Antithrombin III Deficiency
Antithrombin III
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)
Antithrombins
Methionine Adenosyltransferase
Cytochromes b
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.
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) Antithrombin III (ATIII) deficiency is a rare genetic disorder that affects the blood's ability to form clots and regulate blood platelet activity. It occurs when the body does not produce enough or produces abnormal antithrombin III protein, which is essential for maintaining normal blood clotting function.
People with ATIII deficiency may experience a range of symptoms, including:
* Prolonged bleeding after injuries or surgery
* Spontaneous bruising or petechiae (small red or purple spots on the skin)
* Nosebleeds or easy bruising
* Bleeding into the joints (hemarthrosis)
* Easy bleeding in the gastrointestinal tract
ATIII deficiency can be caused by inherited mutations in the ATIII gene or acquired due to certain medical conditions, such as liver disease, sepsis, or autoimmune disorders.
Diagnosis of ATIII deficiency involves blood tests to measure the level of antithrombin III activity and genetic testing to identify mutations in the ATIII gene. Treatment typically involves infusions of antithrombin III concentrates to replace the missing or abnormal protein, and management of underlying conditions that may be contributing to the deficiency.
In rare cases, individuals with severe ATIII deficiency may require regular infusions throughout their lives to prevent bleeding complications. However, with proper treatment and close monitoring, many people with ATIII deficiency can lead normal lives without significant limitations.
Protein S deficiency refers to a condition where the body does not produce enough protein S, a protein that plays a crucial role in blood clotting and platelet function. Protein S deficiency can increase the risk of developing venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE).
Protein S is a vitamin K-dependent protein that is produced in the liver and circulates in the blood. It works by inhibiting the activity of thrombin, a clotting factor that helps to form blood clots. In people with protein S deficiency, there may be an overactivation of thrombin, leading to an increased risk of blood clots forming.
Protein S deficiency can be caused by several factors, including genetic mutations, vitamin K deficiency, and certain medical conditions such as liver disease or cancer. It is usually diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies.
Treatment for protein S deficiency typically involves replacing the missing protein with intravenous immune globulin (IVIG) or recombinant human protein S. In some cases, medications that inhibit thrombin activity, such as heparins or direct thrombin inhibitors, may also be used to reduce the risk of blood clots forming.
Preventing protein S deficiency involves ensuring adequate intake of vitamin K through dietary sources or supplements, managing underlying medical conditions, and avoiding factors that can increase the risk of bleeding or thrombosis, such as smoking, obesity, and inactivity.
In summary, protein S deficiency is a condition characterized by low levels of protein S, which increases the risk of developing blood clots. It can be caused by several factors and treated with replacement therapy or medications that inhibit thrombin activity. Prevention involves ensuring adequate vitamin K intake and managing underlying medical conditions.
Thrombosis is a medical condition where a blood clot (thrombus) forms inside a blood vessel, and it can occur in both arteries and veins. Thrombosis can cause blockages in the affected blood vessels, which can lead to serious health problems such as heart attack, stroke, or pulmonary embolism.
There are several types of thrombosis, including:
1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.
The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:
1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic
Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.
Thrombophlebitis is a type of inflammation that occurs in the veins, specifically in the walls of the veins. It is caused by the formation of a blood clot or thrombus within the vein, which can lead to swelling and irritation of the vein wall. Thrombophlebitis can occur in any vein in the body, but it most commonly affects the superficial veins near the surface of the skin.
There are two main types of thrombophlebitis:
1. Superficial thrombophlebitis: This type of thrombophlebitis affects the superficial veins, which are located just under the skin. It is often caused by injury or trauma to the vein, and it can cause redness, swelling, and pain in the affected area.
2. Deep vein thrombophlebitis: This type of thrombophlebitis affects the deep veins, which are located deeper in the body. It is often caused by blood clots that form in the legs or arms, and it can cause symptoms such as pain, swelling, and warmth in the affected limb.
Thrombophlebitis can be caused by a variety of factors, including:
1. Injury or trauma to the vein
2. Blood clotting disorders
3. Prolonged bed rest or immobility
4. Surgery or medical procedures
5. Certain medications, such as hormone replacement therapy or chemotherapy
6. Age, as the risk of developing thrombophlebitis increases with age
7. Family history of blood clotting disorders
8. Increased pressure on the veins, such as during pregnancy or obesity
Thrombophlebitis can be diagnosed through a variety of tests, including:
1. Ultrasound: This test uses sound waves to create images of the veins and can help identify blood clots or inflammation.
2. Venography: This test involves injecting a dye into the vein to make it visible under X-ray imaging.
3. Blood tests: These can be used to check for signs of blood clotting disorders or other underlying conditions that may be contributing to the development of thrombophlebitis.
Treatment for thrombophlebitis typically involves anticoagulation therapy, which is designed to prevent the blood clot from growing larger and to prevent new clots from forming. This can involve medications such as heparin or warfarin, or other drugs that work by blocking the production of clots. In some cases, a filter may be placed in the vena cava, the large vein that carries blood from the lower body to the heart, to prevent clots from traveling to the lungs.
In addition to anticoagulation therapy, treatment for thrombophlebitis may also include:
1. Elevation of the affected limb to reduce swelling
2. Compression stockings to help reduce swelling and improve blood flow
3. Pain management with medication or heat or cold applications
4. Antibiotics if there is an infection
5. Rest and avoiding strenuous activities until the symptoms resolve.
In some cases, surgery may be necessary to remove the clot or repair the affected vein.
It's important to note that early diagnosis and treatment of thrombophlebitis can help prevent complications such as infection, inflammation, or damage to the valves in the affected vein. If you suspect you or someone else may have thrombophlebitis, it is important to seek medical attention promptly.
Antithrombin III deficiency
... (abbreviated ATIII deficiency) is a deficiency of antithrombin III. This deficiency may be ... Antithrombin Găman AM, Găman GD (2014). "Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature". ... Testing for antithrombin activity can confirm deficiency if the levels are less than 70%. Deficiency can result from genetic ... The causes of acquired antithrombin deficiency are easier to find than the hereditary deficiency. The prevalence of ...
List of OMIM disorder codes
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
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. ...
Warfarin necrosis
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 ...
Cardiopulmonary bypass
A small percentage of patients, such as those with an antithrombin III deficiency, may exhibit resistance to heparin. In these ... or other blood products such as recombinant anti-thrombin III to achieve adequate anticoagulation. A persistent left superior ... For type III reactions, heparin is redosed and the patient may need to go back on bypass. CPB may contribute to immediate ... There are three types of protamine reactions, and each may cause life-threatening hypotension (type I), anaphylaxis (type II), ...
Heparin cofactor II
... heparin cofactor activities in a family with hereditary antithrombin III deficiency: evidence for a second heparin cofactor in ... The structure is similar to antithrombin III (ATIII), which was known to effectively inhibit thrombin as well as coagulation ... This protein shares homology with antithrombin III and other members of the alpha-1 antitrypsin superfamily. Mutations in this ... Pizzo SV (1989). "Serpin receptor 1: a hepatic receptor that mediates the clearance of antithrombin III-proteinase complexes". ...
Reza Razavi
"Pulmonary arterial thrombosis in a neonate with homozygous deficiency of antithrombin III: successful outcome following ... "Pulmonary arterial thrombosis in a neonate with homozygous deficiency of antithrombin III: successful outcome following ... pulmonary thrombectomy and infusions of antithrombin III concentrate". His most cited article is the "Percutaneous pulmonary ... pulmonary thrombectomy and infusions of antithrombin III concentrate". Cardiology in the Young. 10 (3): 275-278. doi:10.1017/ ...
Thrombophilia
The main ones are antithrombin III deficiency, protein C deficiency and protein S deficiency. Milder rare congenital ... antithrombin deficiency, was recognized in 1965 by the Norwegian hematologist Olav Egeberg. Protein C deficiency followed in ... Antithrombin deficiency is present in 0.2% of the general population and 0.5-7.5% of people with venous thrombosis. Protein C ... The first major form of thrombophilia to be identified by medical science, antithrombin deficiency, was identified in 1965, ...
Superficial vein thrombosis
... and antithrombin III and factor XII deficiency. The mechanism for the development of an SVT depends upon the specific etiology ... SVTs that occur within the great saphenous vein within 3 cm of the saphenofemoral junction are considered to be equivalent in ... Anticoagulation is also used for intermediate risk SVTs that are greater than 3 cm from the saphenofemoral junction or are ... Anticoagulation for high risk SVTs includes the use of vitamin K antagonists or novel oral anticoagulants (NOACs) for 3 months ...
Phenprocoumon
... antithrombin III deficiency, atrial fibrillation (a kind of abnormal heart rhythm) with artery embolisms, after venous ... Inhibiting this enzyme effectively creates a vitamin K deficiency, blocking activation of the coagulation factors. After 36 to ... intervals between measurements are increased to twice or three times a week for a week or two, then to two to four weeks if the ... 6 (3): 129-135. doi:10.1007/s007720100143. S2CID 44842896. Karow T, Lang-Roth R (2021). Pharmakologie und Toxikologie (in ...
Fresh frozen plasma
Use in antithrombin III deficiency: FFP can be used as a source of antithrombin III in patients who are deficient of this ... There are purified, human derived, as well as recombinant forms of antithrombin III available in the US. Treatment of ... 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 ...
List of MeSH codes (C16)
... 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 ...
Multifocal stenosing ulceration of the small intestine
Ischemia Thrombotic diseases Degos disease Pseudoxanthoma elasticum Myeloproliferative disorders Antithrombin III deficiency ...
Pre-existing disease in pregnancy
Examples include: Factor V Leiden Prothrombin G20210A Protein C deficiency Protein S deficiency Antithrombin III deficiency ... Journal of Acquired Immune Deficiency Syndromes. 23 (3): 246-254. doi:10.1097/00042560-200003010-00006. PMID 10839660. S2CID ... 108 (3 Pt 1): 667-81. doi:10.1097/01.AOG.0000235059.84188.9c. PMID 16946229. Louik, C; Schatz, M; Hernández-Díaz, S; Werler, MM ... 18 (3): 32. doi:10.1007/s11920-016-0664-7. ISSN 1535-1645. PMID 26879925. S2CID 38045296. Kwon, Helen L.; Triche, Elizabeth W ...
Hypercoagulability in pregnancy
... 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 ...
Purpura fulminans
... 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 ...
Feminizing hormone therapy
... antithrombin III, and protein C or S deficiency) are not absolute contraindications for hormonal therapy. A 2018 cohort study ... June 2002). "Androgen deficiency, Meibomian gland dysfunction, and evaporative dry eye". Annals of the New York Academy of ... A report of three cases". Andrologia. 21 (5): 456-461. doi:10.1111/j.1439-0272.1989.tb02447.x. PMID 2530920. S2CID 30370123. ... The Endocrine Society recommends that patients have blood tests every three months in the first year of HRT for estradiol and ...
List of diseases (C)
... 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 ... adrenal hyperplasia due to 11β-hydroxylase deficiency Congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency ...
Protein S deficiency
... 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 ...
Deep vein thrombosis
Deficiencies of three proteins that normally prevent blood from clotting-protein C, protein S, and antithrombin-contribute to ... These deficiencies in antithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors. They ... Genetic factors include non-O blood type, deficiencies of antithrombin, protein C, and protein S and the mutations of factor V ... Three compression ultrasound scanning techniques can be used, with two of the three methods requiring a second ultrasound some ...
Serpin
Austin RC, Rachubinski RA, Ofosu FA, Blajchman MA (May 1991). "Antithrombin-III-Hamilton, Ala 382 to Thr: an antithrombin-III ... October 2000). "Complete antithrombin deficiency in mice results in embryonic lethality". The Journal of Clinical Investigation ... "Primary structure of antithrombin III (heparin cofactor): partial homology between alpha-1-antitrypsin and antithrombin III". ... Petitou M, van Boeckel CA (June 2004). "A synthetic antithrombin III binding pentasaccharide is now a drug! What comes next?". ...
SRD5A3-CDG
... clotting due to antithrombin III activity Hypertrichosis or excessive hair growth Hypothyroidism Growth hormone deficiency The ... patient-derived cell models could be crucial in understanding the impact of polyprenol reductase enzyme deficiency and be used ... doi:10.1038/s41431-020-0647-3. PMC 7609305. PMID 32424323. "Chromosome 4: Medline Plus Genetics". Medline Plus. US National ... doi:10.1038/s41431-020-0647-3. PMC 7609305. PMID 32424323. "Disease Models". Cure SRD5A3. 30 August 2020. Retrieved 9 October ...
Prothrombinase
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 ...
Transferrin
... and anti-thrombin III, can manifest as iron-resistant microcytic anemia. An example reference range for transferrin is 204-360 ... 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) but ... Drosophila melanogaster has three transferrin genes and is highly divergent from all other model clades, Ciona intestinalis one ...
List of MeSH codes (C15)
... antithrombin iii deficiency MeSH C15.378.100.425.080 - bernard-soulier syndrome MeSH C15.378.100.425.300 - factor v deficiency ... antithrombin iii deficiency MeSH C15.378.147.333 - dysgammaglobulinemia MeSH C15.378.147.333.500 - iga deficiency MeSH C15.378. ... antithrombin iii deficiency MeSH C15.378.925.220 - disseminated intravascular coagulation MeSH C15.378.925.795 - protein c ... factor v deficiency MeSH C15.378.100.141.310 - factor vii deficiency MeSH C15.378.100.141.320 - factor x deficiency MeSH ...
Reptilase time
Unlike thrombin, reptilase is resistant to inhibition by antithrombin III. Thus, the reptilase time is not prolonged in blood ... Reptilase time (RT) is a blood test used to detect deficiency or abnormalities in fibrinogen, especially in cases of heparin ...
Activated protein C resistance
... antithrombin deficiency, protein C deficiency, or protein S deficiency), should be considered for lifelong oral anticoagulation ... 3 (1): 13-24. doi:10.1055/s-2003-38329. PMID 15199489. Asscheman H, T'Sjoen G, Lemaire A, Mas M, Meriggiola MC, Mueller A, Kuhn ... 90 (3): 642-72. doi:10.1016/j.fertnstert.2007.07.1298. PMID 17923128. Morimont L, Haguet H, Dogné JM, Gaspard U, Douxfils J ( ... 3 (1): 33-46. doi:10.1055/s-2003-38331. PMID 15199491. Kujovich JL (January 2011). "Factor V Leiden thrombophilia". Genet Med. ...
Alpha-1 antitrypsin
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 ( ... The presence of deviant bands on IEF can signify the presence of alpha-1 antitrypsin deficiency. Since the number of identified ...
Anticoagulant
UFH binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation. The ... or after surgery or birthing in patients with hereditary antithrombin deficiency. Many other anticoagulants exist, for use in ... Allingstrup M, Wetterslev J, Ravn FB, Møller AM, Afshari A (April 2016). "Antithrombin III for critically ill patients: a ... The antithrombin protein itself is used as a protein therapeutic that can be purified from human plasma or produced ...
Inverted repeat
The antithrombin III gene's coding region is an example of an imperfect inverted repeat as shown in the figure on the right. ... Specifically, the missense mutation would lead to a defective gene and a deficiency in antithrombin which could result in the ... The three main repeats which are largely found in particular DNA constructs include the closely precise homopurine- ... Sets 1 and 2 are the stem of stem-loop A and are part of the loop for stem-loop B. Similarly, sets 3 and 4 are the stem for ...
Factor XIII
... Deficiency is also known as Laki-Lorand factor, after Kalman Laki and Laszlo Lorand, the scientists who first ... antithrombin and TFPI are the most relevant proteolytic inhibitors of the active factor XIIIa. α2-macroglobulin is a ... Deficiency of Factor XIII (FXIIID), while generally rare, does occur, with Iran having the highest global incidence of the ... Deficiency of XIII worsens clot stability and increases bleeding tendency. Human XIII is a heterotetramer. It consists of 2 ...
Cerebral venous sinus thrombosis
... deficiency of protein C, protein S or antithrombin, or related problems Nephrotic syndrome, a kidney problem causing protein ... The three major mechanisms for such an imbalance are enumerated in Virchow's triad: alterations in normal blood flow, injury to ... If the thrombosis developed under temporary circumstances (e.g. pregnancy), three months are regarded as sufficient. If the ... 4 (3): 419-30. doi:10.1161/01.str.4.3.419. PMID 4713031. Ribes MF (1825). "Des recherches faites sur la phlebite". Rev. Med. Fr ...
Acute fatty liver of pregnancy
Castro MA, Goodwin TM, Shaw KJ, Ouzounian JG, McGehee WG (1996). "Disseminated intravascular coagulation and antithrombin III ... Deficiency of LCHAD (3-hydroxyacyl-CoA dehydrogenase) leads to an accumulation of medium and long chain fatty acids. When this ... LCHAD deficiency is autosomal recessive in inheritance and mothers are often found to be heterozygous for the affected mutation ... deficiency in infants". Advances in Neonatal Care. 4 (1): 26-32. doi:10.1016/j.adnc.2003.12.001. PMID 14988877. S2CID 29356240 ...
Factor X
Deficiency of vitamin K or antagonism by warfarin (or similar medication) leads to the production of an inactive factor X. In ... Factor Xa plays a key role in all three of these stages. In stage 1, Factor VII binds to the transmembrane protein TF on the ... antithrombin (AT) to inactivate several coagulation factors IIa, Xa, XIa and XIIa. The affinity of unfractionated heparin and ... Apart from congenital deficiency, low factor X levels may occur occasionally in a number of disease states. For example, factor ...
Coagulation
The three main forms are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency or "Christmas disease") and ... Quantitative or qualitative deficiency of antithrombin (inborn or acquired, e.g., in proteinuria) leads to thrombophilia.[ ... Vitamin K deficiency from other causes (e.g., in malabsorption) or impaired vitamin K metabolism in disease (e.g., in liver ... Quantitative or qualitative deficiency of either (protein C or protein S) may lead to thrombophilia (a tendency to develop ...
Sepsis
Within the first three hours, someone with sepsis should have received antibiotics and, intravenous fluids if there is evidence ... Vasopressin can be used in septic shock because studies have shown that there is a relative deficiency of vasopressin when ... On the other hand, the use of antithrombin to treat disseminated intravascular coagulation is also not useful. Meanwhile, the ... Within the first three hours of suspected sepsis, diagnostic studies should include white blood cell counts, measuring serum ...
Renal vein thrombosis
Cystathionine beta synthase deficiency, also known as homocystinuria, is an autosomal recessive inherited disorder in which the ... Rudolf Virchow, was the first to describe the physiological mechanism behind venous thrombosis (blood clots) using three ... and a decrease in coagulation inhibiters like antithrombin. Hypercoagulability can be inherited and/or acquired. ... vitamin B12 and folic acid deficiency. Factor V Leiden and mutations of the prothrombin gene are the two most common genetic ...
Acute-phase protein
Chua E, Clague JE, Sharma AK, Horan MA, Lombard M (October 1999). "Serum transferrin receptor assay in iron deficiency anaemia ... Examples include albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin. The decrease of such ... 3 (1): 118-27. doi:10.4103/0975-7406.76489. PMC 3053509. PMID 21430962. Abbas A, Lichtman A, Pillai S (2012). Basic immunology ... 156 (3): 488-94. doi:10.1111/j.1365-2249.2009.03929.x. PMC 2691978. PMID 19438602. Lippincott's Illustrated Reviews: Immunology ...
CSL Behring
... freeze-dried human antithrombin III concentrate Streptase, freeze-dried streptokinase Wound healing Beriplast P Combi-Set, ... "CSL Behring , Immune Deficiency Foundation". primaryimmune.org. Retrieved 2022-03-27. "CSL Behring's Global Products List". www ... primary immune deficiencies (PIDD); hereditary angioedema; inherited respiratory disease; and neurological disorders. The ... for acute bleeding episodes in patients with congenital fibrinogen deficiency and the Swiss government awarded CSL Behring the ...
Venous thrombosis
... and polycythemia vera Chemotherapy Heart failure Antithrombin deficiency Protein C deficiency Protein S deficiency (type I) ... 9 (49): iii-iv, ix-x, 1-78. doi:10.3310/hta9490. PMID 16336844. Lederle, FA; Zylla, D; Macdonald, R; Wilt, TJ (2011-11-01). " ... The three factors of stasis, hypercoagulability, and alterations in the blood vessel wall represent Virchow's triad, and ... The American College of Physicians (ACP) gave three strong recommendations with moderate quality evidence on VTE prevention in ...
Pharmacodynamics of estradiol
Three escalating doses (10 mg, 20 mg, 40 mg) of intramuscular estradiol valerate were administered every 2 weeks in 12 patients ... Eberhard Nieschlag; Hermann M. Behre; Susan Nieschlag (26 July 2012). Testosterone: Action, Deficiency, Substitution. Cambridge ... has been found to increase markers of coagulation and plasminogen system activation such as levels of thrombin-antithrombin ... a phase III randomised trial". Br J Urol. 52 (3): 208-15. doi:10.1111/j.1464-410x.1980.tb02961.x. PMID 7000222. Sander S, ...
Budd-Chiari syndrome
... protein S deficiency, the Factor V Leiden mutation, hereditary anti-thrombin deficiency and prothrombin mutation G20210A. An ... Examples of genetic tendencies include protein C deficiency, ... In general, nearly 2/3 of patients with Budd-Chiari are alive ... 232 (3): 340-52. doi:10.1097/00000658-200009000-00006. PMC 1421148. PMID 10973384. "Ascites". The Lecturio Medical Concept ...
Syndecan
This deficiency is attributed to the lack of syndecan 1 expression. Syndecan 4 also interacts with integrin proteins for cell- ... More specifically, these core proteins carry three to five heparan sulfate and chondroitin sulfate chains, i.e. they are ... fibronectin and antithrombin-1. Interactions between fibronectin and some syndecans can be modulated by the extracellular ... These myeloma cells had a deficiency in the ability to adhere to one another in a rotation-mediated aggregation matrix. ...
Congenital antithrombin III deficiency: MedlinePlus Medical Encyclopedia
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 Deficiency: Practice Essentials, Pathophysiology, Epidemiology
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 ... have heterozygous antithrombin III deficiency rather than the homozygous state.. Acquired antithrombin III deficiency is a ...
Antithrombin III deficiency - wikidoc
Differentiating Antithrombin III deficiency from other Diseases. Epidemiology and Demographics. Risk Factors. Screening. ... Retrieved from "https://www.wikidoc.org/index.php?title=Antithrombin_III_deficiency&oldid=1626862" ... Synonyms and keywords: Antithrombin 3 deficiency, Congenital AT-III Deficiancy, Overview. Historical Perspective. ...
Congenital antithrombin III deficiency | Lima Memorial Health System
Congenital antithrombin III deficiency. Site Map Congenital antithrombin III deficiency. Deficiency - antithrombin 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 ... Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. ...
A patient defines the interstitial 1q deletion syndrome characterized by antithrombin III deficiency - PubMed
A patient defines the interstitial 1q deletion syndrome characterized by antithrombin III deficiency R Pallotta 1 , L Dalprà, M ... A patient defines the interstitial 1q deletion syndrome characterized by antithrombin III deficiency R Pallotta et al. Am J Med ... As expected, antithrombin III (AT3, 1q23-q25.1) serum level and activity were half of normal. We performed a review of the ... and antithrombin III. Takano T, Yamanouchi Y, Mori Y, Kudo S, Nakayama T, Sugiura M, Hashira S, Abe T. Takano T, et al. Am J ...
Hereditary antithrombin deficiency: MedlinePlus Genetics
Hereditary antithrombin deficiency is a disorder of blood clotting. Explore symptoms, inheritance, genetics of this condition. ... This gene provides instructions for producing a protein called antithrombin (previously known as antithrombin III). This ... medlineplus.gov/genetics/condition/hereditary-antithrombin-deficiency/ Hereditary antithrombin deficiency. ... Hereditary antithrombin deficiency is a disorder of blood clotting. People with this condition are at higher than average risk ...
Antithrombin III Deficiency? - NEJS
High frequency of antithrombin 3 and protein C deficiency following autologous bone marrow transplantation for lymphoma<...
Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement ... Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement ... Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement ... Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement ...
Hereditary antithrombin deficiency (Concept Id: C0272375)
- MedGen - NCBI
Two categories of AT-III deficiency have been defined on the basis of AT-III antigen levels in the plasma of affected ... The majority of AT-III deficiency families belong in the type I (classic) deficiency group and have a quantitatively abnormal ... The second category of AT-III deficiency has been termed type II (functional) deficiency. Affected individuals from these ... Type I (low functional and immunologic antithrombin) has been subdivided into subtype Ia (reduced levels of normal antithrombin ...
Pulmonary embolus: MedlinePlus Medical Encyclopedia
Etiology of Pulmonary Embolism
Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other risk factors. Deficiency of these ... such as antithrombin III, protein C, or protein S deficiency. [16] In 1997, Nuss et al reported that 70% of children with a ... Is the Field of Electrophysiology Stuck? Three Hot Topics Reviewed * JAK-Inhibitor Safety in Adolescents With AD: Long-Term ... Three primary influences predispose a patient to blood clot formation; these form the so-called Virchow triad, which consists ...
DeCS - Termos Novos
Livedoid vasculopathy - About the Disease - Genetic and Rare Diseases Information Center
Biomarkers Search
Familial antithrombin III deficiency.. Winter JH; Fenech A; Ridley W; Bennett B; Cumming AM; Mackie M; Douglas AS. Q J Med; ... Hereditary antithrombin III deficiency and pregnancy: report of two cases and review of the literature.. Nelson DM; Stempel LE ... 6. Hereditary deficiency of antithrombin III, protein C and protein S: prevalence in patients with a history of venous ... 5. [Antithrombin III deficiency and tendency to thrombosis (authors transl)].. Lechner K; Thaler E; Niessner H; Nowotny C; ...
DailyMed - HEPARIN SODIUM injection, solution
Patients with hereditary antithrombin III deficiency receiving concurrent antithrombin III therapy. - The anticoagulant effect ... Antithrombin III (human) - The anticoagulant effect of heparin is enhanced by concurrent treatment with antithrombin III (human ... Antithrombin III, to induce a conformational change, which markedly enhances the serine protease activity of Antithrombin III, ... and patients with antithrombin III deficiency. Close monitoring of coagulation tests is recommended in these cases. Adjustment ...
RFA-DD-07-005: Thrombosis and Hemostasis Centers Research and Prevention Network (U01)
Factor II), Protein C deficiency, Protein S deficiency Antithrombin III deficiency). *Provide evidence that the Principal ... Deficiencies in anticoagulant proteins C, S, or antithrombin III are responsible for less than 10% of cases of VTE. ... and deficiencies of proteins C, S, and antithrombin III have been implicated in fetal loss. ... Section III. Eligibility Information 1. Eligible Applicants A. Eligible Institutions 2.Cost Sharing or Matching. 3.Other - ...
Classifications for Combined Hormonal Contraceptives | CDC
Thrombotic risk of women with hereditary antithrombin III-, protein C- and protein S-deficiency taking oral contraceptive ... Gene-gene and gene-environment interactions determine risk of thrombosis in families with inherited antithrombin deficiency. ... and antithrombin deficiencies). This condition is associated with increased risk for adverse health events as a result of ... iii. Indinavir (IDV). 1. Evidence: One small study found no pregnancies in women using COCs and IDV (277).. ...
Pregnancy and Hematology - Brigham and Women's Hospital
Vol. 30 No. 2 (2021)
| Journal of Dhaka Medical College
SMART: SERPIN domain annotation
Antithrombin-III (P01008) (SMART). OMIM:107300: Antithrombin III deficiency. Alpha-1-antichymotrypsin (P01011) (SMART). OMIM: ... Crystal Structure of Antithrombin-III. 2b5t. 2.1 Angstrom structure of a nonproductive complex between antithrombin, synthetic ... ANTITHROMBIN-ANHYDROTHROMBIN-HEPARIN TERNARY COMPLEX STRUCTURE. 1t1f. Crystal Structure of Native Antithrombin in its Monomeric ... THE INTACT AND CLEAVED HUMAN ANTITHROMBIN III COMPLEX AS A MODEL FOR SERPIN-PROTEINASE INTERACTIONS. ...
MeSH Browser
Congenital Antithrombin III Deficiency Deficiency, Antithrombin III Hereditary Antithrombin Deficiency Previous Indexing. ... Antithrombin III Deficiency Preferred Concept UI. M0029883. Scope Note. An absence or reduced level of Antithrombin III leading ... Antithrombin III/deficiency (1979-1998). Antithrombins/deficiency (1971-1978). Public MeSH Note. 99. History Note. 99. Date ... Hereditary Antithrombin Deficiency Narrower Concept UI. M0583594. Terms. Hereditary Antithrombin Deficiency Preferred Term Term ...
Microbial L-asparaginase as a Potential Therapeutic Agent for the Treatment of Acute Lymphoblastic Leukemia: The Pros and Cons
Risk of thrombotic complications in L-asparaginase-induced antithrombin III deficiency. Blood, 83: 386-391.. PubMed ... 1969) reported three patients with severe central nervous disorders who had a marked improvement of symptoms after ... Comparative pharmacokinetic studies of three asparaginase preparations. J. Clin. Oncol., 11: 1780-1786.. PubMedDirect Link ... and wastes from three leguminous crops-bran of Cajanus cajan, Phaseolus mungo and Glycine max (Mishra, 2006). ...
Cerebral Venous Thrombosis: Background, Etiology, Epidemiology
... antithrombin III deficiency, lupus anticoagulant, and the Leiden factor V mutation may result in CVT. Antibodies against the ... Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2-4 weeks after completion of ... Testing for prothrombotic conditions (including protein C, protein S, or antithrombin deficiency), antiphospholipid syndrome, ... deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), ...
Mixed platelet and coagulation disorders: Pathology review | Osmosis
Pathophysiological Changes in the Hemostatic System and Anti... : Transplantation
... or antithrombin III deficiency, activated protein C resistance, and antiphospholipid or anticardiolipin antibodies.40,58 In ... UFH potentiates antithrombin III to inhibit several coagulation factors: mainly FXa and FIIa but, to a lesser extent, also ... Various serine protease inhibitors (serpins), such as antithrombin and activated protein C, regulate the coagulation cascade by ... van den Berg, Tamar A.J. MD1,2; Nieuwenhuijs-Moeke, Gertrude J. MD, PhD3; Lisman, Ton PhD1,2; Moers, Cyril MD, PhD1,2; Bakker, ...
Ethinyl Estradiol and Norelgestromin (Professional Patient Advice) - Drugs.com
... antithrombin-III-deficiency, protein C deficiency, protein S deficiency, hyperhomocysteinemia [eg, due to MTHFR C677T, A1298 ... antithrombin deficiency) may have increased risk of VTE. Age ,35 years, hypertension, obesity, and tobacco use also increase ... If used as hormone replacement therapy, monitor for estrogen deficiency. Monitor all patients using tipranavir/ritonavir and ... Women with inherited thrombophilias (eg, protein C or S deficiency, factor V Leiden mutation, prothrombin mutation, ...
Thrombosis6
- Once a patient with congenital antithrombin III deficiency has developed thrombosis, anticoagulation is more strongly indicated. (medscape.com)
- 3. [Hereditary deficiency of antithrombin III, protein C, protein S and factor XII in 121 patients with venous or arterial thrombosis]. (nih.gov)
- 4. [A family with venous thrombosis and hereditary antithrombin III deficiency]. (nih.gov)
- 6. Hereditary deficiency of antithrombin III, protein C and protein S: prevalence in patients with a history of venous thrombosis and criteria for rational patient screening. (nih.gov)
- 17. Inherited antithrombin III deficiency in an Italian family, associated with venous and arterial thrombosis. (nih.gov)
- An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis. (nih.gov)
Antiphospholipid2
- Testing for prothrombotic conditions (including protein C, protein S, or antithrombin deficiency), antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden can be beneficial for the management of patients with CVT. (medscape.com)
- Antinuclear antithrombin, protein C, protein S or pres- antibodies were investigated with standard- ence of antiphospholipid antibodies, are ized enzyme-linked immunosorbent assay common in patients with retinal vein occlu- sions and may contribute to the etiology of (ELISA). (who.int)
Disseminated intravascul1
- 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)
Protein11
- Antithrombin III is a protein in the blood that blocks abnormal blood clots from forming. (medlineplus.gov)
- The abnormal gene leads to a low level of the antithrombin III protein. (medlineplus.gov)
- This gene provides instructions for producing a protein called antithrombin (previously known as antithrombin III). (medlineplus.gov)
- Antithrombin blocks the activity of proteins that promote blood clotting, especially a protein called thrombin. (medlineplus.gov)
- Most of the mutations that cause hereditary antithrombin deficiency change single protein building blocks (amino acids) in antithrombin, which disrupts its ability to control blood clotting. (medlineplus.gov)
- Brouwer JL, Lijfering WM, Ten Kate MK, Kluin-Nelemans HC, Veeger NJ, van der Meer J. High long-term absolute risk of recurrent venous thromboembolism in patients with hereditary deficiencies of protein S, protein C or antithrombin. (medlineplus.gov)
- By day 14 there had been a significant drop in protein C activity (mean of 95% of normal to 52%), protein C antigen (mean of 105% of normal to 70%), and antithrombin 3 activity (111% of normal to 83%), and an increase in fibrinogen (471-621mg/dl) and tissue plasminogen activator (6.9-13.8ng/ml). (nebraska.edu)
- The decreases in protein C and antithrombin 3 persisted through day 28 after transplantation. (nebraska.edu)
- Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement in fibrinolytic variables create a potentially hypercoagulable state which may contribute to the thrombotic complications of autologous BMT. (nebraska.edu)
- Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2-4 weeks after completion of anticoagulation. (medscape.com)
- Additional causes include inherent thrombophilic states, such as those caused by systemic lupus erythematosus, protein C or S deficiency, and antithrombin III deficiency. (jefferson.edu)
Hereditary antithrombin13
- Hereditary antithrombin deficiency is a disorder of blood clotting. (medlineplus.gov)
- In hereditary antithrombin deficiency, abnormal blood clots usually form only in veins, although they may rarely occur in arteries. (medlineplus.gov)
- About half of people with hereditary antithrombin deficiency will develop at least one abnormal blood clot during their lifetime. (medlineplus.gov)
- Other factors can increase the risk of abnormal blood clots in people with hereditary antithrombin deficiency. (medlineplus.gov)
- The combination of hereditary antithrombin deficiency and other inherited disorders of blood clotting can also influence risk. (medlineplus.gov)
- Women with hereditary antithrombin deficiency are at increased risk of developing an abnormal blood clot during pregnancy or soon after delivery. (medlineplus.gov)
- Hereditary antithrombin deficiency is estimated to occur in about 1 in 2,000 to 3,000 individuals. (medlineplus.gov)
- Of people who have experienced an abnormal blood clot, about 1 in 20 to 200 have hereditary antithrombin deficiency. (medlineplus.gov)
- Hereditary antithrombin deficiency is caused by mutations in the SERPINC1 gene. (medlineplus.gov)
- 1. The prevalence of hereditary antithrombin-III deficiency in patients with a history of venous thromboembolism. (nih.gov)
- 8. Impact of the type of SERPINC1 mutation and subtype of antithrombin deficiency on the thrombotic phenotype in hereditary antithrombin deficiency. (nih.gov)
- 11. Hereditary antithrombin III deficiency and pregnancy: report of two cases and review of the literature. (nih.gov)
- 20. [Severe pulmonary embolism and recurrent thrombophlebitis caused by hereditary antithrombin III deficiency]. (nih.gov)
Proteins1
- Individuals with this condition do not have enough functional antithrombin to inactivate clotting proteins, which results in the increased risk of developing abnormal blood clots. (medlineplus.gov)
Thromboembolic disease1
- Deficiency of antithrombin III is a major risk factor for venous thromboembolic disease. (nih.gov)
Pathogenesis1
- Hereditary and acquired antithrombin deficiency: epidemiology, pathogenesis and treatment options. (medlineplus.gov)
Congenital4
- Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. (medlineplus.gov)
- Congenital antithrombin III deficiency is an inherited disease. (medlineplus.gov)
- Congenital antithrombin III deficiency is an autosomal dominant disorder in which an individual inherits one copy of the SERPINC1 (also called AT3 ) gene on chromosome 1q25.1, which encodes antithrombin III. (medscape.com)
- Severe congenital antithrombin III deficiency, in which the individual inherits two defective genes, is a rare autosomal recessive condition associated with increased thrombogenesis, typically noted in the neonatal period or early infancy. (medscape.com)
Gene2
- It occurs when a person receives one abnormal copy of the antithrombin III gene from a parent with the disease. (medlineplus.gov)
- Interstitial deletion of chromosome 1q [del(1)(q24q25.3)] identified by fluorescence in situ hybridization and gene dosage analysis of apolipoprotein A-II, coagulation factor V, and antithrombin III. (nih.gov)
Abnormal2
- This low level of antithrombin III can cause abnormal blood clots (thrombi) that can block blood flow and damage organs. (medlineplus.gov)
- The majority of AT-III deficiency families belong in the type I (classic) deficiency group and have a quantitatively abnormal phenotype in which antigen and heparin cofactor levels are both reduced to about 50% of normal. (nih.gov)
Disorders1
- Hemostasis disorders, also known as bleeding disorders, can be broadly divided into three groups. (osmosis.org)
ATIII2
- Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa, IXa, Xa). (medscape.com)
- We performed a review of the literature on proximal and intermediate deletion 1q syndrome, and we hypothesize the existence of only one 1q interstitial deletion syndrome, clinically characterized by ATIII deficiency. (nih.gov)
Subtype1
- Type I (low functional and immunologic antithrombin) has been subdivided into subtype Ia (reduced levels of normal antithrombin), and type Ib (reduced levels of antithrombin and the presence of low levels of a variant). (nih.gov)
Patients9
- In these patients, replacement of antithrombin III using antithrombin III concentrates or fresh frozen plasma is recommended. (medscape.com)
- The study involved 58 VTE patients under age 45 years, 45 of whom had at least one inherited risk factor, including 14 with antithrombin III deficiency. (medscape.com)
- Incidence of factor XII deficiency in patients after recurrent venous or arterial thromboembolism and myocardial infarction]. (nih.gov)
- 12. [Plasma antithrombin III activity in patients with pulmonary thromboembolism]. (nih.gov)
- In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3-6 months, with a target international normalized ratio of 2.0-3.0. (medscape.com)
- Eleven patients, eight (8) females and age over 40 years, obesity and the types of opera- three (3) males aged between 20 and 40 years with tion a patient undergoes. (who.int)
- Pro- els on long haul flights, the so called `economy longed sitting was the main factor in 9 out of class syndrome,2,3,4 where the cramped conditions eleven patients. (who.int)
- All the patients had dresser developed the condition after a three hour a full blood count, sickling test and clotting profile journey in a minibus and the 29 year old busi- performed. (who.int)
- Informed include lupus anticoagulant and anticardio- consent was obtained from patients and lipin antibodies [ 2,3 ]. (who.int)
Disorder2
- Once a person is diagnosed with antithrombin III deficiency, all close family members should be screened for this disorder. (medlineplus.gov)
- One such disorder is antithrombin III deficiency . (nih.gov)
Heparin3
- Antithrombin III activity is markedly potentiated by heparin, the principal mechanism by which both heparin and low-molecular-weight heparin result in anticoagulation. (medscape.com)
- Oral contraceptive use and even heparin administration have also been associated with antithrombin III deficiency. (medscape.com)
- they have reduced heparin cofactor activity levels (about 50% of normal) but levels of AT-III antigen are often normal or nearly normal (summary by Bock and Prochownik, 1987). (nih.gov)
Pulmonary1
- [ 3 ] Validated clinical prediction rules should be used to estimate pretest probability of pulmonary embolism and to interpret test results. (medscape.com)
20221
- 24(3): 681-693, 2022 03. (bvsalud.org)
Activity3
- In antithrombin III deficiency, however, the activity of LMWH is not as reliable as in an otherwise healthy person. (medscape.com)
- As expected, antithrombin III (AT3, 1q23-q25.1) serum level and activity were half of normal. (nih.gov)
- A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. (nih.gov)
Homozygous1
- Most affected neonates, however, have heterozygous antithrombin III deficiency rather than the homozygous state. (medscape.com)
Miscarriage1
- 1. A 38-year-old P1+3 presents after her third miscarriage for investigations. (studyebcog.com)
Functional2
Combination1
- Asparaginases are the cornerstones of treatment protocols for acute lymphoblastic leukemia (ALL), it has been an integral part of combination chemotherapy protocols of pediatric acute lymphoblastic leukemia for almost 3 decades and in the majority of adult treatment protocols. (scialert.net)
Antigen1
- Two categories of AT-III deficiency have been defined on the basis of AT-III antigen levels in the plasma of affected individuals. (nih.gov)
Condition1
- 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method. (cdc.gov)
Clinical1
- The clinical significance of antithrombin III]. (nih.gov)
Risk factor1
- 7. [Factor XII (Hageman factor) deficiency: a risk factor for development of thromboembolism. (nih.gov)
Studies1
- Evidence is inconsistent about whether CHC use affects fracture risk ( 34 - 45 ), although three recent studies show no effect ( 34 , 35 , 45 ). (cdc.gov)