Hirudin therapy. Medical search. Web

Use of HIRUDINS as an anticoagulant in the treatment of cardiological and hematological disorders.

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

An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.

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.

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

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

Annelids of the class Hirudinea. Some species, the bloodsuckers, may become temporarily parasitic upon animals, including man. Medicinal leeches (HIRUDO MEDICINALIS) have been used therapeutically for drawing blood since ancient times.

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.

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

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

Proteins prepared by recombinant DNA technology.

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.

Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.

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

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.

Pro- and anti-inflammatory actions of thrombin: a distinct role for proteinase-activated receptor-1 (PAR1). (1/68)

1. Thrombin has well characterized pro-inflammatory actions that have recently been suggested to occur via activation of its receptor, proteinase-activated receptor-1 (PAR1). 2. In the present study, we have compared the effects of thrombin to those of two peptides that selectively activate the PAR1 receptor, in a rat hindpaw oedema model. We have also examined whether or not thrombin can exert anti-inflammatory activity in this model. 3. Both thrombin and the two PAR1 activating peptides induced significant oedema in the rat hindpaw following subplantar injection. 4. The oedema induced by thrombin was abolished by pre-incubation with hirudin, and was markedly reduced in rats in which mast cells were depleted through treatment with compound 48/80 and in rats pretreated with indomethacin. In contrast, administration of the PAR1 activating peptides produced an oedema response that was not reduced by indomethacin and was only slightly reduced in rats pretreated with compound 48/80. 5. Co-administration of thrombin together with a PAR1 activating receptor resulted in a significantly smaller oedema response than that seen with the PAR1 activating peptide alone. This anti-inflammatory effect of thrombin was abolished by pre-incubation with hirudin. 6. These results demonstrate that the pro-inflammatory effects of thrombin occur through a mast-cell dependent mechanism that is, at least in part, independent of activation of the PAR1 receptor. Moreover, thrombin is able to exert anti-inflammatory effects that are also unrelated to the activation of PAR1. (+info)

Relationship between delay in performing direct coronary angioplasty and early clinical outcome in patients with acute myocardial infarction: results from the global use of strategies to open occluded arteries in Acute Coronary Syndromes (GUSTO-IIb) trial. (2/68)

BACKGROUND: Time to treatment with thrombolytic therapy is a critical determinant of mortality in acute myocardial infarction. Little is known about the relationship between the time to treatment with direct coronary angioplasty and clinical outcome. The objectives of this study were to determine both the time required to perform direct coronary angioplasty in the Global Use of Strategies to Open Occluded Arteries in Acute Coronary Syndromes (GUSTO-IIb) trial and its relationship to clinical outcome. METHODS AND RESULTS: Patients randomized to direct coronary angioplasty (n=565) were divided into groups based on the time between study enrollment and first balloon inflation. Patients randomized to angioplasty who did not undergo the procedure were also analyzed. The median time from study enrollment to first balloon inflation was 76 minutes; 19% of patients assigned to angioplasty did not undergo an angioplasty procedure. The 30-day mortality rate of patients who underwent balloon inflation /=91 minutes after enrollment, 6.4%. The mortality rate of patients assigned to angioplasty who never underwent the procedure was 14.1% (P=0.001). Logistic regression analysis revealed that the time from enrollment to first balloon inflation was a significant predictor of mortality within 30 days; after adjustment for differences in baseline characteristics, the odds of death increased 1.6 times (P=0.008) for a movement from each time interval to the next. CONCLUSIONS: The time to treatment with direct PTCA, as with thrombolytic therapy, is a critical determinant of mortality. (+info)

Lepirudin (recombinant hirudin) for parenteral anticoagulation in patients with heparin-induced thrombocytopenia. Heparin-Associated Thrombocytopenia Study (HAT) investigators. (3/68)

BACKGROUND: We prospectively investigated lepirudin for further parenteral anticoagulation in patients with heparin-induced thrombocytopenia (HIT). METHODS AND RESULTS: Patients with confirmed HIT (n=112) received lepirudin according to need for 2 to 10 days (longer if necessary): A1, treatment: 0.4 mg/kg IV bolus, followed by 0.15 mg. kg(-1). h(-1) intravenous infusion, n=65; A2, treatment in conjunction with thrombolysis: 0.2 mg/kg, followed by 0.10 mg. kg(-1). h(-1), n=4; and B, prophylaxis: 0.10 mg. kg(-1). h(-1), n=43. Outcomes from 95 eligible lepirudin-treated patients were compared with those of historical control patients (n=120). Complete laboratory response (activated partial thromboplastin time ratio >1.5 with /=1 outcome (cumulative incidence 30.9% versus 52.1%; relative risk [RR] 0.71; P=0.12, log-rank test). Bleeding events were more frequent in the lepirudin group than the historical control group (cumulative incidence at 35 days, 44.6% versus 27.2%; RR 2.57; P=0.0001, log-rank test). No difference was observed in bleeding events requiring transfusion (cumulative incidence at 35 days, 12.9% versus 9.1%; RR 1.66; P=0.23, log-rank test); no intracranial bleeding was observed in the lepirudin group. CONCLUSIONS: Lepirudin effectively prevents death, limb amputations, and new thromboembolic complications and has an acceptable safety profile in HIT patients. Treatment should be initiated as soon as possible if HIT is suspected. (+info)

Assessment of the treatment effect of enoxaparin for unstable angina/non-Q-wave myocardial infarction. TIMI 11B-ESSENCE meta-analysis. (4/68)

BACKGROUND: Two phase III trials of enoxaparin for unstable angina/non-Q-wave myocardial infarction have shown it to be superior to unfractionated heparin for preventing a composite of death and cardiac ischemic events. A prospectively planned meta-analysis was performed to provide a more precise estimate of the effects of enoxaparin on multiple end points. METHODS AND RESULTS: Event rates for death, the composite end points of death/nonfatal myocardial infarction and death/nonfatal myocardial infarction/urgent revascularization, and major hemorrhage were extracted from the TIMI 11B and ESSENCE databases. Treatment effects at days 2, 8, 14, and 43 were expressed as the OR (and 95% CI) for enoxaparin versus unfractionated heparin. All heterogeneity tests for efficacy end points were negative, which suggests comparability of the findings in TIMI 11B and ESSENCE. Enoxaparin was associated with a 20% reduction in death and serious cardiac ischemic events that appeared within the first few days of treatment, and this benefit was sustained through 43 days. Enoxaparin's treatment benefit was not associated with an increase in major hemorrhage during the acute phase of therapy, but there was an increase in the rate of minor hemorrhage. CONCLUSIONS: The accumulated evidence, coupled with the simplicity of subcutaneous administration and elimination of the need for anticoagulation monitoring, indicates that enoxaparin should be considered as a replacement for unfractionated heparin as the antithrombin for the acute phase of management of patients with high-risk unstable angina/non-Q-wave myocardial infarction. (+info)

Recombinant hirudin (lepirudin) for the improvement of thrombolysis with streptokinase in patients with acute myocardial infarction: results of the HIT-4 trial. (5/68)

OBJECTIVES: The purpose of this study was to compare recombinant hirudin and heparin as adjuncts to streptokinase thrombolysis in patients with acute myocardial infarction (AMI). BACKGROUND: Experimental studies and previous small clinical trials suggest that specific thrombin inhibition improves early patency rates and clinical outcome in patients treated with streptokinase. METHODS: In a randomized double-blind, multicenter trial, 1,208 patients with AMI < or =6 h were treated with aspirin and streptokinase and randomized to receive recombinant hirudin (lepirudin, i.v. bolus of 0.2 mg/kg, followed by subcutaneous (s.c.) injections of 0.5 mg/kg b.i.d. for 5 to 7 days) or heparin (i.v. placebo bolus, followed by s.c. injections of 12,500 IU b.i.d. for 5 to 7 days). A total of 447 patients were included in the angiographic substudy in which the primary end point, 90-min Thrombolysis in Myocardial Infarction (TIMI) flow grade 3 of the infarct-related artery, was evaluated, while the other two-thirds served as "safety group" in which only clinical end points were evaluated. As an additional efficacy parameter the ST-segment resolution at 90 and 180 min was measured in all patients. RESULTS: TIMI flow grade 3 was observed in 40.7% in the lepirudin and in 33.5% in the heparin group (p = 0.16), respectively. In the entire study population the proportion of patients with complete ST resolution at 90 min (28% vs. 22%, p = 0.05) and at 180 min (52% vs. 48%, p = 0.18) after start of therapy tended to be higher in the lepirudin group. There was no significant difference in the incidence of hemorrhagic stroke (0.2% vs. 0.3%) or total stroke (1.2% vs. 1.5%), reinfarction rate (4.6% vs. 5.1%) and total mortality rate (6.8% vs. 6.4%) at 30 days, as well as the combined end point of death, nonfatal stroke, nonfatal reinfarction, rescue-percutaneous transluminal coronary angioplasty and refractory angina (22.7 vs. 24.3%) were not statistically different between the two groups. CONCLUSIONS: Lepirudin as adjunct to thrombolysis with streptokinase did not significantly improve restoration of blood flow in the infarct vessel as assessed by angiography, but was associated with an accelerated ST resolution. There was no increase in the risk of major bleedings with lepirudin compared to heparin. (+info)

Comparison of the predictive value of ST segment elevation resolution at 90 and 180 min after start of streptokinase in acute myocardial infarction. A substudy of the hirudin for improvement of thrombolysis (HIT)-4 study. (6/68)

AIMS: Previous studies revealed that >/=70% or <30% ST segment elevation resolution 180 min after the start of thrombolysis is a strong predictor of either favourable or poor outcome. The aim of this study was to compare the prognostic value of ST segment elevation resolution at 90 and 180 min after the start of streptokinase infusion. METHODS AND RESULTS: The Hirudin for Improvement of Thrombolysis (HIT)-4 study of 1208 patients compared streptokinase therapy in conjunction with either r-hirudin or heparin. Complete ST segment elevation resolution (>/=70%) at 90 and 180 min identified 25% and 50%, respectively, of all patients with a 30 day cardiac mortality of less than 2%. Forty-four percent of patients had no ST segment elevation resolution (<30%) at 90 min and the 30 day cardiac mortality was 7.3%. At 180 min, the no ST segment elevation resolution group decreased to 15% of all patients while the mortality risk increased to 13.6%. CONCLUSIONS: ST segment elevation resolution is a useful tool for early risk stratification and the strategy of rescue angioplasty. Complete ST segment elevation resolution within 180 min of the start of streptokinase therapy indicates excellent survival prospects in 50% of patients. A half of these low risk patients can be identified at 90 min. A high risk group appears to be best characterized by no ST segment elevation resolution at 180 min rather than at 90 min. (+info)

Reduction in vascular lesion formation by hirudin secreted from retrovirus-transduced confluent endothelial cells on vascular grafts in baboons. (7/68)

BACKGROUND: The hypothesis that thrombin mediates the formation of neointimal vascular lesions at sites of mechanical vascular injury has been tested in baboons by measurement of the effects of hirudin delivered by retrovirus-transduced hirudin-secreting vascular endothelial cells (ECs) lining surgically implanted arterial vascular grafts (AVGs). METHODS AND RESULTS: The antithrombotic efficacy of baboon ECs transduced with cDNA encoding hirudin was assessed in vitro and in vivo on thrombogenic segments in chronically exteriorized femoral arteriovenous (AV) shunts. Bilateral brachial AVGs lined with hirudin-transduced versus nonhirudin control ECs at confluent density were surgically implanted, and vascular lesion formations at distal graft-vessel anastomoses were compared after 30 days. Hirudin-transduced ECs secreted 20+/-6 ng x 10(6) cells(-1) x 24 h(-1) (range, 14 to 24 ng x 10(6) cells(-1) x 24 h(-1)) hirudin in supernatants of static cultures. Hirudin-secreting ECs on segments of collagen-coated graft interposed in chronic AV shunts decreased the accumulation of (111)In-labeled platelets to 0.52+/-0.34 x 10(9) platelets, compared with 0.82+/-0.49 x 10(9) platelets in controls (P = 0.03) and reduced platelet deposition in propagated thrombotic tails extending downstream from segments of vascular graft from 1.38+/-0.41 x 10(9) platelets in controls to 0.59+/-0.22 x 10(9) platelets (P = 0.04). ECs recovered from 30-day AVG implants generated 17+/-9 ng x 10(6) cells(-1) x 24 h(-1) (range, 9 to 25 ng x 10(6) cells(-1) x 24 h(-1)) hirudin. Hirudin-secreting ECs reduced neointimal lesion formation at distal graft-vessel anastomoses, ie, 1.02 mm(2) (range, 0.88 to 1.95 mm(2)) versus 1.82 mm(2) (range, 0.88 to 2.56 mm(2)) in contralateral AVGs bearing nonhirudin control ECs (P<0.01). CONCLUSIONS: Viral vector-directed secretion of hirudin from ECs lining implanted AVGs significantly reduces the formation of thrombus and neointimal vascular lesions. (+info)

Clinical outcomes of bivalirudin for ischemic heart disease. (8/68)

BACKGROUND: Current treatment strategies for percutaneous coronary revascularization and acute coronary syndromes incorporate thrombin inhibition with either unfractionated or fractionated heparin. The peptide bivalirudin (Hirulog) is a direct thrombin inhibitor whose pharmacological properties differ from those of heparin. We conducted a systematic overview (meta-analysis) to assess the effect of bivalirudin on 4 end points: death, myocardial infarction, major hemorrhage, and the composite of death or infarction. METHODS AND RESULTS: Six trials (5674 patients) represent the randomized, controlled bivalirudin experience, including 4603 patients undergoing elective percutaneous coronary revascularization and 1071 patients with acute coronary syndromes. ORs for the 4 clinical end points were calculated for each trial. Four trials (4973 patients) that compared bivalirudin with heparin were combined with the use of a random-effects model. In these trials, bivalirudin was associated with a significant reduction in the composite of death or infarction (OR 0.73, 95% CI 0.57 to 0.95; P=0.02) at 30 to 50 days, or 14 fewer events per 1000 patients so treated. There also was a significant reduction in major hemorrhage for the same trials (OR 0.41, 95% CI 0. 32 to 0.52; P<0.001, or 58 fewer events per 1000 patients so treated). A similar analysis combined 2 dose-ranging trials (701 patients) that compared therapeutic (activated partial thromboplastin time more than twice the control time) with subtherapeutic bivalirudin anticoagulation (activated partial thromboplastin time less than twice the control time). CONCLUSIONS: Bivalirudin is at least as effective as heparin, with clearly superior safety. Thus, it provides an unprecedented net clinical benefit over heparin in patients with ischemic heart disease. (+info)

Hirudin therapy, also known as leech therapy, is a type of treatment that uses the saliva of medicinal leeches (Hirudo medicinalis) to alleviate symptoms and promote healing. The saliva of these leeches contains various bioactive compounds, including hirudin, which is a potent anticoagulant that prevents blood clotting.

In hirudin therapy, leeches are applied to specific areas of the body, usually on congested tissues or sites of stasis, where they feed on the patient's blood and release their saliva into the bite site. The hirudin in the saliva helps to dissolve blood clots, improve circulation, reduce swelling, and relieve pain.

Hirudin therapy is used in various medical conditions, such as arterial and venous insufficiency, skin ulcers, joint diseases, and post-surgical recovery, particularly after reconstructive surgery or organ transplantation. It can also be used to treat thrombophlebitis, varicose veins, and other circulatory disorders.

It is essential to note that hirudin therapy should only be performed by trained medical professionals in a controlled environment due to the potential risks associated with infection transmission and bleeding complications.

Hirudin is not a medical term itself, but it is a specific substance with medical relevance. Hirudin is a naturally occurring anticoagulant that is found in the saliva of certain species of leeches (such as Hirudo medicinalis). This compound works by inhibiting the activity of thrombin, a key enzyme in the coagulation cascade, which ultimately results in preventing blood clot formation.

Medically, hirudin has been used in some research and therapeutic settings for its anticoagulant properties. For instance, recombinant hirudin (also known as lepirudin) is available for clinical use as an injectable anticoagulant to treat or prevent blood clots in specific medical conditions, such as heparin-induced thrombocytopenia (HIT).

In summary, Hirudins are a group of anticoagulant substances, primarily derived from leeches, that inhibit the activity of thrombin and have potential medical applications in preventing or treating blood clots.

Thrombin is a serine protease enzyme that plays a crucial role in the coagulation cascade, which is a complex series of biochemical reactions that leads to the formation of a blood clot (thrombus) to prevent excessive bleeding during an injury. Thrombin is formed from its precursor protein, prothrombin, through a process called activation, which involves cleavage by another enzyme called factor Xa.

Once activated, thrombin converts fibrinogen, a soluble plasma protein, into fibrin, an insoluble protein that forms the structural framework of a blood clot. Thrombin also activates other components of the coagulation cascade, such as factor XIII, which crosslinks and stabilizes the fibrin network, and platelets, which contribute to the formation and growth of the clot.

Thrombin has several regulatory mechanisms that control its activity, including feedback inhibition by antithrombin III, a plasma protein that inactivates thrombin and other serine proteases, and tissue factor pathway inhibitor (TFPI), which inhibits the activation of factor Xa, thereby preventing further thrombin formation.

Overall, thrombin is an essential enzyme in hemostasis, the process that maintains the balance between bleeding and clotting in the body. However, excessive or uncontrolled thrombin activity can lead to pathological conditions such as thrombosis, atherosclerosis, and disseminated intravascular coagulation (DIC).

Antithrombins are substances that prevent the formation or promote the dissolution of blood clots (thrombi). They include:

1. Anticoagulants: These are medications that reduce the ability of the blood to clot. Examples include heparin, warfarin, and direct oral anticoagulants (DOACs) such as apixaban, rivaroxaban, and dabigatran.
2. Thrombolytic agents: These are medications that break down existing blood clots. Examples include alteplase, reteplase, and tenecteplase.
3. Fibrinolytics: These are a type of thrombolytic agent that specifically target fibrin, a protein involved in the formation of blood clots.
4. Natural anticoagulants: These are substances produced by the body to regulate blood clotting. Examples include antithrombin III, protein C, and protein S.

Antithrombins are used in the prevention and treatment of various thromboembolic disorders, such as deep vein thrombosis (DVT), pulmonary embolism (PE), stroke, and myocardial infarction (heart attack). It is important to note that while antithrombins can help prevent or dissolve blood clots, they also increase the risk of bleeding, so their use must be carefully monitored.

Partial Thromboplastin Time (PTT) is a medical laboratory test that measures the time it takes for blood to clot. It's more specifically a measure of the intrinsic and common pathways of the coagulation cascade, which are the series of chemical reactions that lead to the formation of a clot.

The test involves adding a partial thromboplastin reagent (an activator of the intrinsic pathway) and calcium to plasma, and then measuring the time it takes for a fibrin clot to form. This is compared to a control sample, and the ratio of the two times is calculated.

The PTT test is often used to help diagnose bleeding disorders or abnormal blood clotting, such as hemophilia or disseminated intravascular coagulation (DIC). It can also be used to monitor the effectiveness of anticoagulant therapy, such as heparin. Prolonged PTT results may indicate a bleeding disorder or an increased risk of bleeding, while shortened PTT results may indicate a hypercoagulable state and an increased risk of thrombosis.

Fibrinopeptide A is a small protein molecule that is cleaved and released from the larger fibrinogen protein during the blood clotting process. Specifically, it is removed by the enzyme thrombin as part of the conversion of fibrinogen to fibrin, which is the main structural component of a blood clot. The measurement of Fibrinopeptide A in the blood can be used as a marker for ongoing thrombin activation and fibrin formation, which are key events in coagulation and hemostasis. Increased levels of Fibrinopeptide A may indicate abnormal or excessive blood clotting, such as in disseminated intravascular coagulation (DIC) or deep vein thrombosis (DVT).

Leeches are parasitic worms that belong to the family Hirudinidae and the phylum Annelida. They are typically cylindrical in shape, have a suction cup at both ends, and possess rows of sharp teeth that allow them to attach to a host and feed on their blood.

In a medical context, leeches have been used for therapeutic purposes in a practice known as hirudotherapy. This technique involves applying leeches to certain parts of the body to draw out blood and promote healing. The saliva of some leech species contains substances that act as anticoagulants, which can help improve circulation and reduce swelling in the affected area.

However, it's important to note that the use of leeches for medical purposes is not without risks, including infection and allergic reactions. Therefore, it should only be performed under the supervision of a trained healthcare professional.

Heparin is defined as a highly sulfated glycosaminoglycan (a type of polysaccharide) that is widely present in many tissues, but is most commonly derived from the mucosal tissues of mammalian lungs or intestinal mucosa. It is an anticoagulant that acts as an inhibitor of several enzymes involved in the blood coagulation cascade, primarily by activating antithrombin III which then neutralizes thrombin and other clotting factors.

Heparin is used medically to prevent and treat thromboembolic disorders such as deep vein thrombosis, pulmonary embolism, and certain types of heart attacks. It can also be used during hemodialysis, cardiac bypass surgery, and other medical procedures to prevent the formation of blood clots.

It's important to note that while heparin is a powerful anticoagulant, it does not have any fibrinolytic activity, meaning it cannot dissolve existing blood clots. Instead, it prevents new clots from forming and stops existing clots from growing larger.

Fibrinopeptide B is a small protein molecule that is cleaved and released from the larger fibrinogen protein during the blood clotting process, also known as coagulation. Fibrinogen is converted to fibrin by the action of thrombin, an enzyme that activates the coagulation cascade. Thrombin cuts specific peptide bonds in fibrinogen, releasing fibrinopeptides A and B from the resulting fibrin monomers.

The release of fibrinopeptide B is a critical step in the formation of a stable blood clot because it allows for the exposure of binding sites on the fibrin molecules that facilitate their polymerization into an insoluble network, trapping platelets and other components to form a clot. The measurement of fibrinopeptide B levels can be used as a marker for thrombin activity and fibrin formation in various clinical settings, such as monitoring the effectiveness of anticoagulant therapy or diagnosing conditions associated with abnormal blood clotting.

Thrombin receptors are a type of G protein-coupled receptor (GPCR) that play a crucial role in hemostasis and thrombosis. They are activated by the protease thrombin, which is generated during the coagulation cascade. There are two main types of thrombin receptors: protease-activated receptor 1 (PAR-1) and PAR-4.

PAR-1 is expressed on various cell types including platelets, endothelial cells, and smooth muscle cells, while PAR-4 is primarily expressed on platelets. Activation of these receptors triggers a variety of intracellular signaling pathways that lead to diverse cellular responses such as platelet activation, aggregation, and secretion; vasoconstriction; and inflammation.

Dysregulation of thrombin receptor signaling has been implicated in several pathological conditions, including arterial and venous thrombosis, atherosclerosis, and cancer. Therefore, thrombin receptors are considered important therapeutic targets for the treatment of these disorders.

Recombinant proteins are artificially created proteins produced through the use of recombinant DNA technology. This process involves combining DNA molecules from different sources to create a new set of genes that encode for a specific protein. The resulting recombinant protein can then be expressed, purified, and used for various applications in research, medicine, and industry.

Recombinant proteins are widely used in biomedical research to study protein function, structure, and interactions. They are also used in the development of diagnostic tests, vaccines, and therapeutic drugs. For example, recombinant insulin is a common treatment for diabetes, while recombinant human growth hormone is used to treat growth disorders.

The production of recombinant proteins typically involves the use of host cells, such as bacteria, yeast, or mammalian cells, which are engineered to express the desired protein. The host cells are transformed with a plasmid vector containing the gene of interest, along with regulatory elements that control its expression. Once the host cells are cultured and the protein is expressed, it can be purified using various chromatography techniques.

Overall, recombinant proteins have revolutionized many areas of biology and medicine, enabling researchers to study and manipulate proteins in ways that were previously impossible.

Antithrombin III is a protein that inhibits the formation of blood clots (thrombi) in the body. It does this by inactivating several enzymes involved in coagulation, including thrombin and factor Xa. Antithrombin III is produced naturally by the liver and is also available as a medication for the prevention and treatment of thromboembolic disorders, such as deep vein thrombosis and pulmonary embolism. It works by binding to and neutralizing excess clotting factors in the bloodstream, thereby reducing the risk of clot formation.

Fibrinolytic agents are medications that dissolve or break down blood clots by activating plasminogen, which is converted into plasmin. Plasmin is a proteolytic enzyme that degrades fibrin, the structural protein in blood clots. Fibrinolytic agents are used medically to treat conditions such as acute ischemic stroke, deep vein thrombosis, pulmonary embolism, and myocardial infarction (heart attack) by restoring blood flow in occluded vessels. Examples of fibrinolytic agents include alteplase, reteplase, and tenecteplase. It is important to note that these medications carry a risk of bleeding complications and should be administered with caution.

Blood coagulation, also known as blood clotting, is a complex process that occurs in the body to prevent excessive bleeding when a blood vessel is damaged. This process involves several different proteins and chemical reactions that ultimately lead to the formation of a clot.

The coagulation cascade is initiated when blood comes into contact with tissue factor, which is exposed after damage to the blood vessel wall. This triggers a series of enzymatic reactions that activate clotting factors, leading to the formation of a fibrin clot. Fibrin is a protein that forms a mesh-like structure that traps platelets and red blood cells to form a stable clot.

Once the bleeding has stopped, the coagulation process is regulated and inhibited to prevent excessive clotting. The fibrinolytic system degrades the clot over time, allowing for the restoration of normal blood flow.

Abnormalities in the blood coagulation process can lead to bleeding disorders or thrombotic disorders such as deep vein thrombosis and pulmonary embolism.

Fibrinogen is a soluble protein present in plasma, synthesized by the liver. It plays an essential role in blood coagulation. When an injury occurs, fibrinogen gets converted into insoluble fibrin by the action of thrombin, forming a fibrin clot that helps to stop bleeding from the injured site. Therefore, fibrinogen is crucial for hemostasis, which is the process of stopping bleeding and starting the healing process after an injury.

Recombinant hirudin (desirudin), a specific inhibitor of thrombin, represents a new development in antithrombotic therapy. (nih.gov)
New agents such as CGP 39393, a recombinant form of hirudin, may be more effective than existing therapies. (nih.gov)
Recent developments in the therapy of HAT-type II include recombinant hirudin or synthetic analogs, or use of some intravenous immunoglobulin preparations. (shengsci.com)
The anticoagulation characteristics of a newly developed anticoagulant, recombinant neorudin (EPR-hirudin (EH)), were explored using a rat model of SCI to provide a basis for clinical anticoagulation therapy of SCI. (bvsalud.org)
In this study, the toxicity effects on circulatory system and respiratory system, and the acute toxicity test of recombinant neorudin (EPR-hirudin, EH) in cynomolgus monkeys were evaluated to provide reference information for clinical studies. (bvsalud.org)
Lepirudin, (chemical designation: [Leu 1 , Thr 2 ]-63-desulfohirudin) is a recombinant hirudin derived from yeast cells. (nih.gov)
18. Recombinant hirudin for the treatment of disseminated intravascular coagulation in patients with haematological malignancy. (nih.gov)
Agents used for other indications include recombinant hirudin (lepirudin, IV desirudin) and synthetic analogues of hirudin (bivalirudin, IV argatroban). (empendium.com)

From hirudin, the active principle in the salivary secretion of leeches that acts as a potent anticoagulant (bloodthinner). (nih.gov)
rivaroxaban, apixaban, edoxaban) and direct thrombin inhibitors (dabigatran) have revolutionized anticoagulation therapy over the past decade and now account for most oral anticoagulant use. (thieme-connect.de)
The benefits of leech therapy are due, in large part, to the anticoagulant effects ("blood thinning"), vasodilatory effects. (hirudofarmamb.com)
Background: Whether anticoagulant therapy should be used after spinal-cord injury (SCI) surgery was controversial. (bvsalud.org)
The medicinal leech ( Hirudo medicinalis ) is probably the most-studied leech and produces the best-known leech anticoagulant, hirudin, a very potent and specific peptide thrombin inhibitor. (zedira.com)
And they secrete hirudin, an anticoagulant that serves as a localized blood thinner, allowing a leech bite to bleed long after the leech has finished feeding and buying crucial time for the body to connect its own veins. (anaeve.com)
In the United States, edoxaban is indicated to treat deep vein thrombosis and pulmonary embolism following five to ten days of initial therapy with a parenteral anticoagulant. (wikipedia.org)

Unlike thrombin, reptilase is not affected by the presence of heparin, heparinoids, or hirudin and may be a useful tool in evaluating test plasma for their presence. (healthmatters.io)
A prolonged thrombin time in a patient with a normal reptilase time suggest heparin therapy or contamination. (healthmatters.io)
Thrombin time (TT) frequently exceeded 200 seconds even at low plasma concentrations of lepirudin, which renders this test unsuitable for routine monitoring of REFLUDAN therapy. (nih.gov)
Antocoagulants work via different mechanisms, thrombolytic, antiplatelet or plasminogen activator r-hirudin and drotrecogin are both direct thrombin inhibitors. (futurelearn.com)

Hirudin in a European Trial versus Heparin in the Prevention of Restenosis after PTCA (percutaneous transluminal coronary angioplasty) (HELVETICA) was a randomized, double-blind, multicenter study of desirudin versus heparin therapy in patients with unstable angina who underwent coronary angioplasty. (medscape.com)

Leech saliva contains an enzyme called Hirudin, which thins the blood and prevents clotting. (expressdigest.com)
When the leech is 'in place', it releases many active therapeutic enzymes into the human body, including hirudin, which thins the blood. (health-alphabet.com)

The use of leeches for medical therapy. (nih.gov)
The therapy consists of placing leeches on a certain area, allowing them to stick their three jaws with tiny rows of teeth into the skin, infusing it with coagulants in their saliva. (expressdigest.com)
Among the first was the re-creation using biotechnology in plants to produce hirudin, a chemical secreted by leeches to prevent blood clotting for medical use. (thefishsite.com)
Hirudotherapy: The use of leeches for medical therapy. (extraviagra.com)
Before the designated day of therapy with medicinal leeches, do not eat garlic and onions or too spicy food. (health-alphabet.com)

Novel IIb/IIIa platelet inhibitors appear to offer a significant therapeutic advance: major bleeding is variable and depends in part on the use of concomitant procedures, and heparin therapy. (duke.edu)
The prevention of HAT-type II requires history taking preference of LMWH to UH, early start of oral anticoagulation, and platelet monitoring from the fifth day of heparin therapy. (shengsci.com)
Some of the predictors of heparin resistance include antithrombin activity level, platelet count, age, and prior heparin therapy. (your-doctor.net)

Most patients with rickettsial diseases, such as Japanese spotted fever and scrub typhus, do not notice a tick or mite bite ( 4 ), but a leech bite is easy to detect because the site bleeds for an extended time due to hirudin in leech saliva. (cdc.gov)
Chemically, it is a synthetic congener of the naturally occurring drug hirudin, found in the saliva of the medicinal leech Hirudo medicinalis . (worldsbest.rehab)

Traditional leech therapies are very rarely applied in modern medicine. (zedira.com)
As a rule, subsequent leech therapies are carried out at weekly intervals. (health-alphabet.com)

Hirudin (extracted from Hirudo medicinalis) is very important substance used in drug industry. (hirudofarmamb.com)
For over 3,000 years, leech therapy or Hirudo therapy is known. (cultu.be)

While in the clinical setting, anticoagulation therapy is successful in preventing propagation of venous thrombi, current therapies are not designed to inhibit inflammation, which can lead to the development of PTS. (frontiersin.org)
American Society of Hematology 2018 guidelines for management of venous thromboembolism: optimal management of anticoagulation therapy. (empendium.com)

Several of these secreted proteins serve as anticoagulants (such as hirudin), platelet aggregation inhibitors (most notably apyrase, collagenase, and calin), vasodilators, and proteinase inhibitors. (wikipedia.org)
The therapy of HAT-type II implies immediate discontinuation of heparin and avoidance of platelet transfusions, unless severe bleeding occurs. (shengsci.com)

The biosynthetic molecule (lepirudin) is identical to natural hirudin except for substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63. (nih.gov)

This gene was then transferred into Brassica napus, where hirudin accumulates in seeds. (apcnet.org)

Therefore, the efficacy observed with r-hirudin did not come at a price of increased severe or life-threatening bleeding. (medscape.com)
A definitive answer regarding the role of hirudin and the balance of safety and efficacy awaits completion of ongoing trials. (duke.edu)
12. Efficacy of gene therapy for Wiskott-Aldrich syndrome using a WAS promoter/cDNA-containing lentiviral vector and nonlethal irradiation. (nih.gov)

Recent experience with the experimental use of antithrombin agents such as hirudin, indicates a delicate dose-response relationship as it relates to the risk of cerebral haemorrhage, when used in conjunction with thrombolytic agents. (duke.edu)

Assessment of the risks of new antithrombotic therapies is best undertaken by evaluating risk factors for bleeding in individual patients, and risks associated with specific antithrombotic agents. (duke.edu)
It is important to identify the source and severity of bleeding with the use of antithrombotic therapy and its haemodynamic consequences in constructing a management plan. (duke.edu)
Antithrombotic Therapy for Atrial Fibrillation: CHEST Guideline and Expert Panel Report. (empendium.com)

Reperfusion using thrombolytic agents will therefore remain an important therapy for hyperacute ischemic stroke. (j-stroke.org)

A gene that produces hirudin is introduced into the plant, resulting in the accumulation of hirudin in its seeds from where it gets extracted for medical purposes. (vedantu.com)

Unless some definite contraindication exists, antiplatelet therapy ( low-dose aspirin ) should be considered routinely for all patients whose medical history implies a significant risk of occlusive vascular disease over the next few months or years (secondary prevention), and should generally be continued for as long as the risk remains high. (practicalpointers.org)
[3] It is also used together with aspirin in heart attacks and following the placement of a coronary artery stent ( dual antiplatelet therapy ). (mdwiki.org)
Consensus-based therapeutic guidelines also recommend the use of clopidogrel rather than ASA for antiplatelet therapy in people with a history of gastric ulceration, as inhibition of the synthesis of prostaglandins by ASA can exacerbate this condition. (mdwiki.org)

It uses a combination of massage, acupressure, and manual therapy to correct pelvic asymmetry. (rehealth.me)
Combination therapy is a logical approach, given the multiple pathophysiological lesions in DM2. (practicalpointers.org)

Hirudin Therapy" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (sdsu.edu)

A retrospective comparison of 30-day outcomes for the EPIC and HELVETICA studies revealed that r-hirudin was superior to heparin for the triple endpoint of death, MI, or urgent re-vascularization and similar to the triple endpoint benefit achieved with heparin plus the glycoprotein IIb/IIIa inhibitor abciximab (ReoPro) versus heparin alone. (medscape.com)
This significant difference continued with a 27% reduction at 48 hours (r-hirudin 2.3% versus heparin 3.1%, OR 0.73, CI 0.59-0.91, p = 0.001). (medscape.com)
[ 12 ] Treatment with r-hirudin versus heparin was not associated with an increase in severe bleeding (1.2% versus 1.1%, p = 0.49) or intracranial hemorrhage (0.3% versus 0.2%, p = 0.24), but was associated with a slight increase in moderate bleeding (8.8% versus 7.7%, p = 0.03). (medscape.com)
Coronary angioplasty versus medical therapy for angina: the second Randomised Intervention Treatment of Angina (RITA-2) trial. (medscape.com)

By reading this document one can find out all the answers to the important questions related to the chapter such as what is biotechnology, what are its applications in different fields, what is gene therapy, what are ethical issues, etc. (vedantu.com)

After piercing the skin, they suck out blood while injecting anticoagulants (hirudin). (wikipedia.org)
Hirudin keeps the blood flowing and reduces this potentially life-threatening clotting. (expressdigest.com)
Hiruding is the BEST natural blood thinner (hirudin is 10 times stronger than modern blood thinners). (leechtherapyus.com)
Leech oil contains hirudin that suppresses blood clotting and improves blood circulation, leading to healthier scalp & hair growth. (naturessure.com)

A study by Lupi-Herrera et al indicated that primary percutaneous coronary intervention (PPCI) leads to lower mortality rates than does thrombolytic therapy in patients with right ventricular infarction. (medscape.com)
Parisi AF, Folland ED, Hartigan P. A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. (medscape.com)

Despite recent advances in recanalization therapy, mechanical thrombectomy will never be a treatment for every ischemic stroke because access to mechanical thrombectomy is still limited in many countries. (j-stroke.org)

BACKGROUND: Thrombolytic therapy improves survival after myocardial infarction through reperfusion of the infarct-related artery. (ox.ac.uk)

Well developed treatment algorithms for patients with severe bleeding exist, and although laboratory testing may be helpful, it is on balance of marginal benefit since patients usually require urgent therapy. (duke.edu)
YuMeiHo® therapy, also known as Yumeiho therapy or just Yumeiho, is a therapeutic treatment that uses manual and physical therapy to deliver whole-body wellness through a collection of over 100 manoeuvres designed to restore functional balance throughout the patient's entire body. (rehealth.me)

Molecular targeting with fusion proteins that attract to a specific antigen, thereby delivering more effective and safe therapy, offer new promise. (duke.edu)

Until 2014, the only evidence-based therapy to reverse the neurological deficit in acute ischemic stroke was the administration of intravenous tissue plasminogen activator (tPA) within 4.5 hours from symptom onset [ 2 ]. (j-stroke.org)

Of all of them, 148 patients underwent thrombolytic therapy and 351 patients were treated with PPCI. (medscape.com)
Yumeiho is a form of therapy developed by Professor Saionji Masayuki, to use massage, acupressure, and manual therapy to help patients suffering from a wide range of health complaints. (rehealth.me)
Patients who experience a range of ongoing and chronic conditions linked to pelvic asymmetry will benefit from manual therapies. (rehealth.me)
5. B-cell reconstitution after lentiviral vector-mediated gene therapy in patients with Wiskott-Aldrich syndrome. (nih.gov)
Factor VIII assays are used to help replacement therapy in patients with hemophilia. (medscape.com)
Despite the advances in recanalization therapy, approximately half of patients with severe ischemic stroke remain disabled or die [ 3 - 5 ]. (j-stroke.org)

11. Development of hematopoietic stem cell gene therapy for Wiskott-Aldrich syndrome. (nih.gov)

Leech therapy, or Hirudotherapy, has become common for healing after facial surgery and for its ability to preserve soft tissue. (expressdigest.com)

Nitroglycerin is preferable to morphine , which should be used judiciously (eg, if a patient has a contraindication to nitroglycerin or is in pain despite nitroglycerin therapy). (msdmanuals.com)

Basic and Clinical Research The overall concept of a SCOR program focuses on scientific issues related to diseases and therapies relevant to the mission of the NHLBI. (nih.gov)
The plant-derived insulin was found to match commercially available human insulin products in in-vivo , in-vitro and clinical trials and offers the potential to provide an inexpensive yet effective therapy for diabetes sufferers across the world. (thefishsite.com)
A comprehensive understanding of basic and clinical research pipelines as well as the current status of thrombolytic therapy will help facilitate the development of new thrombolytics. (j-stroke.org)

The physical massage therapy focuses on repositioning the pelvis, which is achieved by manipulating bones and muscle tissues through applied targeted pressure and manual movements. (rehealth.me)

Leech therapy dates back to 1500 BC when ancient Egyptians used it for remedial purposes well before people had any concept of disease. (expressdigest.com)
15. Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. (nih.gov)

This graph shows the total number of publications written about "Hirudin Therapy" by people in this website by year, and whether "Hirudin Therapy" was a major or minor topic of these publications. (sdsu.edu)
Below are the most recent publications written about "Hirudin Therapy" by people in Profiles. (sdsu.edu)
Leech therapy carries the risk of bacterial infection and people with compromised immune systems are discouraged from trying it. (expressdigest.com)

This is not the first time MGK has professed his love of leech therapy. (expressdigest.com)

Organisms1

Chemicals and Drugs11

Analytical, Diagnostic and Therapeutic Techniques and Equipment2

Phenomena and Processes2

Pro- and anti-inflammatory actions of thrombin: a distinct role for proteinase-activated receptor-1 (PAR1). (1/68)

Relationship between delay in performing direct coronary angioplasty and early clinical outcome in patients with acute myocardial infarction: results from the global use of strategies to open occluded arteries in Acute Coronary Syndromes (GUSTO-IIb) trial. (2/68)

Lepirudin (recombinant hirudin) for parenteral anticoagulation in patients with heparin-induced thrombocytopenia. Heparin-Associated Thrombocytopenia Study (HAT) investigators. (3/68)

Assessment of the treatment effect of enoxaparin for unstable angina/non-Q-wave myocardial infarction. TIMI 11B-ESSENCE meta-analysis. (4/68)

Recombinant hirudin (lepirudin) for the improvement of thrombolysis with streptokinase in patients with acute myocardial infarction: results of the HIT-4 trial. (5/68)

Comparison of the predictive value of ST segment elevation resolution at 90 and 180 min after start of streptokinase in acute myocardial infarction. A substudy of the hirudin for improvement of thrombolysis (HIT)-4 study. (6/68)

Reduction in vascular lesion formation by hirudin secreted from retrovirus-transduced confluent endothelial cells on vascular grafts in baboons. (7/68)

Clinical outcomes of bivalirudin for ischemic heart disease. (8/68)

No images available that match "hirudin therapy"

Hirudin Therapy

Hirudins

Thrombin

Antithrombins

Partial Thromboplastin Time

Fibrinopeptide A

Leeches

Heparin

Fibrinopeptide B

Receptors, Thrombin

Recombinant Proteins

Antithrombin III

Fibrinolytic Agents

Blood Coagulation

Fibrinogen

Pro- and anti-inflammatory actions of thrombin: a distinct role for proteinase-activated receptor-1 (PAR1). (1/68)

Relationship between delay in performing direct coronary angioplasty and early clinical outcome in patients with acute myocardial infarction: results from the global use of strategies to open occluded arteries in Acute Coronary Syndromes (GUSTO-IIb) trial. (2/68)

Lepirudin (recombinant hirudin) for parenteral anticoagulation in patients with heparin-induced thrombocytopenia. Heparin-Associated Thrombocytopenia Study (HAT) investigators. (3/68)

Assessment of the treatment effect of enoxaparin for unstable angina/non-Q-wave myocardial infarction. TIMI 11B-ESSENCE meta-analysis. (4/68)

Recombinant hirudin (lepirudin) for the improvement of thrombolysis with streptokinase in patients with acute myocardial infarction: results of the HIT-4 trial. (5/68)

Comparison of the predictive value of ST segment elevation resolution at 90 and 180 min after start of streptokinase in acute myocardial infarction. A substudy of the hirudin for improvement of thrombolysis (HIT)-4 study. (6/68)

Reduction in vascular lesion formation by hirudin secreted from retrovirus-transduced confluent endothelial cells on vascular grafts in baboons. (7/68)

Clinical outcomes of bivalirudin for ischemic heart disease. (8/68)

Recombinant8

Anticoagulant7

Thrombin4

Desirudin1

Thins the blood2

Leeches5

Heparin therapy3

Saliva2

Leech therapies2

Hirudo2

Anticoagulation therapy2

Platelet2

Lepirudin1

Brassica1

Efficacy3

Antithrombin1

Antithrombotic3

Thrombolytic agents1

Seeds1

Antiplatelet therapy3

Combination2

Descriptor1

Versus4

Biotechnology1

Blood4

Coronary2

Thrombectomy1

Improves1

Treatment2

Specific1

Acute1

Patients6

Gene therapy1

Hirudotherapy1

Contraindication1

Clinical3

Focuses1

Disease2

People3

Time1

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