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)

Mercuric chloride (HgCl2) induces in Brown Norway (BN) rats an autoimmune disease characterized by a biphasic glomerulonephritis (GN). A transient nephrotic syndrome occurs during the third and fourth weeks after the first HgCl2 injection. Related to nephrotic syndrome, an hypercoagulable state develops with decreased factor XII and anti-thrombin III (AT III) levels and increased factor V activity and fibrinogen concentration. Moreover, during the same period, most of the rats were found thrombocytopenic. The presence of soluble fibrin monomer complexes and of fibrin degradation products (FDP) in the plasma of these rats associated with fibrin thrombi in glomerular capillary lumen proved the occurrence of disseminated intravascular coagulation (DIC). DIC was responsible for the death of several rats but most of these survived and clotting abnormalities were no longer found. Numerous factors can explain the occurrence of DIC in this model: anti glomerular basement membrane antibodies, circulating immune complexes, complement activation and/or glomerular endothelial cell detachment. The HgCl2 induced autoimmune disease appears as a good experimental model to study the relation between coagulation process and glomerulonephritis.
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PMID:Involvement of hemostasis during an autoimmune glomerulonephritis induced by mercuric chloride in brown Norway rats. 622 1

The clinico-pathological features of four patients with placental-site trophoblastic tumour (trophoblastic pseudotumour) are presented. One patient had the nephrotic syndrome associated with evidence of disseminated intravascular coagulation, with complete resolution after hysterectomy. In two patients the tumour extended beyond the uterus, and one of them died with many metastases in spite of intensive post-operative chemotherapy and 'second look' laparotomy. In three patients the tumour behaved as an actively infiltrative neoplasm resistant to chemotherapeutic regimes usually effective for choriocarcinoma. Serum HCG levels were relatively low compared with those of choriocarcinoma. Histologically the tumours were predominantly composed of mononuclear cells supported by a variable amount of vascular stroma and lacked the bilaminar structure characteristic of choriocarcinoma. Scattered cells stained positively with anti-beta HCG and anti-alpha HCG antisera. Prior curettage was diagnostic in two of three cases. We did not find a clear correlation between mitotic activity and subsequent behaviour. Inflammatory cell infiltration and evidence of organisation around the tumour may be favourable prognostic indicators. We agree with a recent publication stressing the variable behaviour of this tumour, and emphasize the importance of serum HCG monitoring. Total surgical excision is usually feasible and in aggressive cases offers the best chance of eradication. We support the recent suggestion that 'trophoblastic pseudotumour' is an unsuitable name for a potentially lethal disease.
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PMID:Placental site trophoblastic tumour (trophoblastic pseudotumour): a study of four cases requiring hysterectomy including one fatal case. 628 Nov 56

Hematologic alterations unrelated to neoplastic bone marrow involvement include polycythemia, anemia, leukocytosis, leukopenia, thrombocytosis, thrombocytopenia and coagulopathies. Serum globulin levels may be increased or decreased, depending on the type of neoplasm. Plasma fibrinogen and fibrin degradation product concentrations are usually elevated in cancer patients, whereas cancer patients with DIC have low plasma fibrinogen concentrations. Hypercalcemia can be a sequel of osseous metastases. Neoplasia may cause the nephrotic syndrome in some patients. Effusions should be examined microscopically for signs of malignancy. Elevated serum enzyme levels are not specific in neoplastic disease.
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PMID:Laboratory aspects of cancer. 650 15

AT III substitution is indicated in patients with inherited antithrombin III deficiency if these patients suffer acute thrombosis, if they have to be treated surgically and in the case of pregnancy in women with AT III deficiency who have an abortion or thrombosis, as well as during and after delivery. In acquired antithrombin III deficiency such as in patients with liver cirrhosis or the nephrotic syndrome, AT III substitution may be necessary if thrombotic complications occur. AT III substitution has been propagated especially in patients with polytrauma, septicaemia, DIC, acute liver failure and in toxaemia. In AT III substitution initial doses of 1 U/kg body weight are used to reach a 1,5% rise in plasma AT III level. If AT III turnover is normal a rise above 80% of normal should be achieved. If AT III turnover is increased, much higher initial and maintenance doses may be needed to normalize plasma AT III levels and to block DIC.
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PMID:Substitution of antithrombin III. 652 16

In three different disease entities associated with acquired antithrombin III (AT III) deficiency some of the pathogenetic mechanisms were studied. In liver cirrhosis (23 patients) the AT III level was closely correlated to the activity of hepatocellular synthesized clotting factors, indicating decreased AT III synthesis. In glomerular proteinuria (20 patients not on steroid therapy) the plasma level of AT III correlated inversely to the renal AT III clearance. In contrast to liver cirrhosis and proteinuria, in septicaemia (33 patients) the ratio between AT III antigen (radial immunodiffusion) and functional AT III (heparin cofactor assay using a chromogenic substrate) demonstrated an excess of AT III antigen probably due to inactive AT III-enzyme complexes. Therefore consumption of AT III appears to be an important cause of AT III deficiency in septicaemia. There was an inverse correlation between this ratio and the plasma AT III activity. It is well documented that congenital AT III deficiency predisposes to deep venous thrombosis (DVT) and sometimes to disseminated intravascular coagulation. A similar clinical relevance may be assumed for an acquired AT III deficiency, though so far a relationship between AT III deficiency and DVT has been only established in the nephrotic syndrome.
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PMID:[Pathogenetic mechanism and clinical relevance of acquired anti-thrombin III deficiency in internal medicine (author's transl)]. 702 26

Plasma fibronectin was determined in 121 normal adults and in 149 patients. Fibronectin levels in normals were strongly influenced by sex and age. The mean value of the protein in cancer patients did not differ from that in normal controls; however, patients with cryofibrinogenaemia or extensive liver metastases had lower values whereas those with obstructive jaundice due to pancreatic carcinoma had higher values than normal controls. Fibronectin levels were greatly increased in patients with primary biliary cirrhosis and moderately elevated in nephrotic syndrome. In patients with severe infection or sepsis, plasma fibronectin did not show a consistent pattern. Patients with overt disseminated intravascular coagulation, irrespective of its cause, had the lowest plasma fibronectin concentrations.
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PMID:Plasma fibronectin in normal subjects and in various disease states. 725 92

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in three patients with increased serum FDP, that were caused by various diseases. In the patient suffering from tuberculous constrictive pericarditis (case 1), the most part of the FDP fragments were DD and D. In the patient suffering from infection in addition to liver cirrhosis (case 2), the most part of the FDP fragments were high molecular weight (HMW) and D. In case 1 and 2, serum FDP levels were increased in parallel with the elevations of CRP levels. Although DD and HMW fragments were remarkably increased in case 1 and 2 with our immunoblotting analysis, DD levels assayed with LPIA system were much lower than FDP levels. The reason this discrepancy was explained by the observation that affinities of the monoclonal antibody used in LPIA system with DD and HMW fragment were markedly lower than that to DD-E fragment. In the patient suffering from deep vein thrombosis probably caused by steroid therapy of nephrotic syndrome (case 3), the most part of detected FDP fragments were DD and HMW in the period when APTT was shorter than normal, whereas D was mainly observed in the period when APTT was normal. In case 3, FDP and DD levels were increased in parallel with the shortening of APTT. In these non-DIC patients, increased serum FDP levels were induced by the presence of ascites and/or pleural effusion plus infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on the fragments of FDP in 3 non-DIC patients with increased FDP levels in the sera]. 836 Oct 25

We describe a male infant with early myoclonic encephalopathy (EME) associated with the congenital nephrotic syndrome, microcephaly, multiple minor anomalies, and cerebellar hypoplasia. He had erratic and massive myoclonus, and partial seizures from the neonatal period. Electroencephalography showed the so-called suppression-burst pattern. He died of disseminated intravascular coagulation caused by the congenital nephrotic syndrome at the age of two months. Our patients is the first reported case with EME associated with the congenital nephrotic syndrome.
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PMID:A case of early myoclonic encephalopathy with the congenital nephrotic syndrome. 910 63

A 41-year-old woman with complete protein S (PS) deficiency who developed diffuse proliferative lupus nephritis is reported. She was referred to our hospital with nephrotic syndrome and thrombocytopenia. Her medical history included colorectostomy and amputation of the extremities because of repeated thrombotic episodes during her teens without any evidence of systemic lupus erythematosus. The diagnosis of PS deficiency was made from the patient's clinical course, undetectable serum PS in either the active or inactive form, normal protein C activity, and no evidence of the antiphospholipid syndrome. However, there was no definitive family history. A depressed level of complements and a positive antinuclear acid antibody suggested a diagnosis of systemic lupus erythematosus. The patient had a rapidly progressive course and died of disseminated intravascular coagulation. An autopsy showed generalized thrombotic lesions and diffuse proliferative lupus nephritis on both ordinal light and immunoperoxidase microscopy. Our observations suggest that PS-deficient patients may have a hyperinflammatory response.
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PMID:A 41-year-old woman with protein S deficiency and diffuse proliferative lupus nephritis: is protein S deficiency associated with a hyperinflammatory response? 918 80

Thromboembolic disease and progression to disseminated intravascular coagulation (DIC) are potential life-threatening complications for dogs with nephrotic syndrome. Platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), plasma concentration of fibrinogen degradation products (FDPs), antithrombin III (ATIII), protein C, and plasminogen were used to identify hemostatic abnormalities in a dog with nephrotic syndrome. Pulmonary thromboembolic disease was diagnosed by thoracic radiography, arterial blood gas analysis, and pulmonary scintigraphy. Prompt recognition and treatment of hemostatic complications is necessary in dogs with nephrotic syndrome.
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PMID:Nephrotic syndrome resulting in thromboembolic disease and disseminated intravascular coagulation in a dog. 927 13


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