைடு வாயுவை செலுத்தினால் தங்கம்(III) சல்பைடு உருவாகிறது. அறை ...
目前胃癌的细胞毒药物治疗已进入一个平台期。随着分子生物学研究的深入开展,胃癌的诊断及治疗进入了分子水平。大量的基础和临床研究正在探索胃癌的分子靶点包括:人表皮生长因子受体2、人表皮生长因子受体1、哺乳动物雷帕霉素靶蛋白、血管内皮生长因子、血管内皮生长因子2、纤维母细胞生长因子受体2、肝细胞生长因子受体以及聚腺苷酸二磷酸核糖转移酶等。目前,仅有人表皮生长因子受体2的靶向药物曲妥珠单抗及血管内皮生长因子受体2靶向药物ramucirumab被III期临床研究证实在晚期胃癌中有显著疗效,针对上述靶点的其他药物需进一步研究和开发。
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... Levels of protein C, free and total protein S, factor VIII, antithrombin, plasminogen, tissue plasminogen activator (TPA) and ... a) Vascular thrombosis in three or more organs or tissues and. *b) Development of manifestations simultaneously or in less than ... and two antibody blood tests spaced at least three months apart that confirm the presence of either lupus anticoagulant or anti ...
Antithrombin III deficiency. altered coagulation. [14] Falls and hip fracture. related to immobility. [17] ... Three factors are important in the formation of a blood clot within a deep vein-these are the rate of blood flow, the thickness ... "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, ... Protein C and/or S deficiency. congenital; associated with Warfarin necrosis. [14] ...
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... doi:10.1016/s0140-6736(97)06356-3.. *^ Gando, S (1999). "Disseminated intravascular coagulation and sustained systemic ... Laboratory markers consistent with DIC include:[3][7][12] *Characteristic history (this is important because severe liver ... Treatment is mainly directed towards the underlying condition.[2][3] Other measures may include giving platelets, ...
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... Factor V deficiency Prolonged Prolonged Unaffected Unaffected Factor X deficiency as seen in amyloid purpura Prolonged ... Vitamin K deficiency or warfarin Prolonged Normal or mildly prolonged Unaffected Unaffected ... 3] There are several possible risks to treating coagulopathies, such as transfusion-related acute lung injury, acute ...
PITX3 Antithrombin III deficiency; 613118; AT3 Antley-Bixler syndrome; 207410; FGFR2 Antley-Bixler syndrome-like with ... SDHAF1 Mitochondrial complex III deficiency; 124000; BCS1L Mitochondrial complex III deficiency; 124000; UQCRB Mitochondrial ... GATA1 Leukocyte adhesion deficiency; 116920; ITGB2 Leukocyte adhesion deficiency, type III; 612840; KIND3 Leukodystrophy, adult ... SDHD CPT deficiency, hepatic, type IA; 255120; CPT1A CPT deficiency, hepatic, type II; 600649; CPT2 CPT II deficiency, lethal ...
antithrombin III. Inhibits IIa, Xa, and other proteases. Antithrombin III deficiency. heparin cofactor II. Inhibits IIa, ... The three main forms are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency or "Christmas disease") and ... AntithrombinEdit. Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases: thrombin, FIXa, FXa ... III (tissue factor or tissue thromboplastin ). Co-factor of VIIa (formerly known as factor III). ...
Kiehl R, Hellstern P, Wenzel E (January 1987). "Hereditary antithrombin III (AT III) deficiency and atypical localization of a ... including protein S deficiency, activated protein C resistance (Factor V Leiden) and antithrombin III deficiency. Although the ... These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, ... Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of ...
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... "Factor I deficiency (Fibrinogen deficiency) - Canadian Hemophilia Society". www.hemophilia.ca. Retrieved 2015-11-12.. ... Factor I Deficiency. References[edit]. *^ Neerman-Arbez, Marguerite; De Moerloose, Philippe (2007). "Mutations in the ... Gallastegui, N.; Kimble, E. L.; Harrington, T. J. (2015-09-01). "Resolution of fibrinogen deficiency in a patient with ...
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... Balgir RS (2012). "Community expansion and gene geography of sickle cell trait and G6PD deficiency, and natural selection ... 62 (3): 247-62. doi:10.1111/j.1574-695X.2011.00819.x. PMID 21585562.. Unknown parameter ,month=. ignored (tulong)CS1 maint: ... 3] Ang Sickle-cell anaemia ay isang anyo ng sakit na sickle-cell kung saan may homozygosity para sa mutasyon na nagsasanhi ng ...
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... quantitative deficiency).[10] Of those who have severe deficiency (defined as ,1% activity of factor VIII), 45-50% have the ... Haemophilia A (or hemophilia A) is a genetic deficiency in clotting factor VIII, which causes increased bleeding and usually ... Two of the most common differential diagnoses are haemophilia B which is a deficiency in Factor IX and von Willebrand Disease ...
... heparin cofactor activities in a family with hereditary antithrombin III deficiency: evidence for a second heparin cofactor in ... Pizzo SV (1989). "Serpin receptor 1: a hepatic receptor that mediates the clearance of antithrombin III-proteinase complexes". ... Mutations in this gene are associated with heparin cofactor II deficiency. Heparin Cofactor II deficiency can lead to increased ... 2006). "Homozygous deficiency of heparin cofactor II: relevance of P17 glutamate residue in serpins, relationship with ...
Screening for protein C, protein S, or antithrombin III deficiency is sometimes recommended but these are more usually ... 3] Savitz SI, Caplan LR (2005). "Vertebrobasilar disease". N. Engl. J. Med. 352 (25): 2618-26. doi:10.1056/NEJMra041544. PMID ...
Use in antithrombin III deficiency FFP can be used as a source of antithrombin III in patients who are deficient of this ... Greater care should be taken in people with protein S deficiency, IgA deficiency, or heart failure. Fresh frozen plasma is made ... Single-donor plasma is efficacious in the treatment of mild deficiencies of stable clotting factors. It also is of value in ... FFP is the usual treatment for factor V deficiency. Reversal of warfarin effect Patients who are anticoagulated with warfarin ...
... antithrombin iii deficiency MeSH C16.320.099.080 --- bernard-soulier syndrome MeSH C16.320.099.300 --- factor v deficiency MeSH ... factor x deficiency MeSH C16.320.099.325 --- factor xi deficiency MeSH C16.320.099.330 --- factor xii deficiency MeSH C16.320. ... pyruvate dehydrogenase complex deficiency disease MeSH C16.320.565.240 --- cytochrome-c oxidase deficiency MeSH C16.320.565.390 ... pyruvate carboxylase deficiency disease MeSH C16.320.565.150.750 --- pyruvate dehydrogenase complex deficiency disease MeSH ...
Ischemia Thrombotic diseases Degos disease Pseudoxanthoma elasticum Myeloproliferative disorders Antithrombin III deficiency ...
... proteins C and S deficiencies, and antithrombin III deficiency. Hypercoagulability in pregnancy, particularly due to ... However, the other major anticoagulants, protein C and antithrombin III, remain constant. Fibrinolysis is impaired by an ... Both anti-IIa and anti-Xa activity may return up to three hours after protamine reversal, possibly due to release of additional ... Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal ...
Acquired antithrombin deficiency occurs as a result of three distinctly different mechanisms. The first mechanism is increased ... Antithrombin is also termed Antithrombin III (AT III). The designations Antithrombin I through to Antithrombin IV originate in ... Antithrombin III (AT III) refers to a substance in plasma that inactivates thrombin. Antithrombin IV (AT IV) refers to an ... AT III is generally referred to solely as "Antithrombin" and it is Antithrombin III that is discussed in this article. ...
... acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates". Intensive Care Med. 16 (2): 121 ... Acquired protein C deficiency is caused by either depletion of available protein C in plasma or decreased protein C synthesis ( ... Report of the Working Party on Homozygous Protein C Deficiency of the Subcommittee on Protein C and Protein S, International ... Regardless of the underlying cause of purpura fulminans, the mechanism of disease is similar with deficiency in protein C ...
... (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary ... Information on antithrombin from UIUC Non-profit advocacy group for patients and families with antithrombin deficiency. ... "Inherited antithrombin deficiency causing thrombophilia". Thromb Diath Haemorrh. 13:516-520. PMID 14347873. Edward F. Goljan ( ... ATIII binds to thrombin and then forms the thrombin-anti thrombin complex or TAT complex. This is a major natural pathway of ...
... alopecia X linked Congenital amputation Congenital aneurysms of the great vessels Congenital antithrombin III deficiency ... II deficiency Carnitine transporter deficiency Carnitine-acylcarnitine translocase deficiency Carnosinase deficiency ... chain deficiency Complex 4 mitochondrial respiratory chain deficiency Complex 5 mitochondrial respiratory chain deficiency ... Caratolo-Cilio-Pessagno syndrome Carbamoyl phosphate synthetase deficiency Carbamoyl-phosphate synthase I deficiency disease ( ...
... disseminated intravascular coagulation and antithrombin deficiency (though this list is not exhaustive) There are three types ... "Protein S Deficiency. Learn about Protein S Deficiency , Patient". Patient. Retrieved 2016-10-16. "Protein S Deficiency: ... GG frameshift mutation in a family with mixed type I/type III protein S deficiency". Haematologica. 91 (8): 1151-2. PMID ... specifically 3q11.1 Protein S deficiency can also be acquired due to vitamin K deficiency, treatment with warfarin, liver ...
Deficiencies in antithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors. These three ... Antithrombin deficiency, a strong or moderately strong risk factor, carries an annual risk of VTE of only 0.8-1.5%; as such, ... Genetic factors include deficiencies of antithrombin, protein C, and protein S, and factor V Leiden mutation. The underlying ... A three-month course is also recommended for those with proximal DVT provoked by a transient risk factor, and three months is ...
... and an increase in circulating antithrombin. Patients in the late stage had significant thrombocytopenia; deficiency of ... William III lost his mother to the disease when he was only ten years old in 1660, and named his uncle Charles as legal ... 978-3-642-76200-0. .. *^ a b c d e f g Fenner, F. (1988). "The History of Smallpox and its Spread Around the World" (PDF). ... If successful, a red and itchy bump develops at the vaccine site in three or four days. In the first week, the bump becomes a ...
Factor Xa is inhibited by the antithrombin III/heparin system, which also acts to inhibit thrombin. Deficiencies of either ... After the antithrombin III binds to Factor Xa, the Fondaparinux is released and can activate another antithrombin. Another drug ... Fondaparinux binds to antithrombin III and activates the molecule for Factor Xa inhibition. In fact, Fondaparinux imparts an ... Idraparinux also binds antithrombin III, however with a 30-fold increase in affinity as compared to Fondaparinux. Idraparinux ...
... and anti-thrombin III, can manifest as iron-resistant microcytic anemia. Reference ranges[edit]. An example reference range for ... A high transferrin level may indicate an iron deficiency anemia. Levels of serum iron and total iron binding capacity (TIBC) ... III) binding sites. The affinity of transferrin for Fe(III) is extremely high (association constant is 1020 M−1 at pH 7.4)[7] ... The shape of a transferrin receptor resembles a butterfly based on the intersection of three clearly shaped domains.[8] ...
DeMeo DL, Silverman EK (March 2004). "Alpha1-antitrypsin deficiency. 2: genetic aspects of alpha(1)-antitrypsin deficiency: ... The three N-linked glycosylations sites are mainly equipped with so-called diantennary N-glycans. However, one particular site ... An extremely rare form of Pi, termed PiPittsburgh, functions as an antithrombin (a related serpin), due to a mutation ( ... All three products showed minor differences compared to the normal human plasma A1AT, and are introduced during the specific ...
What is antithrombin III deficiency? Meaning of antithrombin III deficiency medical term. What does antithrombin III deficiency ... Looking for online definition of antithrombin III deficiency in the Medical Dictionary? antithrombin III deficiency explanation ... antithrombin III deficiency. Also found in: Wikipedia. antithrombin III deficiency. Congenital antithrombin III deficiency An ... See Antithrombin III. antithrombin III deficiency. An inherited deficiency of certain protein-splitting enzymes (proteases) ...
Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. ... The abnormal gene leads to a low level of the antithrombin III protein. This low level of antithrombin III can cause abnormal ... Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of the ... Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. ...
Antithrombin III activity is markedly potentiated by heparin, the principle mechanism by which both heparin and low molecular ... Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by lysing thrombin and factor Xa. ... encoded search term (Antithrombin III Deficiency) and Antithrombin III Deficiency What to Read Next on Medscape. Related ... have heterozygous antithrombin III deficiency rather than the homozygous state.. Acquired antithrombin III deficiency is a ...
Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary ... Information on antithrombin from UIUC Non-profit advocacy group for patients and families with antithrombin deficiency. ... "Inherited antithrombin deficiency causing thrombophilia". Thromb Diath Haemorrh. 13:516-520. PMID 14347873. Edward F. Goljan ( ... ATIII binds to thrombin and then forms the thrombin-anti thrombin complex or TAT complex. This is a major natural pathway of ...
No sex-related difference is noted in terms of the prevalence of congenital antithrombin III deficiency. Women of childbearing ... Antithrombin III Deficiency Q&A What are the sexual predilections of antithrombin III (ATIII) deficiency?. Updated: Feb 10, ... Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J. 2014 Apr-Jun. 40 (2):141 ... deficiency?) and What are the sexual predilections of antithrombin III (ATIII) deficiency? What to Read Next on Medscape. ...
Arterial thrombosis due to antithrombin III deficiency is uncommon. Ve... more ... This should be performed in all patients with antithrombin III deficiency, especially if they have evidence of arterial ... Antithrombin III Deficiency Q&A What is the role of echocardiography in the workup of antithrombin III (ATIII) deficiency?. ... Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J. 2014 Apr-Jun. 40 (2):141 ...
Antithrombin III Deficiency Q&A What is the role of Doppler ultrasonography in the workup of antithrombin III (ATIII) ... Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J. 2014 Apr-Jun. 40 (2):141 ... Role of antithrombin concentrate in treatment of hereditary antithrombin deficiency. An update. Thromb Haemost. 2009 May. 101(5 ... Mild Antithrombin Deficiency and Risk of Recurrent Venous Thromboembolism: Results from the MEGA follow-up Study. J Thromb ...
Antithrombin III Deficiency Q&A What is the role of Doppler ultrasonography in the workup of antithrombin III (ATIII) ... Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J. 2014 Apr-Jun. 40 (2):141 ... Uses of antithrombin III concentrate in congenital and acquired deficiency states. Transfusion. 1998 May. 38(5):481-98. [ ... Nagaraja D, Christopher R, Tripathi M. Plasma antithrombin III deficiency in ischaemic stroke in the young. Neurol India. 1999 ...
primary: Antithrombin III deficiency - Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... Differentiating Antithrombin III deficiency from other Diseases. Epidemiology and Demographics. Risk Factors. Screening. ... enzyme: G6PD Deficiency - Pyruvate kinase deficiency - Triosephosphate isomerase deficiency hemoglobin: Thalassemia - Sickle- ... Retrieved from "https://www.wikidoc.org/index.php?title=Antithrombin_III_deficiency&oldid=1494831" ...
Antithrombin deficiency in three Japanese families: one novel and two reported point mutations in the antithrombin gene.. ... AT; Ala; Alanine; Antithrombin; Antithrombin deficiency; Arg; Arginine; Asp; Aspartic acid; CL; CM; COS-1 cells; Cell lysates; ... Inherited antithrombin (AT) deficiency is associated with a predisposition to familial venous thromboembolic disease. We ... We analyzed the SERPINC1 gene in three patients. Additionally, we expressed the three mutants in the COS-1 cells and compared ...
What is antithrombin-III deficiency? Meaning of antithrombin-III deficiency medical term. What does antithrombin-III deficiency ... Looking for online definition of antithrombin-III deficiency in the Medical Dictionary? antithrombin-III deficiency explanation ... antithrombin-III deficiency. Also found in: Dictionary, Thesaurus, Legal, Financial, Encyclopedia. antithrombin-III deficiency ... medical-dictionary.thefreedictionary.com/antithrombin-III+deficiency,antithrombin-III deficiency,/a,. *Facebook ...
Antithrombin (AT III) Deficiency. Posted by Dr. Chris. What is antithrombin deficiency?. Antithrombin deficiency is a condition ... Types of Antithrombin Deficiency. There are two types of antithrombin deficiency - type I and type II. ... Causes of Antithrombin Deficiency. Antithrombin deficiency can be inherited or acquired. Inherited cases are usually present ... With type II antithrombin deficiency, the quantity of antithrombin is normal but it does not function as it should. The ...
Congenital antithrombin III deficiency. Deficiency - antithrombin III - congenital; Antithrombin III deficiency - congenital ... Antithrombin III (AT III) is a protein that helps control blood clotting. A blood test can determine the amount of AT III ... The abnormal gene leads to a low level of the antithrombin III protein. This low level of antithrombin III can cause abnormal ... Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of the ...
Antithrombin Deficiency, type II) with alternative diagnoses, full-text book chapters, misdiagnosis, research treatments, ... and treatment information for Antithrombin 3 Deficiency, type II ( ... Antithrombin Deficiency, type II: »Introduction: Antithrombin Deficiency, type II »Symptoms of Antithrombin Deficiency, type II ... Antithrombin Deficiency, type II »Symptoms of Antithrombin Deficiency, type II »Treatments for Antithrombin Deficiency, type II ...
Among the causes, predisposing an individual to CTPV is natural anticoagulant protein C and antithrombin III deficiencies. ... We discuss a case of a nine-year-old male child diagnosed as CTPV secondary to protein C and antithrombin III deficiency who ... cavernous transformation, portal vein, portal hypertension, protein c deficiency, anti thrombin iii deficiency, pediatric, ... Cavernous Transformation of Portal Vein in the Setting of Protein C and Anti-thrombin III Deficiency Mahwish Nasim , Bushra ...
He was found to be homozygous for the prothrombin G20210A mutation with mild deficiency for antithrombin III (AT III 73%, ... However, combinations of factor V Leiden and protein C deficiency, protein S deficiency or AT III deficiency greatly increase ... Concomitant homozygosity for the prothrombin gene variant with mild deficiency of antithrombin III in a patient with multiple ... with mildly reduced levels of anti-thrombin III (AT III). Subsequent testing of his father and brother revealed heterozygosity ...
hypercoagulable state/thrombophilia due to deficiency in antithrombin III. * *antithrombin III, an anticoagulant *inhibits ... MB BULLETS Step 2 & 3 For 3rd and 4th Year Med Students ... liver disease (antithrombin III is synthesized in the liver). * ... Male: 4.3-5.9 million/mm3. Female: 3.5-5.5 million mm3. ... Bicarbonate (HCO3-). 22-28 mEq/L. Magnesium (Mg2+). 1.5-2.0 mEq ...
THROMBATE III® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and ... Because THROMBATE III is made from human blood, it may carry a risk of transmitting infectious agents, eg, viruses, the variant ... Please see full Prescribing Information for THROMBATE III.. You are encouraged to report negative side effects of prescription ... effect of heparin is enhanced by concurrent treatment with THROMBATE III in patients with hereditary AT deficiency. Thus, in ...
Helping you find trustworthy answers on Factor IX Deficiency , Latest evidence made easy ... Find all the evidence you need on Factor IX Deficiency via the Trip Database. ... Antithrombin III-deficient patients (...) . Previous References Gaman AM, Gaman GD. Deficiency Of Antithrombin III (AT III) - ... Antithrombin III Deficiency (Treatment) of vitamin K-dependent procoagulant factors (II, VII, IX, X) is reduced adequately for ...
Genetics Home Reference related topics: Hereditary antithrombin deficiency Drug Information available for: Antithrombin III ... Experimental: Anti-thrombin III Drug: Anti-thrombin III Intraoperatively- (correcting to 100%) according to the following ... Antithrombin III Deficiency. Blood Coagulation Disorders, Inherited. Blood Coagulation Disorders. Hematologic Diseases. Blood ... Antithrombins. Antithrombin III. Hemostatics. Coagulants. Serine Proteinase Inhibitors. Protease Inhibitors. Enzyme Inhibitors ...
Antithrombin III activity was estimated by a chromogenic assay. Hence, antithrombin III deficiency, though rare, should be ... A deficiency of plasma antithrombin III has been identified as a potential risk factor for thrombosis. In a pilot study of 56 ... Nagaraja D, Christopher R, Tripathi M. Plasma antithrombin III deficiency in ischaemic stroke in the young. Neurology India. ... we detected only one case of plasma antithrombin III deficiency. ... Plasma antithrombin III deficiency in ischaemic stroke in the ...
Antithrombin III replacement in animal models of acquired antithrombin III deficiency. Emerson, T. E. Jr ... Acquired antithrombin III deficiency-rationale for replacement therapy. Introduction and overview-What are the questions?. ... Acquired antithrombin III deficiency secondary to asparaginase therapy in childhood acute lymphoblastic leukaemia. Andrew, M.; ... Panel Discussion: Rationale for replacement therapy for acquired antithrombin III deficiency. Blajchman, Morris A. ...
The results indicate that antithrombin III-heparin cofactor activity is significantly lower... ... The antithrombin III-heparin cofactor activity of 65 baboons and 130 healthy human subjects was measured. ... Antithrombin III deficiency in a Dutch family.J. Clin. Path., 26: 532-538.PubMedGoogle Scholar ... Deficiency of antithrombin III activity associated with hereditary thrombosis tendency.J. Med., 3: 349-358.Google Scholar ...
primary: Antithrombin III deficiency. *Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... Levels of protein C, free and total protein S, factor VIII, antithrombin, plasminogen, tissue plasminogen activator (TPA) and ... a) Vascular thrombosis in three or more organs or tissues and. *b) Development of manifestations simultaneously or in less than ... and two antibody blood tests spaced at least three months apart that confirm the presence of either lupus anticoagulant or anti ...
Antithrombin III deficiency. altered coagulation. [14] Falls and hip fracture. related to immobility. [17] ... Three factors are important in the formation of a blood clot within a deep vein-these are the rate of blood flow, the thickness ... "Virchows triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, ... Protein C and/or S deficiency. congenital; associated with Warfarin necrosis. [14] ...
  • Drugs that may increase AT-III levels include anabolic steroids, gemfibrozil, and warfarin (Coumadin). (thefreedictionary.com)
  • Patients with protein C and S deficiencies can develop warfarin-induced skin necrosis when placed on warfarin, since protein C and S are vitamin K-dependent factors and, hence are suppressed. (medscape.com)
  • Warfarin may be started preoperatively or immediately postoperatively in patients undergoing hip fracture surgery {02}3 . (drugs.com)
  • Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of its development. (wikipedia.org)
  • In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis (blood stream infection) which also involves skin necrosis. (wikipedia.org)
  • Based on the assumption that low levels of protein C are involved in the underlying mechanism, common treatments in this setting include fresh frozen plasma or pure activated protein C. Since the clot-promoting effects of starting administration of 4-hydroxycoumarins are transitory, patients with protein C deficiency or previous warfarin necrosis can still be restarted on these drugs if appropriate measures are taken. (wikipedia.org)
  • Reversal of warfarin effect Patients who are anticoagulated with warfarin are deficient in the functional vitamin K dependent coagulation factors II, VII, IX, and X, as well as proteins C and S. These functional deficiencies can be reversed by the administration of vitamin K. For anticoagulated patients who are actively bleeding or who require emergency surgery prothrombin complex concentrate should be used if available. (wikipedia.org)
  • Defects in SERPINC1 are the cause of antithrombin III deficiency (AT3D) [MIM: (abcam.com)
  • This protein shares homology with antithrombin and other members of the alpha 1-antitrypsin superfamily. (wikipedia.org)
  • Protease inhibitory activity in blood plasma was first reported in the late 1800s, but it was not until the 1950s that the serpins antithrombin and alpha 1-antitrypsin were isolated. (wikipedia.org)
  • When the blood contains inadequate amounts of A1AT or functionally defective A1AT (such as in alpha-1 antitrypsin deficiency), neutrophil elastase is excessively free to break down elastin, degrading the elasticity of the lungs, which results in respiratory complications, such as chronic obstructive pulmonary disease, in adults. (wikipedia.org)
  • The density of yellow coloration is directly proportional to the amount of antithrombin III captured in plate. (abcam.com)
  • GTC states that one genetically modified goat can produce the same amount of antithrombin in a year as 90,000 blood donations. (wikipedia.org)
  • Three factors are important in the formation of a blood clot within a deep vein-these are the rate of blood flow, the thickness of the blood and qualities of the vessel wall. (wikipedia.org)
  • Common conditions that result in acquired antithrombin III deficiency include disseminated intravascular coagulation (DIC) , microangiopathic hemolytic anemias due to endothelial damage (ie, hemolytic-uremic syndrome ), veno-occlusive disease (VOD) (in patients undergoing bone marrow transplantation ), sepsis, liver disease, and nephrotic syndrome. (medscape.com)
  • white lines (leukonychia) that extend all the way across the nail and lie parallel to the lunula The main signs of nephrotic syndrome are: A proteinuria of greater than 3.5 g /24 h /1.73 m2 (between 3 and 3.5 g/24 h /1.73 m2 is considered to be proteinuria in the nephrotic range) or greater than 40 mg/h/m2 in children. (wikipedia.org)
  • The claims of this new patent relate to a method of treating subjects having an antithrombin III deficiency or inflammation with the administration of recombinant antithrombin III produced in the mammary gland of a non-human mammal. (thefreedictionary.com)
  • [3] There are several possible risks to treating coagulopathies, such as transfusion-related acute lung injury , acute respiratory distress syndrome , multiple organ dysfunction syndrome , major hemorrhage , and venous thromboembolism . (wikipedia.org)
  • [ 3 ] One study assessed the performance of four4 clinical decision rules in addition to D-dimer testing to exclude acute PE. (medscape.com)
  • However, a prospective study did find free protein S deficiency in 23% of young patients with stroke of uncertain cause, but this finding could be associated with higher levels of C4b (an acute phase reactant that decreases free protein S levels). (medscape.com)
  • Acute coronary syndrome in a young woman with antithrombin III deficiency. (nih.gov)
  • The three factors of Virchow's triad-venous stasis, hypercoagulability, and changes in the endothelial blood vessel lining (such as physical damage or endothelial activation)-contribute to DVT and are used to explain its formation. (wikipedia.org)
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