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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three kinds of anticoagulant therapy for obstetrical DIC were studied. 1. Antithrombin-III (AT) or gabexate mesilate for acute DIC, mainly for abruptio placentae. 2. Heparin or heparin-AT combination therapy for toxemia pregnancy. 3. Low molecular weight heparin (LMWH) for fetus of intrauterine growth retardation (IUGR). The results obtained were as follows, 1. a) Platelet count, and fibrinogen were significantly increased in AT therapy group compared with gabexate mesilate group. b) In clinical manifestation, renal failure and hemorrhagic diathesis were improved especially in AT group. 2. In heparin-AT group, high systolic blood pressure was improved during administration of AT, the high level of thrombin antithrombin complex was also found in these period. 3. a) The improvement of the gain of estimated fetal body weight was found after administration of LMWH. b) Redistribution of blood flow in one case of severe IUGR was observed during administration of LMWH.
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PMID:[Anticoagulant therapy in obstetrical disorders]. 217 Jul 3

Six adult specific-pathogen-free cats were inoculated intraperitoneally with a cell culture-adapted strain of feline infectious peritonitis virus. Plasma samples were evaluated for antithrombin-III (AT-III) activities at post-inoculation days (PID) 0, 4, and 11 and at termination on PID 16 (1 cat) or 21 (5 cats). Other hemostatic values evaluated were activated partial thromboplastin times, prothrombin times, thrombin times, fibrinogen, platelet counts, and fibrin/fibrinogen degradation products. Antithrombin-III activity remained within normal or above normal range (89 to 246%) in all cats, with the exception of one cat on PID 4 (AT-III, 70%). Mean baseline AT-III activity for 6 cats at PID 0 was 123%. Mean AT-III activity on PID 4, 11, and 16 or 21 was 98, 162, and 130%, respectively. On PID 4 and 16 or 21, results of coagulation screening tests indicated that all cats had disseminated intravascular coagulation. Histologically, cats also had severe fibrinonecrotizing thrombovasculitis.
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PMID:Evaluation of antithrombin-III activity as a coindicator of disseminated intravascular coagulation in cats with induced feline infectious peritonitis virus infection. 255 30

A detailed review of the dynamic processes of coagulation and fibrinolysis precedes a discussion of clinical applications, especially for users of oral contraception and others with antithrombin-III disorders. Coagulation and fibrinolysis are both initiated by activation of circulating pro-enzymes, namely thrombin and plasmin. Both of these have circulating and local inhibitors that modify stages of the clotting and fibrinolytic processes. The circulating system, also called the intrinsic coagulation system, can be regarded as an amplification system related to the extrinsic, or cellular system. Antithrombin-III (AT-III) is a specific plasma protein that inhibits coagulation at the step (after platelets aggregate) of fibrin formation. At-III can be measured immunologically, or functionally by its ability to bind thrombin in the presence of heparin. Familial AT-III deficiencies incur a risk of venous thrombosis, and may be total or partial, depending on the type of genetic defect. Affected individuals may be treated with vitamin-K antagonists, anabolic steroids, or subcutaneous, low-dose heparin. Episodes of thrombosis may also represent acquired AT-III deficiency, such as in pregnancy, abortion, post-surgery, or disseminated intravascular coagulation. The approximately 10% decrease in AT-III seen in women taking estrogen-containing oral contraceptives is within normal limits. The oral route is significant, as AT-III is a protein made by the liver. This fall is not of any physiological significance, since the plasma euglobulin fibrinolytic system is also increased. Some pill users with AT-III deficiency or other thrombosis-prone conditions, however, may be at risk of increased thrombosis.
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PMID:Pathophysiology and clinical aspects of fibrinolysis and inhibition of coagulation. Experimental and clinical studies with special reference to women on oral contraceptives and selected groups of thrombosis prone patients. 327 96

Antithrombin-III assays are performed to assess response to heparin therapy and efficacy of antithrombin concentrate therapy and in diagnosing hereditary thrombophilia, deep venous thrombosis, pulmonary embolus, and disseminated intravascular coagulation. Synthetic substrate assays for antithrombin-III are the methods of choice; however, most existing assay systems are semiautomated. A fully automated, antithrombin-III assay using the Kabi Chromogenic Synthetic Substrate S-2238 COATEST on the MULTISTAT III has been developed. This assay was compared with the Dade Protopath fluorometric assay. The correlation (r-sq) between the two assay systems was 0.82. Additionally, a three-way assay comparison was also performed, incorporating a new fluorometric substrate for antithrombin-III. The three-way comparative assays revealed correlation as follows: MULTISTAT III fluorometric assay and the MULTISTAT III/Kabi COATEST assay r-sq = 0.90; MULTISTAT III fluorometric assay and the Dade fluorometric assay r-sq = 0.86; and the MULTISTAT III/Kabi COATEST assay and the Dade Protopath fluorometric assay r-sq = 0.95. These automated assays were extremely cost effective and were a fraction of the cost of performing other types of antithrombin-III assays.
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PMID:Fully automated antithrombin-III assays by synthetic substrate on the Multistat III. 361 51

Disseminated intravascular coagulation (DIC) syndromes can be defined as the formation of fibrin deposits within the microcirculation, occurring in definite clinical situations. Their biological counterpart is a consumption coagulopathy. The clinical profiles of DIC have been well known for decades, are multiform and range from latency to overwhelming haemorrhagic diatheses, including also characteristic but rare situations, such as purpura fulminans, acral cyanosis and pictures resembling thrombotic thrombocytopenic purpura or haemolytic-uraemic syndrome. Biological tests of DIC show a consumption coagulopathy, displayed on the standard haemostasis sheet; along with signs of paracoagulation and/or of secondary fibrinolysis (FDP). New tests have recently been introduced: D-dimers are specific and sensible; Antithrombin-III, protein C and alpha 2-antiplasmin also can sometimes be useful. The knowledge of the pathophysiology of DIC has made advances with passing years. Fibrin deposits may be non-occlusive, and indeed they are swiftly removed by a secondary fibrinolysis. Except in very rare situations, such as those leading to a cortical renal necrosis, and perhaps in some ARDS, there is little evidence relating DIC to organ failure syndromes. Moreover, there is no clear relationship between the severity of the consumption coagulopathy and the prognosis. For instance, the mortality is much lower in abruptio placentae, where the coagulopathy is very severe, than in septic shock, where it is usually moderate. In septic shock, the disorders of haemostasis were related initially to a platelet activation, then to an activation of the contact system (releasing kinins and triggering complement cascade), and nowadays to the activation of the extrinsic coagulation system. The treatment of DIC is mainly the treatment of its cause. Indications for heparin therapy should be strictly limited to a few exceptional circumstances. When haemorrhagic diathesis threatens, FPC and/or platelet transfusion may be indicated. Aprotinin can be useful in rare cases of overwhelming secondary fibrinolysis. Trials with antithrombin-III or C1-esterase inhibitors are in progress.
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PMID:[Disseminated intravascular coagulations]. 900 11