Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since disseminated intravascular coagulation (DIC) may directly reflect the abnormal regulation of the fibrinolytic system by endothelial cells, we have measured the levels of tissue-type plasminogen activator (t-PA), type 1 PA inhibitor (PAI-1) and t-PA . PAI-1 complex which is formed as a result of interaction on the two factors, in the plasma of patients with DIC (n = 51) and healthy controls (n = 42). Antigens of t-PA, PAI-1 and t-PA . PAI-1 complex were significantly increased in the DIC plasma (36.4 +/- 25.1, 106.8 +/- 54.7 and 46.6 +/- 34.5 ng/ml, respectively) compared with those in normal plasma (8.5 +/- 4.3, 54.4 +/- 21.2 and 8.6 +/- 3.5 ng/ml, respectively). The molar ratio of t-PA to PAI-1 was much higher in the DIC plasma (1:3) than in normal plasma (1:6), which caused enhancement of the whole fibrinolytic activity in the DIC plasma. These changes resulted in significant consumption of plasminogen, alpha 2-plasmin inhibitor (alpha 2-PI) and a significant increase of plasmin . alpha 2-PI complex (PPI) and D-dimer. These results suggest that t-PA and its specific inhibitor PAI-1 both of which are secreted from endothelial cells into blood, play an important role on the progress of DIC.
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PMID:[Levels of tissue-type plasminogen activator and plasminogen activator inhibitor 1 in disseminated intravascular coagulation syndrome]. 192 Aug 64

The hematologic disorders in patients with acute cardioembolic stroke are not fully understood, and no reliable measures are available to identify patients at high risk for recurrent embolism. We analyzed coagulation and fibrinolytic functions in 22 patients with cardiogenic cerebral embolism less than or equal to 24 hours after onset and in 25 age-matched controls. The levels of antithrombin III, protein C, and alpha 2-plasmin inhibitor were significantly lower in the patients than in the controls (p less than 0.001, 0.02, and 0.05, respectively). In contrast, the plasma concentrations of thrombin-antithrombin III complex and crosslinked D-dimer were markedly higher in the patients than in the controls (p less than 0.01 and 0.001, respectively). At the time of admission, the plasma concentrations of thrombin-antithrombin III complex and crosslinked D-dimer in the eight patients at high risk for recurrent embolization (one with prodromal embolism, three with intracardiac thrombi, and four with recurrent embolization) were 2.8 and 3.5 times, respectively, higher than those in the 14 patients without recurrence or thrombus formation. The lowest concentration of crosslinked D-dimer in the eight patients at high risk for recurrent embolization was 600 ng/ml on admission. Our results suggest that patients with acute cardioembolic stroke have various degrees of consumption coagulopathy and that the plasma concentrations of thrombin-antithrombin III complex and crosslinked D-dimer can be useful indicators of those who are prone to recurrent embolization during this stage.
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PMID:Activation of coagulation in acute cardioembolic stroke. 198 67

The alpha 2-plasmin inhibitor-plasmin complex (alpha 2-PI-PM), alpha 2-plasmin inhibitor (alpha 2-PI) and some functions of coagulation and hemostasis were assayed on aged patients who were operated for femoral neck fracture. After the surgery, APTT, PT, fibrinogen, AT-III and platelet counts were in normal range or slightly deviated, which did not match with the DIC diagnostic standard. FDP levels in the operation group (337 +/- 303 ng/ml) were significantly increased compared to the level of the normal aged persons (64 +/- 9.9 ng/ml). The alpha 2-PI-PM in the operation group was 2.92 +/- 3.56 micrograms/ml, which was significantly higher than the alpha 2-PI-PM level (0.76 +/- 0.45 micrograms/ml) in the normal aged persons. Moreover, 3 in 7 operation cases, showed the increase of alpha 2-PI-PM levels over 5 micrograms/ml. The alpha 2-PI-PM in DIC group was 5.29 +/- 5.17 micrograms/ml. These data suggest that the patients are in the pre DIC state after surgery. In titers of FDP and alpha 2-PI, there were no differences between patients treated with and without heparin. alpha 2-PI-PM levels were improved in 5 out of 7 cases with the heparin treatment. On the other hand only one in 6 cases who did not receive heparin therapy showed the improvement of alpha 2-PI-PM level. In some cases without heparin treatment, the alpha 2-PI-PM level increased in the course of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Alpha 2-plasmin inhibitor plasmin complex in patients undergone surgery in femoral neck fracture]. 213 77

We have studied the activation state of the fibrinolytic system in 39 patients with systemic meningococcal disease (SMD). Patients defined as having fulminant septicemia (n = 13) with high (greater than 700 ng/L) levels of endotoxin (LPS) in plasma and severe coagulopathy, had significantly lower functional levels of plasminogen (P less than 0.05) and alpha-2-antiplasmin (P less than 0.01) and higher antigen levels of plasminogen activator inhibitor 1 (PAI-1) (P less than 0.01), and fibrin degradation products (FDP) (P less than 0.01), but not of PAI-2 (P greater than 0.1) as compared with less severely ill patients (meningitis and meningococcemia) (n = 25). A positive correlation existed between the admission (maximum) levels of LPS and PAI-1 (r = 0.86, P less than 0.0001). Decreasing admission levels of platelets were associated with increasing levels of PAI-1 (r = -0.55, P less than 0.001). After initiation of treatment with antibiotics and fresh frozen plasma, the PAI-1 levels declined rapidly. PAI-1 levels greater than 360 micrograms/L on admission predicted the development of a severe septic shock combined with renal impairment correctly in 12 of 13 patients (92%). None of 25 patients without multiple organ failure had PAI-1 levels greater than 260 micrograms/L. PAI-1 levels greater than 1850 micrograms/L were associated with 100% fatality. The results suggest that in the early phase of fulminant meningococcal septicemia an extensive plasmin generation occurs. On admission, however, high levels of PAI-1 seem to inhibit the plasmin generation, and thereby promote DIC.
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PMID:Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease. 231 89

In the present study, the first case of ruptured hepatoma followed by disseminated intravascular coagulation is reported. An elastase-like enzyme which possessed elastolytic and caseinolytic activities was confirmed from patient plasma. On the other hand, no elastase activity was detected in the plasma of patients with hepatitis, liver cirrhosis or hepatoma without disseminated intravascular coagulation. The patient plasma did not possess H-D-Val-Leu-Lys-p-nitroanilide hydrochloride, succinyl-L-alanyl-L-alanyl-p-nitroanilide, and pyro-Glu-Pro-Val-p-nitroanilide amidolytic activities. However, when chromatographed on Sephadex G-200, the presence of low-molecular weight plasminogen was confirmed. Its molecular weight was approximately 52,000. A slight decrease of alpha 2-plasmin inhibitor was noted, but no decrease of alpha 2-macroglobulin was detected.
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PMID:A case of ruptured hepatoma followed by elastase-induced disseminated intravascular coagulation. 241 97

Plasmin-alpha 2-plasmin inhibitor (alpha 2PI) complex, an indicator of in vivo plasmin generation, was measured in the plasma of 48 patients with disseminated intravascular coagulation (DIC), by enzyme-linked immunosorbent assay (ELISA). Plasmin-alpha 2PI complex was markedly elevated to 7.9 +/- 4.26 mg/liter (mean +/- SD) in DIC at presentation, with normal values at less than 0.8 mg/liter. The concentration of plasmin-alpha 2PI complex changed in parallel with the course of DIC and decreased to 1.9 +/- 1.49 mg/liter (n = 28) in remission. Among various underlying disorders, DIC, in patients with acute promyelocytic leukemia, had the highest complex levels (mean 10.8 mg/liter), and septic patients had the lowest levels (mean 3.4 mg/liter). No significant correlation was found between FDP and plasmin-alpha 2PI complex. These results indicate that the quantitative assay of plasmin-alpha 2PI complex in plasma would be valuable in the assessment of hyperfibrinolysis in DIC.
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PMID:Plasmin-alpha 2-plasmin inhibitor complex in plasma of patients with disseminated intravascular coagulation. 245 7

The levels of alpha-2-antiplasmin (alpha 2-AP), antithrombin III (At III) and plasminogen were studied in 21 patients with acute nonlymphoblastic leukemia (ANLL) before and after induction chemotherapy and during bone marrow cellularity recovery after the postchemotherapy aplastic phase. In the patients with M2, M3 or M4 leukemia who had clinical and laboratory evidence of DIC, the alpha 2-AP levels were very low in the initial phase of the disease but improved significantly during recovery of marrow cellularity. At III and plasminogen values were in the normal range at disease onset and showed no significant modification during the course of leukemia. Proteolytic cleavage of alpha 2-AP by granulocyte proteases, rather than hyperfibrinolysis, may be responsible for the low levels of the inhibitor in the proliferative phase of ANLL. This alpha 2-AP deficiency may well contribute to hemorrhagic diathesis in ANLL independently of the presence or absence of hyperfibrinolysis or DIC. Moreover, the lower alpha 2-AP levels observed during the proliferative phase of ANLL may relate to disease activity.
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PMID:Alpha-2 antiplasmin in acute nonlymphoblastic leukemia. 246 77

Plasma samples from patients with disseminated intravascular coagulation (DIC) associated with acute promyelocytic leukemia (APL) exhibited higher levels of the D-fragment of fibrin and fibrinogen degradation products [FDP(D)], with relatively lower levels of cross-linked fibrin degradation products (XDP), than samples of DIC with non-APL. The difference between FDP(D) and XDP levels increased only when alpha 2-plasmin inhibitor (alpha 2-PI) fell below 60% of the normal level in APL patients. These findings suggest that fibrinogenolysis occurs in APL patients when the alpha 2-PI level has decreased significantly.
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PMID:Characterization of the fibrinolytic state by measuring stable cross-linked fibrin degradation products in disseminated intravascular coagulation associated with acute promyelocytic leukemia. 249 30

The pathophysiology of bleeding manifestations in hemorrhagic fever with renal syndrome (HFRS) was elucidated by serially evaluating coagulation and fibrinolytic profiles and complement alterations in patients with HFRS. In the early stage of the disease, platelet counts, platelet survival time, and platelet aggregation in vitro decreased. Prolongation of bleeding time, prothrombin time, and activated partial thromboplastin time was noted, with decreases in coagulation factors II, V, VIII, IX, and X. Levels of fibrinogen were decreased, and those of fibrinogen-fibrin degradation products in serum and urine were increased. Concentrations of plasminogen, alpha 2-plasmin inhibitor, and antithrombin III in plasma were depressed. Procoagulant activity was present in plasma. Circulating immune complexes were found, whereas serum levels of C3 were decreased. In the early stage of HFRS, thrombocytopenia, defects in platelet function, and disseminated intravascular coagulation may play central roles in the pathogenesis of bleeding manifestations. Vasculopathy and immunologic aberrations also may play a role.
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PMID:Coagulopathy in hemorrhagic fever with renal syndrome (Korean hemorrhagic fever). 256 77

Hemostatic plugs consist of platelet aggregates and fibrin mesh containing blood cells and plasma components. Hemostatic efficiency depends on the rate of formation of hemostatic plugs as well as the structural integrity and stability of the formed hemostatic plugs. Fibrin elements are major constituents contributing to the structural integrity and stability, but they are subject to fibrinolytic activity occurring spontaneously after fibrin formation. Fibrinolysis is usually suppressed by endogenous inhibitors. Increase of a profibrinolytic component or deficiency of an inhibitor would result in an accelerated fibrinolysis, causing a premature lysis of hemostatic plugs before restoration of injured vessels, leading to a hemorrhagic tendency. Such a state can be seen typically in patients with congenital deficiency of alpha 2-plasmin inhibitor or a hereditary increase of plasminogen activator, and it is also seen in acquired situations such as amyloidosis, liver cirrhosis, disseminated intravascular coagulation (particularly in patients with acute promyelocytic leukemia) and thrombolytic therapy. The hemorrhagic tendency can be well controlled by an administration of an antifibrinolytic agent: epsilon-aminocaproic acid or tranexamic acid. In contrast to an accelerated fibrinolysis causing a hemorrhagic tendency, retarded fibrinolysis may predispose an individual to a thrombotic tendency. Retarded fibrinolysis may be due to either an increase in plasminogen activator inhibitors or decrease of plasminogen activators. Quantitative or qualitative deficiency of plasminogen may also lead to a thrombotic tendency.
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PMID:Hemostasis associated with abnormalities of fibrinolysis. 265 Jul 72


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