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

A prothrombin complex concentrate rich in factor VII has been used in the management of the clotting defect in thirteen patients with liver disease. Adequate correction of coagulation was achieved immediately after infusion in all cases. Within 4 hours there was some deterioration and by 24 hours the results approximated to pre-fusion values. Liver biopsies were performed without haemorrhagic complication in the immediate post-infusion period. There was no evidence of induced intravascular coagulation. Since other prothrombin complex concentrates have proved disappointing, both in their failure to correct the clotting defect and in their production of disseminated intravascular coagulation, this factor-VII-rich concentrate may be the treatment of choice in patients with liver disease who require temporary correction of their coagulation defect.
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PMID:Use of factor-VII-rich prothrombin complex concentrate in liver disease. 4 16

Serial prospective studies of coagulation status have been undertaken on 73 babies with a positive Coombs test. No abnormalities were detected in the babies with mild haemolytic disease, but seven of the 36 babies with severe haemolytic disease (cord Hb less than 11 g/dl or cord bilirubin greater than 85 mumol/1) showed evidence of transient defibrination 1 d after birth and another six had evidence of coagulation failure at birth with a platelet count of less than 150 x 10(9)/1 and a severe deficiency of multiple coagulation factors. The level of factor II and factor X was less than a fifth of the normal cord blood level in these six babies and the level of I, VII and IX was severely reduced; the factor VIII level was normal or high. Exchange transfusion started within 1 h of birth corrected the immediate factor deficiency in these six babies, but evidence of defibrination then became apparent with afibrinogenaemia, a marked fall in factors II and V, less constant falls in factors VII, IX and X, and a raised fibrin:fibrinogen degradation product level. One of these six babies died with severe pulmonary hypoplasia within an hour of birth; the other five died from haemorrhage into the lung or brain 1 1/2--6 d after birth. The very low vitamin-K dependent factor levels in the cord blood of the babies who died are presumably the result of liver damage in utero, but the subsequent changes are those of a comsumption coagulopathy. Simple screening tests at birth served to indicate which babies were at risk and it is concluded that death due to haemorrhage might be reduced by more intensive factor replacement before there is overt evidence of haemorrhage in these babies.
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PMID:Coagulation failure in babies with rhesus isoimmunization. 11 26

A case of liver hemangioma complicated by intravascular coagulopathy is presented because of the rarity of the association. Hemangioma of the liver was suspected by palpation of the liver tumor, scintigraphy and x-ray examination, and confirmed by selective hepatic arteriography in combination with exploratory laparotomy. Intravascular coagulopathy was established by demonstrating secondary fibrinolysis and consumption of platelets and coagulation factors. Unconjugated hyperbilirubinemia due to micro-angiopathic hemolytic anemia was also present. The clinical course of the clotting abnormalities was basically a chronic one with an occasional acute or subacute defibrination process associated with further enlargement of the hepatic tumor. These provide sufficient evidence that the intravascular coagulopathy was closely related with the hemangioma in the liver. Neither ligation of a presumed nutritional artery of the hemangioma nor radiation therapy caused any demonstrable reduction in the tumor size.
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PMID:A case of giant cavernous hemangioma of the liver complicated by intravascular coagulopathy. 14 35

This report concerns 20 patients with intrauterine fetal death. Blood samples for coagulation studies were obtained before, during and after delivery. No clinical defibrination or bleeding was noted. Coagulation defects were observed as follows: 2 biological defibrinations: The first case was a pregnancy of 32 wk with retention for more than 12 wk; hypofibrinogenemia was noted in all 6 samples, between 180 and 280 mg/100 ml. The second was a pregnancy of 32 wk with retention for more than 8 wk; fibrinogenemia was between 170 mg/100 ml and 140 mg/100 ml. 2 intravascular coagulations with normal fibrinogenemia, increase of fibrin degradation products and positive ethanol tests. 3 cases with slight coagulation defects that were difficult to explain. The coagulation defects appeared to be transient, and sometimes resolved themselves spontaneously. Induction of labour was made in 19 cases; quinine sulfate, used in 17 cases, was remarkably successful (1 intolerance, 1 failure). Study of the half-life of [125I]fibrinogen was made in 18 of the 20 cases. On average, it was reduced by half in comparison with the half-life of healthy men. The decrease was noted even in cases of fetal deaths without the coagulation defects detected by classical tests. The half-life of [125I]fibrinogen in 6 pregnant women before therapeutic abortion was also studied. The decrease of half-life was noted. Changes of metabolism of fibrinogen during pregnancy are discussed.
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PMID:Fetal death: coagulation defects and management. Report of 20 cases with study of the half-life of [125I]fibrinogen. 26 51

Seven adults with acute promyelocytic leukemia (APL) and disseminated intravascular coagulation were treated for remission induction with daunorubicin hydrochloride and prednisone. In all patients the coagulopathy was managed with continuous-infusion heparin sodium and vigorous transfusion with platelets, cryoprecipitate, and fresh frozen plasma. Five patients survived induction; they all achieved complete remission (CR). Median duration of CR was 27 + months; two patients presently survive in their initial CR at 28 and 48 months. Recognition of APL as a distinct type of acute leukemia and prompt initiation of treatment aimed at rapid cytoreduction and control of the coagulopathy has resulted in a prolonged disease-free survival for the majority of patients.
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PMID:Acute promyelocytic leukemia. Management of the coagulopathy during daunorubicin-prednisone remission induction. 28 Nov 91

Disseminated intravascular coagulation (DIC) is not a disease but a pathological process with widespread thrombus formation in small vessels; it occurs in many systemic conditions that stimulate the intravascular clotting mechanism. There may be widespread tissue involvement, and any tissue in the body may be affected, especially in the kidney, brain, liver, heart, and lungs. This abnormal coagulation is now commonly referred to as disseminated intravascular coagulopathy. It is prone to occur in obstetrical complications, in cancer, after transplantations, and where there has been tissue damage, such as burning, crushing, and surgery, all of which release thromboplastin into the circulation. It may also occur in Gram negative bacterial systemic infections, in antigen-antibody reactions, and in thrombotic thrombocytopenic purpura. When the eye is involved, the thrombi occur in the choriocapillaris, and are usually limited to the submacular and peripapillary choroid. The anterior parts of the eye generally escape involvement. Visual symptoms may be early, and may be due to central choroidopathy or to secondary retinal detachment.
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PMID:Disseminated intravascular coagulopathy. 29 Dec 17

The clinical and laboratory features of nine patients with chronic myelomonocytic leukemia are described. Hepatic or splenic enlargement accompanied by an absolute monocytosis in an older patient with an elevated serum or urine lysozyme and serum vitamin B12 levels were characteristic of the majority of patients in this series. No single clinical or laboratory finding was diagnostic for the disease. Most importantly, seven of nine patients had abnormal coagulation values; in two cases the abnormalities were consistent with disseminated intravascular coagulation and correlated with a hemorrhagic diathesis. It is concluded that patients with chronic myelomonocytic leukemia who have thrombocytopenia or a bleeding tendency should be evaluated for evidence of disseminated intravascular coagulation.
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PMID:Disseminated coagulopathy in chronic myelomonocytic leukemia. 29 10

The evidence for intravascular coagulation in liver diseases is critically reviewed. Alternative mechanisms for hypofibrinogenemia and the accelerated disappearance of fibrinogen from blood are proposed, such as loss into extravascular compartments (e.g., ascites, areas of liver necrosis, etc.). Possible mechanisms other than DIC for the elevation of serum FDP are also considered, such as extravascular fibrinogen proteolysis with subsequent transfer of FDP to blood. Therapy is discussed with reference to the current knowledge on pathophysiology of the coagulation defect in liver diseases.
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PMID:Diffuse intravascular coagulation in liver disease? 33 13

Acute promyelocytic leukemia (APL) is characterized by proliferation of morphologically abnormal promyelocytes and a severe bleeding diathesis. The abnormal promyelocyte is characterized by abundant, large granules, many of which are spindle-shaped. Electron microscopic appearance of the granules closely resembles that of Auer rods. The granules appear to possess tissue thromboplastin activity by both immunologic and clotting assays. Coagulation studies in APL are generally consistent with disseminated intravascular coagulation. Prolongation of the prothrombin time and elevation of fibrinogen degradation products are the tests that are most commonly abnormal. Although occasional reports indicate a favorable response of the coagulopathy to drugs that inhibit fibrinolysis, the use of prophylactic heparin appears to be the treatment of choice. The response rate of APL to chemotherapy regimens that contain an anthracycline is comparable to that of acute myelogenous leukemia. The recent description of the 15;17 chromosomal translocation which may be pathognomonic for APL is only the second example of a chromosomal marker of human neoplasia. Marked elevation of serum vitamin B12 and B12 binding proteins appears to be another characteristic feature of APL. An in vitro cell line of APL cells has been demonstrated to have the capacity to differentiate to functional polymorphonuclear leukocytes, but the cause for the maturation arrest is unknown.
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PMID:Acute promyelocytic leukemia. 39 71

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


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