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

Low molecular weight heparins are increasingly prescribed in France. Prepared from standard heparin by depolymerisation, they show a markedly decreased anti IIa activity and a anti Xa/anti IIa ratio ranging from 2 to 4. Their mode of action in the coagulation system is still not well known and it is difficult to explain the mechanism of their antithrombotic effect, demonstrated in vivo. They seem to inhibit the first traces of thrombin and then counteract the priming and amplification of coagulation. Their fibrinolytic activity is also a disputed question, but seems to be lower than that of standard heparin. The pharmacological studies show a venous as well as arterial antithrombotic activity of a low molecular weight heparin on several animal models, a lower but not negligible bleeding risk as compared to unfractionated heparin. Furthermore heparin fragments have a weak interaction with platelets, which allow to foresee a greater efficacy of LMWH than standard heparin in arterial thrombosis. Some very rare cases of thrombocytopenia in patients treated with LMW heparins have been recently reported. The compared pharmacokinetics of heparins gave proof of a renal elimination of low molecular weight heparin and a bio availability of about 90% after subcutaneous injection. Many clinical studies allowed to define indications of heparin fragments in prophylactic treatment after surgery as well as in medical patients and in curative treatment in case of deep vein thrombosis. However, others studies must be carried out to define the real efficacy of such a treatment during pulmonary embolism, disseminated intravascular coagulation and myocardial infraction, or during thrombotic complications after vascular surgery.
J Mal Vasc 1992
PMID:[The new heparins]. 131 47

Five cases of neonatal infective endocarditis are reported. The mitral, tricuspid and pulmonary valves were involved either alone or in association. The predisposing factors were multiple: umbilical catheter, respiratory distress with assisted ventilation, septicemia, osteoarthritis or gastroenteritis. Only one child had a minor cardiac malformation. The causal organism was a staphylococcus aureus in all cases. All children had disseminated intravascular coagulation and a cardiac murmur. The diagnosis was confirmed by echocardiographic demonstration of bacterial vegetations. Three of the 5 children died despite long-term antibiotic therapy. In one case, a vegetation embolised to the pulmonary artery. In the two cured neonates the vegetations disappeared. These cases illustrate the value of echocardiography which should be performed in all neonates with septicemia or disseminated intravascular coagulation, especially when there is an associated cardiac murmur.
Arch Mal Coeur Vaiss 1990 May
PMID:[Neonatal infectious endocarditis. Apropos of 5 cases]. 211 75

The authors report the case of a Bothrops lanceolatus snake bite complicated by severe pulmonary embolism a few hours after admission. This thromboembolic complication developed despite heparin therapy and was followed by disseminated intravascular coagulation (DIC). Vascular thrombosis and pulmonary embolism are rare after Bothrops lanceolatus snake bite as patients are usually hypocoagulable due to DIC. In this case, the thromboembolism was probably caused by the procoagulant effect of the thrombin-like enzymes of the snake venom which may have been injected directly into the vein of a young woman taking a contraceptive pill. A specific antivenin which has recently become available fort treatment may decrease the complications of Bothrops lanceolatus snake bite.
Arch Mal Coeur Vaiss 1989 Nov
PMID:[Pulmonary embolism and disseminated intravascular coagulation after being bitten by a Bothrops lanceolatus snake. Apropos of a case]. 251 45

A group of 37 patients with myocardial infarction less than 6 hours old was given 5,000 IU of heparin and 0.75 mg/kg of tissue plasminogen activator (rt-PA) (Group A, N = 18) or placebo (Group B, N = 19) intravenously over 90 minutes in a double blind study. Blood sampling was performed before, during and after treatment. The plasma rt-PA concentrations (micrograms/ml) of Group A were as follows: (Table: see text) The concentrations of plasminogen and antiplasmin have decreased significantly as did the fibrinogen level: a concentration of 1 g/l was observed in 7 cases during rt-PA therapy, lasting for 4 to 8 hours after the end of the infusion of rt-PA in 3 cases. The increase of FDP during rt-PA (m = 551 and 222 micrograms/ml at the 60th and 90th minutes) was relatively moderate considering the average level of defibrination (61%). No significant biological changes were observed in Group B. These results support those of our in vitro trials: at comparable thrombolytic activities, the reduction of plasma fibrinogen is less with rt-PA than with streptokinase (SK) or urokinase (UK). However, at concentrations 1 microgram/ml, rt-PA causes almost complete defibrination.
Arch Mal Coeur Vaiss 1986 Oct
PMID:[Tissue plasminogen activator (t-PA) in myocardial infarction. Biological aspects]. 310 72

Six cases of gravidic toxemia (4) and thrombotic thrombocytopenic purpura (Moschowitz's disease) in puerperium with choriocapillaris occlusion, were examined. At the acute stage, the vision is improved, ophthalmoscopy of the fundus revealed cystlike bullous exudative subretinal with retinal detachment, yellowish spots (of retinal pigment epithelium) and often minimal localized arteriolar narrowing. The evolution included retina application pigmentary disturbances and Elschnig's spots. Fluorescein angiography showed delayed filling of the capillaris and dye leakage in the subretinal space (first hypofluorescence and late hyperfluorescence). There are various stages of ischaemic involvement but in all cases visual symptoms may be due to central obstructive choroidopathy with delayed filling and occlusion. The retinal detachment in toxemia or Moschowitz disease in pregnancy in secondary to microcirculatory choroidal damage (short ciliary vessels essentially) with rupture of blood retinal barrier. Other constatations are made in disseminated intravascular coagulation, periarteritis nodosa, accelerated nephrosclerosis, hemolytic uremic syndrome in puerperium, and these suggested possible relationship between the various conditions.
J Mal Vasc 1985
PMID:[Acute choriocapillaris occlusion in pregnancy and puerperium. Toxemias, thrombotic microangiopathies]. 407 90

Haemorrhage or thromboembolism during heparin therapy are usually attributed to a prescribing error. However, these clinical manifestations--especially thromboembolism--may occur with heparin therapy during severe thrombocytopenia. The authors describe the clinical, biological and physiopathological features characterising this thrombocytopenia with reference to 7 personal cases and a review of the literature. The incidence of heparin-induced thrombocytopenia varies between 0.5 and 1%. It seems to be more common (4%) during heparin therapy for thromboembolic disease. The thrombocytopenia appears 8 days after the onset of heparin therapy. It is characterised by the high incidence of thromboembolism (70% of cases) compared to haemorrhagic phenomena (10% of cases). Thrombocytopenia is asymptomatic in 20% of cases. The thrombocytopenia is peripheral, i.e. the bone marrow is normal, and isolated, i.e. there are no deficiencies in the factors of coagulation. One of our cases was of special interest because it was complicated by disseminated intravascular coagulation. Eight cases of disseminated intravascular coagulation have previously been reported. Analysis of platelet aggregation demonstrates the relationship between heparin and thrombocytopenia. Mixing the plasma of patients with thrombocytopenia and plasma rich in platelets in the presence of heparin lead to thrombo-agglutination. In contrast, in control and non-thrombocytopenic heparinised subjects, no reaction was found. These observations prove the existence of a platelet aggregant factor in the plasma during thrombocytopenia. This disappears 6 weeks to 2 months after stopping heparin. This platelet aggregant factor initiates platelet aggregation which is responsible for thrombocytopenia and for the initiation of phenomena of coagulation, so explaining the thromboembolic phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1983 Oct
PMID:[Severe thrombopenias during heparin therapy. A phenomenon of intra-vascular platelet aggregation]. 641 95

A case of intravascular coagulation in a patient with a very large ventricular aneurysm is reported. Biological signs of defibrination with a low serum fibrin of 0,80 g/1, thrombocytopaenia of 80,000/mm3 and the presence of soluble complexes and FDPs were detected after recurrent haematuria. Low dose heparin (0,15 to 0,20 ml x 2/day by subcutaneous injection) led to normalisation of the fibrinogen levels, increased the platelet count and reversed the consumptive coagulopathy. Each withdrawal of heparin (5 attempts over 16 months) led to a biological relapse. At the final withdrawal of therapy, the biological abnormalities remained minor; the consumption of fibrinogen and platelets was well compensated. Similar cases have been published in aortic aneurysms with and without dissection, but the association with a cardiac aneurysm has not been reported previously. The physiopathological mechanism of the coagulopathy is discussed and the authors suggest routine study of the coagulation system in all patients with cardiac aneurysms. This case illustrates the efficacity of moderate doses of heparin in a patient with "biological hypercoagulability" well documented by laboratory investigations.
Arch Mal Coeur Vaiss 1981 Jan
PMID:[Chronic disseminated intravascular coagulation in a case of ventricular aneurysm. Correction by low-dose heparin]. 678 33

Following operation for bladder papilloma and subcutaneous heparin therapy, a patient developed severe thrombopenia with biological signs of disseminated intravascular coagulation (D. I. C.). Heparin therapy was discontinued and the platelet count became normal, no further signs of (D. I. C.) being apparent. Histological examination of the excised tumor showed that it was non-malignant, the thrombopenia being directly related to the heparin treatment. A review of the published literature demonstrated variations in the frequency of this complication reported, with an apparently higher incidence in the USA than in France. This could possibly depend upon whether the heparin was prepared from pulmonary or intestinal tissue. The thrombopenia may be severe (platelet count less than 100,000/mm3) with resulting hemorrhages or more commonly thromboses, or moderate without clinical expression. The dose or mode of administration of the heparin does not appear to be a factor in the development of the thrombopenia, its mechanism not being clearly elucidated. From the practical point of view, a platelet count should be performed before heparin treatment, and this should be repeated if the treatment is continued for more than four days.
J Mal Vasc 1982
PMID:[Thrombopenia caused by heparin. Review of the literature apropos of a personal case]. 714 30

We report a case of alveolar haemorrhage in all probability, attributable to the use of anti-vitamin K. The favourable outcome of this type of disease has rarely been reported with anticoagulants and fibrinolytics, most frequently in a disturbed haematological setting with disseminated intravascular coagulation or profound thrombocytopaenia. One should not forget this diagnosis in cases of acute respiratory failure in association with an alveolar syndrome in an exposed patient due to the fact that the outcome is generally favourable after correcting the disturbed coagulation.
Rev Mal Respir 1995
PMID:[Diffuse alveolar hemorrhage secondary to oral anticoagulant use]. 856 83

The search for a cancer is part of the classical investigation of unexplained venous thrombosis. Arterial thrombosis associated with neoplasia is more rare. The authors report two cases in which arterial thrombosis was the final event of their malignant disease. The first case had abacterial thrombotic endocarditis and disseminated intravascular coagulation at the origin of multiple thrombotic complications. The initially unknown cancer was a pancreatic adenocarcinoma. The second case presented with acute occlusion of the iliac artery after ablation of a malignant melanoma. Despite embolectomy with a Fogarty catheter and effective anticoagulation, the thrombosis recurred several times at the same site. The clinical features and the mechanisms of these two cases suggestive of Trousseau's syndrome are discussed.
Arch Mal Coeur Vaiss 1996 Oct
PMID:[Paraneoplastic arterial thrombosis. Apropos of 2 cases]. 895 28


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