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

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

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

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

Thrombin or factor Xa added to plasma are inactivated by antithrombin III (At-III). The inactivation is accelerated by heparin, permitting assay systems which rapidly measure the At-III content of diluted plasma. Without heparin, the slow inactivation rates may be measured. Existing activity assays (fibrinogen or chromogenic substrates) and immunoassays of At-III have been reviewed. Correlation studies show a close correlation between the results of immunoassay and the results of most activity assays. In health, a narrow range of At-III has been found. The level is low in infancy. Fertile women have on the average somewhat lower levels than men. In old age, the level tends to drop. In clinical material studied with amidolytic assays, subnormal At-III levels were found in hereditary deficiency, liver disease, disseminated intravascular coagulation and in some cases with acute thrombosis. The amidolytic assays are rapid to perform, do not require experience in clotting technique and seem preferable in clinical routine work.
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PMID:Antithrombin III: critical review of assay methods. Significance of variations in health and disease. 35 Jul 29

The case of a nineteen-year-old women with the cerebral form of malaria tropica is reported. She showed hyperpyrexia, abdominal manifestations, haemolysis and disseminated intravascular coagulation. Cerebral symptoms amounting to grade IV encephalopathy occurred. The patient responded rapidly to the administration of chloroquine, anticonvulsants, dextran, corticosteroids, antipyretics, blood and antithrombin III and her symptoms had almost completely vanished one week after the onset of therapy.
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PMID:[Course and intensive treatment of acute falciparum malaria (author's transl)]. 37 59

Endotoxin from E. coli was infused into the distally ligated common bile duct of rabbits under the static pressure of 25 cm H2O. Fibrinogen, soluble fibrin monomer complexes, antithrombin III, leukocyte and platelet counts were estimated before, and 2, 4, and 6 h after endotoxin infusion. All parameters were found significantly changed 2 h after endotoxin infusion. While fibrinogen level, AT III, leukocyte and platelet counts decreased after the endotoxin infusion the amount of SFMC increased. The change of hematological parameters showed a pattern characteristic of disseminated intravascular coagulation (DIC). In accordance with this microclots in the glomeruli of the kidneys could be demonstrated in all endotoxin-treated animals by pathological study. The findings suggest that by endotoxin infusion into the common bile duct, as a focal origin, DIC can be produced.
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PMID:[Disseminated intravascular coagulation (DIC) after endotoxin infusion into the common bile duct of rabbits (author's transl)]. 38 87

Anticoagulants in the form of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III were administered in separate experiments prior to endotoxin infusion in the dog. The pattern of disseminated intravascular coagulation (DIC) developed consistently when endotoxin alone was administered. Heparin dosages from 1 to 10 mg/kg did not influence the appearance of thrombocytopenia but effectively eliminated the decrease in fibrinogen levels ordinarily found. Antithrombin III (AT III), obtained from the National Red Cross, administered in a dose designed to provide a doubling of the circulating AT III, reduced the fibrinogen utilization to a similar degree as heparin without affecting the platelet loss. Dipyridimole, as administered, was ineffective in this model, and did not alter the development of thrombocytopenia or the hypofibrinogenemia. Steroids, Macrodex, and prostaglandin E1 had minimal effect on the coagulopathy. Our finding would suggest that the endotoxin effect on dog platelets id direct, and not mediated by thrombin, and that the role of heparin in the clinical management of DIC should be considered only in instances in which renal complications exist.
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PMID:Endotoxin-induced intravascular coagulation (DIC) and its therapy. 40 May 81

Coagulation factors and plasma proteins are significantly decreased in patients with hyperdynamic septic shock. Besides the activation of the coagulation system, the endotoxin-induced release of granulocyte proteases is responsible for a septic disseminated intravascular coagulation. In this situation special emphasis should be placed on the levels of antithrombin III regarding application of heparin.
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PMID:[Hyperdynamic septic shock in man: concentration course of selected coagulation factors and plasma proteins]. 45 50


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