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)

"Hemorrhage in the newborn" has long been recognized as merely a result of vitamin K deficiency. However, it is also recognized that fibrinolysis, especially the correlation between the plasminogen-activator and plasmin-inhibitors, play an important role in this disease during the neonatal period. With this in mind, we compared thromboelastograms (TEG) from samples with and without urokinase (plasminogen-activator). In 13 out of 15 newborn infant blood-samples (prior to and after addition of urokinase) the thromboelastogram showed the pattern of a consumption coagulopathy. The change in the concentration of plasmin-inhibitor during the neonatal period was also measured using alpha2-macroglobulin, alpha1-antitrypsin and antithrombin III with M-partigen-plates. The value of alpha2-macroglobulin showed normal adult levels but the value of alpha1-antitrypsin and antithrombin III did not even reach half of the adult level. During the newborn period, the plasmin-inhibitor shows a remarkable lowering tendency and it may be surmised that with such a lowering tendency plasmin-inhibitor may constitute an exceptionally large handicap when the activator is working. This is especially true in the case of lung hemorrhage since the activator arises from a severe pathological state in the lungs and in addition because this is complicated by the lowering of plasmin-inhibitor. These results indicate that the low level of plasmin-inhibitors work synergistically with the high value of activator. The low level of antithrombin III could be the reason for coagulation disorders such as disseminated intravascular coagulation, (DIC).
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PMID:New neonatal problems of blood coagulation and fibrinolysis. I. The change of plasmin inhibitor levels in the newborn infant. 6 4

During pregnancy, 12 women who smoked more than 10 cigarettes/day and 12 nonsmokers had blood taken and analyzed at 12, 20, 25, 30, 34, and 38 weeks of gestation. Fibrinogen, plasminogen, plasminogen activator, serum fibrin degradation products, antithrombin 3, alpha 1 antitrypsin, and alpha 2 macroglobulin were measured. The only significant (p .05) difference was that plasma fibrinogen was lower among smokers at 20 weeks. However, there were other patterns of difference -- mean fibrinogen and plasminogen levels were slightly lower throughout pregnancy and reached a lower peak in the smoking group. Fibrinolytic activity fell in the smokers to the same low level as in nonsmokers by 38 weeks, but at a slower rate. Serum fibrin degradation products and alpha 2 macroglobulin were consistently higher in the smoking group. Although the findings showed no major disseminated intravascular coagulation in smokers, there was a pattern of a possible low-grade syndrome.
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PMID:The influence of smoking on the haemostatic mechanism in pregnancy. 6 96

Human plasma alpha2-plasmin inhibitor in fibrinolytic states was studied using immunochemical methods and radioiodinated plasminogen. The concentration and activity of plasma alpha2-plasmin inhibitor decreased when urokinase was added to plasma in vitro or infused intravenously in man. The decrease was associated with the appearance of plasmin-alpha2-plasmin inhibitor complex which subsequently disappeared from the circulation in a short time. A decrease of other major inhibitors, such as alpha2-macroglobulin and alpha1-antitrypsin, was not observed when the amount of urokinase added or infused was relatively small, and conversion of plasminogen to plasmin was not extensive. The formation of plasmin-alpha2-macroglobulin complex was observed only when plasma plasminogen was activated with a larger amount of urokinase, and after most of the alpha2-plasmin inhibitor was consumed by forming complexes with plasmin. The formation of plasmin-alpha1-antitrypsin complex was not observed even in the highly activated plasma unless exogenous plasmin was added to the plasma. alpha2-Plasmin inhibitor was the only inhibitor of which the concentration in plasma was significantly decreased in patients with disseminated intravascular coagulation and fibrinolysis among the major plasmin inhibitors in plasma. The most reactive inhibitor for regulating plasma fibrinolysis very likely is alpha2-plasmin inhibitor.
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PMID:The behavior of alpha2-plasmin inhibitor in fibrinolytic states. 6 62

Long-term determinations of haemostasis factors in a case of Osler's telangiectasia revealed the temporarily simultaneous existance of periods of thrombocytopenia, a decrease of prothrombine and a reduction of the fibrinogen and plasminogen level. These findings considered as signs of consumption coagulopathy coincided with an increased bleeding tendency of the patient. The correlation existing between the clinical symptoms and the observed disorders of coagulation may possibly be explained by the appearance of an intravascular coagulation during the late period of the haemorrhagic diathesis, which could be proved by the simultaneous increase of fibrinogen degradation products. Moreover, the patient's plasma was capable of strongly inhibiting factor VIII of a normal plasma. The possible influence of plasmatic disorders of coagulation which are caused by secondary reasons on the clinical picture of a haemorrhagic diathesis primarily based on vascular conditions is discussed.
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PMID:[A case of Osler-Rendu disease with simultaneous thrombopenia and a factor VIII inhibitor]. 6 66

Coagulation and fibrinolysis studies were performed on 64 newborns; 16 premature infants with hyaline membrane disease (HMD), 17 newborns with other forms of respiratory distress syndrome (RDS) (8 of them were premature), 31 healthy newborns (11 of them were premature). All the babies were studied once in the first 48 hours of life. There was no significant difference between sick and healthy babies for 5 parameters; platelet count, factor VIII, fibrinogen, fibrin(ogen) degradation products, euglobulin lysis time. Factor II, VII and X were low in all infants, and premature infants had significantly lower levels compared to full term newborns. Factor V, plasminogen, alpha 2 macroglobulin (alpha 2M) and antithrombin III (AT III) levels were significantly lower in sick infants. Except for AT III, these deficiencies were not related to prematurity. No significant difference was found between HMD and other RDS. Of the 33 sick infants, 5 developed laboratory findings consistent with disseminated intravascular coagulation (DIC). The results indicate that the coagulation and fibrinolytic abnormalities reported are not specific to HMD.
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PMID:Haemostatic disorders and respiratory distress in the newborn. 7 54

Human newborns have certain hemostatic "deficiencies" which seem to be peculiar to this period of life, such as reduced factors II, VII, IX, X, XI, and XII, reduced antithrombin III levels, and reduced plasminogen levels. However, they are capable of activating the coagulation mechanism to elicit either the entity of disseminated intravascular coagulation or the occurrence of localized and diffuse thrombotic events. The mechanisms involved have yet to be defined. Evidence has been presented to suggest that preterm infants may manifest a variant form of disseminated intravascular coagulation in which thrombocytopenia is not present.
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PMID:Activation of coagulation and disseminated intravascular coagulation in the newborn. 12 Jun 82

Complement component C3, component C4, and total hemolytic complement CH50 were measured in blood from ten patients with acute disseminated intravascular coagulation (aDIC) syndromes. The study group was selected on the basis of history to exclude antecedent immunologic, infectious, or hepatic disease. The mortality rate was high (90%), the average duration of illness short (8.5 days), and the utilization of blood products extensive. The behaviors of C3 and C4 were found to be analogous to fibrinogen, plasminogen, antiplasmin, and platelets. CH50 activity paralled C3 and C4, as well as results of the soluble coagulation factor screening tests. It is concluded that serum complement is consumed as part of the multisystem dysfunction, aDIC, and that in conjunction with traditional indicators it may be utilized to gauge the severity of this syndrome.
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PMID:Complement consumption in acute disseminated intravascular coagulation without antecedent immunopathology. 13 95

In 27 multiple trauma patients receiving standard shock management and intensive care, coagulation and fibrinolysis were investigated after early heparinization. The general coagulation tests did not imply any impaired clotting function. Platelets and factors I, II, and V decreased without induction of hypocoagulability. There was considerable decrease in plasminogen, whereas FDP ranged within normal; thus, a hyperplasminemia can be excluded. Antithrombin III remained within normal range; even in nonsurvivors there was no depletion, although their antithrombin III activity was significantly lower. In comparison to 50 trauma patients - a comparable group with regard to trauma patterns, shock management, and intensive care - there were no significant differences in volume requirements or mortality rate. Whether early heparinization is effective in preventing disseminated intravascular coagulation (DIC) related organ failure remains to be seen.
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PMID:Coagulation and fibrinolysis in multiple trauma after early heparinizing. 26 99

Bleeding is common in acute myeloblastic leukemia (AML). At the time of diagnosis, the danger of bleeding cannot be predicted by laboratory means. However, the following factors represent increased risks: Promyeloblastic leukemia, high blast count, low fibrinogen, low plasminogen. From coagulation studies performed at the time of bleeding complications, the pathomechanism leading to bleeding complications usually cannot be detected. The question whether impairment of production, consumption coagulopathy, or primary fibrinolysis causes the bleeding complications can only be answered by controlling frequently clinical and hemostatic criteria, which include the thrombocytic stystem as well as plasmatic coagulation and fibrinolysis. At the present time, the therapy of bleeding complications in AML is symptomatic. It consists of transfusion with thrombocytes or fresh whole blood, respectively. Coagulation factor concentrates should only be given in combination with Heparin to prevent the deterioration of consumption coagulopathy.
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PMID:[Bleeding complications in acute myeloblastic leukemia (author's transl)]. 28 49

Coagulation studies were done on 78 consecutive cases of obstructive jaundice with or without biliary tract infection. Among 26 cases with biliary tract infection 20 cases showed no bleeding tendency but remarkable hypercoagulability with decreased fibrinolytic activity. Other six cases developed diffuse bleeding tendency in addition to the signs of hypotension and multiorgan dysfunction such as oliguria, respiratory distress and mental confusion. Most showed marked coagulation defects characterized by thrombocytopenia, decreased fibrinogen, antithrombin III and plasminogen levels and narrowing of maximal amplitude in thrombelastogram as well as the increase of fibrin degradation products and positive soluble fibrin monomer complexes. All except one died and three cases were autopsied. In two cases postmortem examination revealed multiple fibrin thrombi in lungs and other organs. A cause of the development of bleeding tendency in obstructive jaundice presently observed may likely to be due to the occurrence of disseminated intravascular coagulation (DIC), i.e. hypercoagulability caused by the biliary tract infection is responsible.
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PMID:Occurrence of disseminated intravascular coagulation (DIC) in obstructive jaundice and its relation to biliary tract infection. 32 28


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