Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes of hemostatic markers in 226 patients with disseminated intravascular coagulation (DIC) and hematopoietic disorders were examined after treatment of DIC. The changes in prothrombin time (PT) ratio, fibrinogen, fibrin and fibrinogen degradation products (FDP), antithrombin, and protein C, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), and soluble fibrin monomer complex (SFMC) in all patients with DIC were significant during the clinical course of DIC, but those of D-dimer, thrombomodulin (TM), tissue factor (TF), and tissue factor pathway inhibitor (TFPI) were not. Activated partial thromboplastin time (aPTT) and PT were significantly longer in the poor response group than in good response group. Plasma levels of FDP, TAT, PPIC, SFMC, TM, and DIC score were significantly higher in poor response group than in good response. Protein C and antithrombin levels were significantly lower in poor response group than in good response group. The changes of PT ratio, fibrinogen, FDP, DIC score, antithrombin, plasmin inhibitor, and protein C were significant in the good response group, but these levels were not significant in the poor response group. The changes in plasma TAT and SFMC levels were significant in the good response group but were not in poor response group. The changes in D-dimer, TM, TF, or TFPI were not significant in both groups. These findings suggest that anticoagulant agents should be administered at levels below TAT 40 ng/mL or SFMC 300 microgram/mL in patients with DIC and hematopoietic disorders.
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PMID:Good or poor responses of hemostatic molecular markers in patients with hematopoietic disorders after treatment of disseminated intravascular coagulation. 1264 27

Venous thromboembolism and associated complications often leading to permanent disability or death are an important problem in modern medicine. Congenital or acquired disorders of the hemostatic system, such as hypercoagulation or thrombophilia, predispose to thrombosis. The aims of the study were as follows: 1. To assess the prevalence of thrombophilia in venous thromboembolism and in healthy subjects by testing resistance to activated protein C and other markers of hemostasis; 2. To screen for factor V Leiden with a PCR-based assay; 3. To evaluate the usefulness of the adopted analytical approach for the detection of thrombophilia in clinical practice. 29 patients (17 females and 12 males) with venous thromboembolism and a history of thrombotic episodes before the age of 40, either idiopathic or associated with protracted immobilization, pregnancy or puerperium, were enrolled in the study. The control group consisted of 25 age-matched healthy subjects (14 females and 11 males) without any history of thrombosis. The following hemostatic parameters were measured: 1. Activated protein C resistance (APC-R); 2. Protein C (PC) and antithrombin III (AT III) activities; 3. Protein S (PS) activity; 4. Fibrinogen (FB) concentration; 5. Euglobin lysis time (ELT); 6. Prothrombin time (PT); 7. Activated partial thromboplastin time (APTT). The presence of Leiden mutation was detected by PCR amplification and digestion of products with Mnl 1 restrictase. The results were tested statistically using: 1. Kolmogorov-Smirnov D test; 2. Student's t-test; 3. linear regression analysis; 4. chi 2 test. The following conclusions were drawn: 1. Prevalence of thrombophilia in patients with venous thromboembolism is 31%, a figure consistent with literature data (no signs of thrombophilia were found in the control group); 2. Resistance to activated protein C is sufficient proof of Leiden mutation provided that APCR index (r) is less than 0.9 (borderline r values (0.9-1.1) require further genetic testing). 3. Methods of diagnosis of thrombophilia used in this study could be applied in routine clinical practice, the most useful ones being resistance to activated protein C, fibrinogen concentration and protein S activity. With this approach the detection of higher risk of thrombotic-embolic episodes, either acquired or inborn, is possible in most cases.
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PMID:[Diagnosis of thrombophilia based on coagulation and genetic studies]. 1460 77

Abnormalities of the Protein C (PC) pathway are found in the majority of patients with thrombophilia. ProC Global is a coagulation assay that reflects the net effect of the PC pathway by measuring the activated partial thromboplastin time (APTT) of patient and control plasma, before and after activation of endogenous PC by Protac, a snake venom. Previous studies have suggested that abnormalities in this test are associated with an increased risk of venous thromboembolism (VTE). A retrospective analysis was performed using frozen plasma samples from 140 patients with confirmed VTE to determine whether an abnormal ProC Global result (in the presence and in the absence of known abnormalities in the PC pathway) is a predictor of initial and recurrent VTE. Patients were tested for the presence of activated protein C resistance, Factor V Leiden, PC and protein S (PS) deficiency, and non-specific inhibitor positivity. Mean ProC Global results were significantly lower in patients with recurrent VTE than in patients without recurrent VTE. The association between abnormal ProC Global result and recurrent VTE showed a strong trend, before (odds ratio, OR 3.6) and after (OR 3.1) exclusion of known thrombophilic abnormalities. Patients with a first episode of idiopathic VTE also expressed significant lower ProC Global results than those with secondary VTE. After exclusion of known PC pathway abnormalities, there was a statistically significant association between abnormal ProC Global and initial idiopathic VTE (p=0.04). These results suggest that ProC Global may serve as a predictor of recurrent VTE and potentially for first episode of idiopathic VTE. ProC Global may help identify patients at increased risk of initial and recurrent VTE.
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PMID:"ProC Global": a functional screening test that predicts recurrent venous thromboembolism. 1573 16

Protein C is a plasmatic protein that is synthesized by the liver with the help of vitamin K. It regulates thrombin formation and consequently prevents thrombosis. We present a case of a newborn male with change in the color of the right foot index finger who after 4 h showed cyanosis that reached malleolus level. Upon admission we observed generalized pallor, tachycardia and a necrotic lesion in the rightfoot. We suspected a septic process and thus administered cefotaxime, vancomycin and heparin. Platelet levels were 70,000 mm3, thromboplastin 16/12 sec., partial thromboplastin 5829 sec. PCfunctionality 20% and protein S 100%. Even though the patient evolvedfavourably and showed partial recovery, an intratuberous amputation was needed. One year later a prosthesis was fitted. We need to carry out studies that support the use of PC monoclonal antibodies in order to offer better baseline treatment to patients with PC congenital deficiency and improve their quality of live.
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PMID:[Protein C congenital deficiency. A case report]. 1602 90

New anticoagulants are under development to improve on current ones that, although effective, have limitations in efficacy, safety and convenience. We have reviewed the use of these agents as thromboprophylactic drugs. These new agents have more specific modes of action and can be divided into three groups. Inhibitors of the initiation of coagulation work via inhibition of the factor VIIa/tissue factor complex. Inhibitors of propagation of coagulation include parenteral and oral factor Xa inhibitors, factor IXa inhibitors, inhibitors of factor Va and VIIIa, activated Protein C, soluble thrombomodulin and SNAC-Heparin. Finally, direct inhibitors of thrombin are under development both for parenteral and oral administration. Several new drugs, such as fondaparinux, hirudin, argatroban, bivalirudin and ximelagatran, have already been licensed for specific indications and are being investigated for more general usage. Other drugs reviewed are in much earlier stages of development.
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PMID:New antithrombotics in the prevention of thromboembolic disease. 1608 52

Autoimmune thrombocytopenic purpura (ITP) is a disease that presents with skin and mucous membrane bleeding due to thrombocytopenia. In the literature, there are a few studies about the effect of high-dose steroid therapy on coagulation tests in different diseases, but their results are still controversial. In this study, coagulation parameters were investigated that might have a role in hemostatic compensation in childhood acute ITP before and after high-dose methylprednisolone (HDMP) treatment. The study includes 21 children age 1.5 to 14 years with acute ITP and 21 healthy age-matched control subjects. All patients with acute ITP received HDMP for 7 days. Before and after HDMP treatment (0 and 8 days) prothrombin time, partial thromboplastin time, fibrinogen, Protein C, Protein S, antithrombin III, and the levels of factor II (FII), FV, FVII, FVIII, FIX, FX, FXI, and FXII were studied in all subjects. The results were compared with those of the control group. Pre-treatment Protein C and Protein S levels in the patient group were significantly lower than those in the control groups (p<0.05). Protein S and Protein C levels were significantly improved after HDMP treatment in patient group. There were lower FV, FVII, FX values in the patient group compared to the control groups on admission. There was no difference in AT III and fibrinogen levels before and after treatment. As a result, some changes in the coagulation system associated with thrombocytopenia were observed in patients with acute ITP. These changes may be accepted as compensatory mechanisms to maintain hemostasis.
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PMID:Effects of high-dose methylprednisolone therapy on coagulation factors in patients with acute immune thrombocytopenic purpura. 1624 77

Cancer procoagulant (CP) is a cysteine proteinase that may be produced by malignant and foetal tissue. The possible role of CP in the pathogenesis of cancer-related thrombosis has been suggested recently. The purpose of the study was to evaluate coagulation prothrombotic markers and their relation to CP concentration in the blood of patients with gastrointestinal adenocarcinomas (GIAC). The study group consisted of 45 patients with confirmed diagnosis of adenocarcinoma (stomach, 18 patients; colon, 27 patients) and without evident metastatic disease. In 24 patients further observation showed metastases. The control group for CP was composed of 10 healthy subjects. Blood samples were drawn on the admission day, before any treatment. Among 45 patients with GIAC, deep venous thrombosis was observed in two (4.4%). In all patients the CP activity in the serum was found, and the mean CP activity shortened the coagulation time almost three times compared with the healthy control group. Also, the mean thrombin-antithrombin complex concentration was above the normal range. A significant elevation of the mean prothrombin fragment 1+2 plasma content in this group of patients was noticed. Despite these observations, CP remained within the normal range and did not correlate with thrombin-antithrombin complex or prothrombin fragment 1+2 plasma concentrations. A positive correlation was observed between serum CP and fibrinogen concentration, and a negative correlation between CP and free protein S plasma content (P = 0.04 and P = 0.025, respectively). A negative correlation between activated protein C resistance ratio and protein C activity in the plasma was confirmed. Protein C activity in the plasma showed a correlation with free protein S plasma content. Analysis of factors influencing the activated partial thromboplastin time revealed the presence of antiphospholipid antibodies in seven persons from the study group (in three cases of IgG and in four cases of IgM class). Our data suggest that CP is a minor risk factor for deep venous thrombosis in GIAC patients. To confirm this, however, the number of patients and controls should be larger. After 3 years of observation, the follow-up in 10 living GIAC patients showed nobody with thromboembolic disease.
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PMID:Cancer procoagulant in patients with adenocarcinomas. 1626 26

During the last decades in Georgia was observed significant increase of cases of visceral leishmaniasis and fight against this disease became important problem as far as the management of this disease is rather problematic. According to references and our clinical experience patients with visceral leishmaniasis are predisposed to bleeding. The objective of our study was the assessment of functional status of hemostasis related to the degree of clinical severity. We have studied platelet count, activated partial thromboplastin time (APTT), prothrombin time, thrombin time, plasma concentration of fibrinogen, the soluble fibrin-monomeric complexes (SFMC), fibrinogen/fibrin degradation products (D-dimer) and anticoagulant protein C. Haemostatic functional tests were studied in 45 patients with visceral leishmaniasis before and after treatment (with 20-25 day intervals). Before treatment the reduction of platelet count was observed in 95%. Prolonged APTT and prothrombin time was found in severe forms of the disease. Thrombin time prolonged in 45.7%, SFMC level was increased in 80% (p=0.003) and D-dimer level in 95.6% (p=0.023). Protein C was in normal value in 73%. The results indicate that leishmania infection affects primary haemostasis, coagulation and fibrinolysis and these alterations are related to the severity of clinical symptoms. Investigation of SFMC and D-dimer showed that in case of visceral leishmaniasis activation of intravascular coagulation takes place, particularly during the severe forms of the disease, study of these markers is of the diagnostic and prognostic importance and the treatment at an early stage of infection may potentially avoid the possibility of developing an uncompensated DIC.
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PMID:[Functional status of haemostasis system in patients with visceral leishmaniasis]. 1636 67

In women with polycystic ovary syndrome, C-reactive protein levels and D-dimer, antithrombin III, activated protein C resistance, and activated partial thromboplastin time were unaffected by metformin treatment throughout pregnancy. Protein C levels increased slightly in the metformin group compared with the placebo group.
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PMID:Beneficial effect of metformin on pregnancy outcome in women with polycystic ovary syndrome is not associated with major changes in C-reactive protein levels or indices of coagulation. 1650 Mar 61

Cadmium, a highly toxic heavy metal, is distributed widely in the general environment. The characteristic clinical manifestations of chronic cadmium intoxication include renal proximal tubular dysfunction, osteomalacia and anemia. Accumulating evidence suggests that cadmium toxicity may also affect various organs such as the liver, lung, testis and hematopoietic system. The aim of this study was to determine the effect of chronic cadmium exposure on the anticoagulant system in rats. Fourty-five adult Wistar albino rats were randomly allocated into 2 groups. While the control group was given tap water, the animals in the cadmium group were treated with 15 ppm CdCl(2) for 4 weeks. Blood cadmium concentration, prothrombin time, activated partial thromboplastin time, plasma protein C and antithrombin activity, and platelet count were determined in the rats. Blood cadmium concentrations increased in the experiment group compared to the control group (p < 0.001). Results also show that cadmium exposure shortened prothrombin time (p < 0.05) and activated partial thromboplastin time (p < 0.01) in rats. Protein C (p < 0.001) and antithrombin (p < 0.001) decreased to statistically significantly lower levels in rat plasma after cadmium exposure when compared to the control group. When the number of thrombocytes was compared between 2 groups, a decrease was observed in the group treated with CdCl(2), which was, however, not statistically significant (p > 0.05). In conclusion, when the parameters of the hemolytic system are considered, the decrease in protein C and antithrombin activities and the shortening of prothrombin time and activated partial thromboplastin time suggests the presence of a hypercoagulable state during chronic cadmium intoxication. Therefore, it may be stated that chronic cadmium toxicity sets the stage for hypercoagulation and hence increases the risk of thrombosis.
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PMID:The effects of chronic cadmium toxicity on the hemostatic system. 1756 33


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