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)

Death from traumatic shock has been associated with loss of blood externally or internally. However, many patients die after trauma, even though blood volume restoration is adequate. Death is often due to pulmonary failure (adult respiratory distress syndrome [ARDS]). Death and ARDS have been associated with disseminated intravascular coagulation (DIC) and microclots in the lungs. Dissolution of the microclots after trauma can be achieved by activation of endogenous plasmin. Nine pigs were anesthetized for 48 h. Trauma was administered by 60 standard blows to each thigh resulting in a bruise of muscle but no skin, bone, or major vessel injury. Nutrition and respiration were maintained at normal levels. All nine pigs died with severe lung pathology and low PaO2. Ten other traumatized pigs were treated with a plasminogen activator iv 4 h after trauma. Five of these were treated with tissue plasminogen activator (tPA) and five with urokinase. All treated pigs survived 48 h and maintained a normal PaO2. Autopsy showed minimal lung pathology.
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PMID:Prevention of adult respiratory distress syndrome with plasminogen activator in pigs. 212 44

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

Thrombin-antithrombin III complex (TAT) and Plasmin-alpha 2 plasmin inhibitor complex (PIC) were examined in fifty two cases of various chronic liver diseases. TAT was significantly elevated in cases of hepatocellular carcinoma (HCC), but PIC did not show significant changes in any chronic liver diseases. Elevations of TAT and PIC were seen in cases of HCC accompanied by tumor enlargement and extensive tumor thrombosis. In cases of HCC undergoing transcatheter arterial embolization (TAE), TAT and PIC increased on the next day after TAE, and tended to recover with time, returning to almost normal at fourth week. Prolongation of prothrombin time, elevation of FDP and positive FM test were noted more often in liver cirrhosis with disseminated intravascular coagulation (DIC) than in severe liver dysfunction without DIC. Of five cases confirmed as DIC, only three cases were diagnosed as DIC by DIC score. On the other hand, TAT and PIC were significantly elevated in DIC cases. Especially, TAT exceeded 30 ng/ml in all DIC cases. TAT was regarded to be useful for the diagnosis of DIC in severe liver dysfunction.
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PMID:[Clinical significance of thrombin-antithrombin III complex and plasmin-alpha 2 plasmin inhibitor complex in chronic liver diseases]. 214 51

Coagulation studies were performed in a patient who had been bitten by a snake of the species Bothrops neuwiedi. The patient presented with hemorrhagic necrosis at the envenomization site and considerable bleeding from venous puncture sites. He developed a severe defibrination syndrome with a clottable fibrinogen level of approximately 0.1 g/l. Fibrinogen was not measurable by clotting time assay. Fibrin degradation products were greatly elevated. Treatment with antivenom caused an anaphylactic reaction within ten minutes and serum sickness after three days. In vitro experiments revealed that B. neuwiedi venom directly activates Factors II and X, but does not activate Factor XIII. In vivo consumption of Factor XIII after B. neuwiedi envenomization is ascribed to the action of Factor IIa. At low venom concentrations clotting is initiated by activation of prothrombin by the venom either directly or via Factor X activation. Treatment with heparin might be beneficial in coagulopathy secondary to snake bite by reducing circulating active thrombin. The venom contains thrombin-like proteases which cause slow clotting of fibrinogen, and plasmin-like components causing further proteolysis of fibrinogen and fibrin. Antivenom has no effect on the proteolytic action of the snake venom. The in vivo effects of antivenom are presumably caused by acceleration of the elimination of venom components from the circulation. Intravenous administration of antivenom caused normalization of blood coagulation parameters within 48 h.
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PMID:Coagulopathy after snake bite by Bothrops neuwiedi: case report and results of in vitro experiments. 229 86

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 order to assess precisely the fibrinolytic state in disseminated intravascular coagulation (DIC), plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP) and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 72 patients with DIC at presentation. Not only FbDP and TDP but also FgDP were markedly elevated in patients with DIC. When analyzed according to the underlying disease categories, the relative proportion of FgDP to TDP was high in patients with acute promyelocytic leukemia and vascular diseases, and it was the lowest in patients with sepsis. Correlation analysis revealed that plasma levels of FgDP correlated negatively with alpha 2-antiplasmin and positively with plasmin-alpha 2-antiplasmin complex (PAP) and a ratio of PAP to thrombin-antithrombin III complex (TAT). These findings indicate that besides fibrinolysis, fibrinogenolysis is markedly accelerated in the majority of the patients with DIC.
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PMID:Fibrinolysis and fibrinogenolysis in disseminated intravascular coagulation. 240 38

Management of cirrhosis with massive ascites involves particular difficulties. The introduction of a peritoneovenous shunt and reinfusion of concentrated ascitic fluid techniques allows increased diuresis and improves renal function. However, these procedures have frequently been associated with disseminated intravascular coagulation and/or activation of fibrinolysis. Factor VIII activity, antigen and ristocetin cofactor, plasminogen, antiplasmin, plasminogen activator activity and plasmin-antiplasmin complex were investigated both in the ascitic fluid and plasma of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicated that no hyperfibrinolysis was seen in the plasma of cirrhotic patients and that activation of fibrinolysis exists in ascites. Significantly higher levels of plasmin-antiplasmin complex and plasminogen activator activity were found in ascitic fluid than in plasma. In post-reinfusion much higher levels of all three Factor VIII components were observed in cirrhotic plasma than in normal plasma. In conclusion, activation of fibrinolysis could explain coagulation complications occurring after ascites reinfusion. Antifibrinolytic treatment could render the concentration-reinfusion technique more acceptable.
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PMID:Fibrinolytic study in plasma and ascitic fluid of cirrhotic patients before and after ascites concentration; reinfusion technique. 241 33

Thrombin (Thr), plasmin (Pl) and elastase (ELP) are serine proteinases which are quickly inactivated by their specific inhibitors (AT III, alpha 2AP, alpha 1AT), if intravascular activation of coagulation and fibrinolytic system or if release from PMN granulocytes by different stimuli (F.I., endotoxin, activated factor XII, a.o.) occurs. The immunological determination of the developing proteinase inhibitor complexes (PIC) AT III-Thr, alpha 2AP-Pl and alpha 1AT-ELP gives information as to whether intravascular coagulation, hyperfibrinolysis or unspecific proteolysis induced by elastase have taken place. Despite the high antiprotease activity in the plasma the a.m. serine proteinases may exert their proteolytic activity towards their specific substrates in vivo. In infectious diseases, fulminant hepatic failure and cardiac shock a complex consumption of coagulation factors and inhibitors may cause severe coagulation defects, microcirculatory disturbances and bleeding tendency. The PICs behaviour was determined in more than 80 patients with infectious diseases, in 5 patients with fulminant hepatic failure (FHF) and 7 patients with cardiac shock. Only in infectious diseases, mainly in septic complications, and septic complications during FHF and cardiac shock, are alpha 1AT-ELP levels found to be highly elevated. After cardiac shock, in FHF and in infectious diseases coagulation and fibrinolysis may additionally be activated. In this case AT III-Thr and alpha 2AP-Pl complexes could be detected in the patients plasma. This indicates that intravascular coagulation and hyperfibrinolysis has additionally taken place. To prevent bleeding complications a replacement therapy with plasma derivatives (AT III, plasminogen concentrate, PPSB and FFP) has been successfully performed in several patients with septic complications and in the 5 patients with FHF and the 7 patients with cardiac shock. No bleeding complication occurred, and the haemostatic balance could be maintained in the treated patients. AT III replacement therapy is necessary to stop DIC, PPSB improves severe coagulation defects, only FFP may additionally provide alpha 1AT, alpha 2AP and factor V. In acute renal failure sometimes plasminogen replacement is necessary to maintain a normal activity of the fibrinolytic system. The complex consumption of coagulation proteins in infectious diseases, FHF and cardiac shock cannot successfully be treated with an anticoagulant such as heparin alone.
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PMID:The proteinase inhibitor complexes (antithrombin III-thrombin, alpha 2antiplasmin-plasmin and alpha 1antitrypsin-elastase) in septicemia, fulminant hepatic failure and cardiac shock: value for diagnosis and therapy control in DIC/F syndrome. 242 25

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

In order to detect even minimal fibrinolysis activation in liver cirrhosis, we measured fibrinopeptide B beta 15-42 (B beta 15-42), an indicator of plasmin activity in vivo and alpha 2-antiplasmin (alpha 2-AP) in a group of cirrhotic patients. The second goal of this study was to investigate whether an increased fibrinolytic activity is related to a chronic disseminated intravascular coagulation. For this purpose we concomitantly measured fibrinopeptide A (FPA), marker of thrombin activity in vivo. Results show significantly higher levels of B beta 15-42 in cirrhotic patients than in control (p less than 0.01). In patients with high FPA levels we found significantly higher values than in patients with normal FPA (p less than 0.01). alpha 2-AP was lower in patients with high FPA levels than in patients with normal FPA (p less than 0.05). A significant negative correlation was found between FPA and alpha 2-AP only in patients with high FPA (p less than 0.05). There was no relationship between B beta 15-42 and FPA nor between B beta 15-42 and alpha 2-AP when all patients were considered. These findings confirm that in liver cirrhosis fibrinolysis activation may occur. The primary pathogenetic role of DIC may be important in this respect. However the lack of correlation between FPA and B beta 15-42 suggests that other pathogenetic factors may be involved in determining fibrinolysis activation.
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PMID:Fibrinopeptide A and B beta 15-42 in liver cirrhosis. 245 43


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