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)

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66

A secific, sensitive, and reproducible radioimmunoassay for human Hageman factor (HF, factory XII) has been developed with purified human HF and monospecific rabbit antibody. Precise measurements of HF antigen were possible for concentrations as low as 0.1% of that in normal pooled plasma. A good correlation (correlation co-efficient = 0.82) existed between the titers of HF measured by clot-promoting assays and radioimmunoassays among 42 normal adults. Confirming earlier studies, HF antigen was absent in Hageman trait plasma, but other congenital deficient plasmas, including those of individuals with Fletcher trait and Fitzgerald trait, contained normal amounts of HF antigen. HF antigen was reduced in the plasmas of patients with disseminated intravascular coagulation or advanced liver cirrhosis, but it was normal in those of patients with chronic renal failure or patients under treatment with warfarin. HF antigen was detected by this assay in plasmas of primates, but not detectable in plasmas of 11 nonprimate mammalian and one avian species.
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PMID:Radioimmunoassay of human Hageman factor (factor XII). 95 1

Calcification of small subcutaneous arteries and arterioles is commonly found in patients with chronic renal failure (CRF), but the syndrome of acute ischemic necrosis of the skin and subcutaneous fat supplied by these vessels is relatively uncommon. The necrosis occurs during dialysis and after successful renal transplantation, and it is often fatal. Occlusion of the calcified arteries and associated microvessels by thrombi is reported infrequently, but it is relevant to the necrosis. However, the pathogenesis remains enigmatic. In the patient described here, who had CRF, bacteremia, and laboratory evidence of disseminated intravascular coagulation (DIC), the distribution of thrombi and necrosis was mainly that of the calcified arteries which, therefore, probably played a role in the localization of the thrombi. An increased susceptibility of the endothelium of calcified vessels to the procoagulant effects of sepsis may be a contributing factor.
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PMID:Acute skin and fat necrosis during sepsis in a patient with chronic renal failure and subcutaneous arterial calcification. 146 96

A study was made of changes in functional status of complementary system in 42 patients with chronic renal failure on programmed hemodialysis. Early stages of hemodialysis were accompanied by short-term and reversible activation of complementary system. 100 sessions were followed by complement depression. Complement system was found to be involved in two pathogenetic mechanisms of respiratory insufficiency: block of pulmonary microcirculation by leukocytic aggregates and DIC syndrome associated with microthrombosis of the lesser circulation vessels. To manage the above complications, plasmapheresis is advocated.
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PMID:[The role of the complement system in the origin of respiratory insufficiency in patients on hemodialysis]. 180 18

Sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by immunoblot analysis of plasma thrombomodulin concentrate revealed that four degraded forms of thrombomodulin with different molecular weights are present in plasma. Plasma concentrations of thrombomodulin in patients with various diseases were measured by two methods of enzyme-linked immunosorbent assay using monoclonal antibodies. One method measures intact thrombomodulin and degraded forms of thrombomodulin; the other does not detect the two smaller degraded forms of thrombomodulin present in plasma. The results indicated that thrombomodulin was increased in the circulating blood of patients with disseminated intravascular coagulation syndrome, pulmonary thromboembolism, adult respiratory distress syndrome, chronic renal failure, or acute hepatic failure. The different values obtained by the two methods indicate that the increase of plasma thrombomodulin found in these patients was mainly due to an increase of the smaller fragments of degraded forms, suggesting that the release of thrombomodulin from endothelial cells was accelerated in various disease states by proteolytic activity generated on the surface of the endothelium and may be removed from the circulation mostly by the kidneys and liver.
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PMID:Plasma thrombomodulin in health and diseases. 217 34

A nephelometric method is described for determination of plasminogen and two types of plasmin inhibitors in human plasma having different affinity toward plasmin. This method is based on the kinetic analysis of effects of whole plasma and plasmin inhibitor fraction obtained from plasma on the activity of exogenously added plasminogen which was determined by measuring the decrease of light scattering of fibrin suspension. With this method we have determined the activity of plasminogen and two types of inhibitors in the plasma of normal subjects and patients with high fibrinogen degradation product values. They include patients with various malignant tumors with DIC, chronic renal failure, sepsis, vascular diseases, and liver cirrhosis with hepatoma.
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PMID:Nephelometric determination of plasminogen and plasmin inhibitors in human plasma using fibrin suspension as a substrate. 622 10

We report the case of a 55-year-old man with chronic renal failure, and a history of prolonged fever and jaundice. Radiological studies revealed a multiloculated irregular liver abscess. Mycobacterium tuberculosis was isolated from the abscess on smear and culture of aspirated pus. Haematological studies revealed the presence of disseminated intravascular coagulation. A detailed search failed to identify any reason for this other than the tuberculous infection. The treatment of tuberculous liver abscess and pathogenesis of disseminated intravascular coagulation in tuberculosis are discussed.
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PMID:Liver abscess and disseminated intravascular coagulation in tuberculosis. 756 59

Eleven patients with chronic subdural hematoma (CSDH) with bleeding tendency (BT) were surgically treated in the last 12 years. To study the clinical problem of CSDH with BT, 11 surgical cases were divided into 3 groups, Group A; CSDH with primary BT (1 case of hemophilia A), Group B; CSDH with BT secondary to a basic disease (3 cases of leukemia, 2 cases of malignant tumor with DIC, 1 case of chronic renal failure and 1 case of liver cirrhosis), Group C; CSDH with BT by anticoagulants (warfarin) (2 cases of replacement of mitral valve, 1 case of A-C bypass). Evacuation of the hematoma was performed by means of one or two burr holes with irrigation of the hematoma cavity and a drainage tube was placed in the subdural space. The outcome was excellent in Groups A and C. In Group B, two patients with DIC due to gastric cancer and prostatic cancer died, and 3 patients with leukemia recovered dramatically from CSDH, but the poor course of the disease itself resulted in death. The outcome of other patients in Group B was excellent. Since CSDH with BT is often fatal, those patient had usually been treated conservatively. However, from this analysis, we stress that CSDH with BT should be surgically treated after checking the blood conditions carefully to determine whether or not the patient has need for surgery.
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PMID:[Chronic subdural hematoma with bleeding tendency; clinical analysis of 11 surgical cases]. 784 20

Pathologies of serial sections of 9 temporal bones from 6 patients without caloric response were studied. The patients died of epipharyngeal cancer, middle ear cancer, chronic renal failure with DIC, pancreatic cancer with DIC, multiple brain metastasis of pancreatic cancer, and leukemia. Under light microscopy, 8 ears showed pathologies in the vestibular end organs and the nerves. Possible causes of the lack of caloric responses in the 8 ears were endolymphatic hemorrhage, labyrinthitis, leukemic infiltration in the labyrinth, degeneration or disappearance of the vestibular sensory cells, reduction in the number of vestibular nerve fibers, and/or brainstem lesions. The remaining one ear did not show abnormal findings in the vestibular end organs or the nerves, but the patient had brainstem lesions. Four types of temporal bone pathologies were observed according to the lesion site responsible for the lack of caloric response; i) sensory type, ii) neural type, iii) mixed type and iv) central type.
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PMID:Temporal bone pathology in patients without caloric response. 787 14

To investigate the clinical significance of determination of plasma tissue factor (TF) antigen, we have developed a highly sensitive enzyme-linked immunosorbent assay (ELISA) for plasma TF, using two different monoclonal antibodies against TF apoprotein, 6B4 (catching antibody) and 5G9 (detecting antibody), and tetramethyl benzidine/H2O2 as substrates. Titration curves of recombinant human TF in buffer containing Triton X-100 were linear within the range from 50 to 2000 pg/ml. The total assay time was 3 h. Ultracentrifugation and immunoblot analysis indicated that human plasma and urine contained 50,000 g sedimentable and non-sedimentable forms of TF, both of which were detected by our ELISA method. Plasma and urine concentrations of TF in healthy subjects and patients with various diseases were measured by the ELISA method. In healthy subjects, plasma and urinary TF levels were found to be 149 +/- 72 pg/ml (n = 30) and 175 +/- 60 pg TF/urine creatinine mg (n = 95), respectively. TF was increased in plasma of patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, vasculitis associated with collagen diseases, diabetic microangiopathy and chronic renal failure receiving haemodialysis, but not in the plasma of endotoxaemic patients without DIC. The plasma TF/serum creatinine ratio did not show a positive correlation. Measurement of TF antigen in plasma may be useful for evaluating the endothelial damage and cell destruction in TF-containing tissues.
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PMID:Determination of plasma tissue factor antigen and its clinical significance. 794 77


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