Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four basic coagulation tests, the prothrombin time, thrombin time, partial thromboplastin time, and prothrombin consumption time, were used, with relatively simple modifications, to demonstrate the presence of two circulating anticoagulants in the blood of a patient with IgG myeloma and a severe bleeding tendency.
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PMID:Antithrombin and antithromboplastin activity accompanying IgG myeloma. Report of a case with a severe bleeding tendency. 111 Dec 75

One hundred and fifty-seven HIV seropositive patients were included in a prospective study of coagulation parameters. Activated partial thromboplastin time, prothrombin time, thrombin time and specific factor assays of the intrinsic pathway were performed using standard techniques. The tissue thromboplastin inhibition test and antiphospholipid antibodies were used to establish the presence of circulating lupus anticoagulant. Among the 46 patients with a prolonged activated partial thromboplastin time, an anti-prothrombinase was present in 33. Of the 111 patients with a normal activated partial thromboplastin time, anti-prothrombinase was present in 51. Circulating lupus anticoagulant seems to be common in HIV seropositive patients, since it was found in 84 patients (53.5%). Our findings confirm that the presence of circulating anticoagulants is not particularly associated with opportunistic infections or the development of the disease. It is possible that these inhibitors could be mediated by anti-phospholipid antibodies. In HIV seropositive patients, defective T cell regulation of B cells leads to polyclonal hypergammaglobulinemia. These antibodies may be directed against endogenous or exogenous phospholipids.
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PMID:[Circulating anticoagulants in immunodeficiency virus infection. Results of a prospective study of 157 seropositive patients]. 259 85

Hemostatic abnormalities associated with malignancy have been described since the middle of the 19th century. Abnormalities associated with hypercoagulability and hemorrhage are reported in various percentages of patients depending upon the underlying neoplasm and the type of therapy. Changes in the quantitative and qualitative aspects of protein coagulation factors, anticoagulant proteins, circulating anticoagulants, platelets, and vascular responses have been noted. Clinical or subclinical disseminated intravascular coagulopathy (DIC) and associated paradoxical bleeding are common. Hemorrhage may be associated with a decrease of particular coagulation factors or alterations of vascular integrity and platelet numbers or function in various combinations. Evaluation of hemostatic abnormalities associated with cancer (HAAC) includes a careful history and physical examination, assessment of the prothrombin and activated partial thromboplastin times, platelet count, a test for fibrin or fibrinogen degradation products, and assay of fibrinogen levels. Specific findings may suggest the need for tests for naturally occurring protein anticoagulants (e.g., protein S, protein C, and antithrombin III), coagulation inhibitors, abnormalities of the fibrinolytic system, or other esoteric tests. Testing for F1 + 2 and fibrinopeptide A may be useful in determining early activation of prothrombin and thrombin, respectively, and a clue to incipient onset of DIC. Besides the disease, therapies for cancer can alter hemostatic activity. Chemotherapy has been reported to be associated with venous and arterial thromboses, cerebrovascular events, and coagulopathies. Radiation therapy decreases platelet production, particularly if the active bone marrow has been included in the field. Laboratory evaluation of HAAC requires consideration of the type of malignant disorder, the history and physical condition of the patient and any therapy.
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PMID:Hemostatic abnormalities associated with cancer and its therapy. 943 35

Hemostasis is initiated by injury to the vascular wall, leading to the deposition of platelets adhering to components of the subendothelium. Platelet adhesion requires the presence of von Willebrand factor and platelet receptors (IIb/IIIa and Ib/IX). Additional platelets are recruited to the site of injury by release of platelet granular contents, including ADP. The "platelet plug" is stabilized by interaction with fibrinogen. In this review, I consider laboratory tests used to evaluate coagulation, including prothrombin time, activated partial thromboplastin time, thrombin time, and platelet count. I discuss hereditary disorders of platelets and/or coagulation proteins that lead to clinical bleeding as well as acquired disorders, including disseminated intravascular coagulation and acquired circulating anticoagulants.
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PMID:Coagulation and bleeding disorders: review and update. 1092 20

In a recent randomized, double-blind, placebo-controlled trial of women with a history of venous thromboembolism (VTE), we found that hormone replacement therapy (HRT) was associated with an early excess risk of recurrent thrombosis. The aims of the present study were to characterize the effects of HRT on coagulation in these women to elucidate the mechanism(s) by which HRT increases the risk of thrombosis. The study comprised 140 women who were randomized to receive continuous treatment for 24 months with once daily 2 mg 17-beta-estradiol plus 1 mg norethisterone acetate (n = 71) or placebo (n = 69). HRT caused significant increases in prothrombin fragments 1+2, thrombin-antithrombin complex, and D-Dimer after 3 months, but these changes were less pronounced on prolonged treatment. The increases in markers of activated coagulation was higher in those women who subsequently developed recurrent thrombosis, but was similar in carriers and non-carriers of the factor V Leiden mutation. HRT had no effects on fibrinogen and factor VIII. Activated factor VII, but not factor VII antigen, decreased significantly on HRT as compared with placebo. The coagulation inhibitors antithrombin, protein C, and TFPI, but not protein S, all showed significant sustained decreases in the HRT group as compared with placebo. Antithrombin and protein C decreased by 8-12% on HRT, whereas TFPI activity decreased by 12-17% and TFPI free antigen by 29-30%. In multivariate analysis, only TFPI activity was a significant predictor for the increased activation of coagulation. We conclude that HRT was associated with early activation of coagulation, which corroborates the finding of an early risk of recurrent VTE. This activation may in part be explained by reduction in circulating anticoagulants.
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PMID:The effects of hormone replacement therapy (HRT) on hemostatic variables in women with previous venous thromboembolism--results from a randomized, double-blind, clinical trial. 1137 67