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)

Subnormal concentrations of alpha 2 Antiplasmin (alpha 2 AP) in liver cirrhosis may be due to an impaired hepatic synthesis and/or to a fibrinolysis activation in disseminated intravascular coagulation (DIC). In order to clarify this problem, in 26 cirrhotic patients (15 compensated and 11 decompensated) alpha 2 AP plasma activity and plasma Fibrinopeptide A (FPA) were measured. Serum albumin, p-Cholinesterase (p-CHE), Fibrinogen and Fibrinogen Degradation Products (FDP) were also carried out. Our data show that alpha 2 AP and FPA were equally abnormal in compensated and decompensated cirrhosis. The significant negative correlation obtained between alpha 2 AP and FPA as well as the lack of correlation between alpha 2 AP and albumin, alpha 2 AP and p-CHE in both groups suggests that, in our patients, alpha 2 AP decrease may be due to a fibrinolysis activation induced by a DIC which appears chronic since Fibrinogen and FDP were normal. These findings are in agreement with the results obtained in the four subgroups a posteriori selected on the basis of FPA levels: alpha 2 AP in subgroups with high FPA was significantly different from controls while it did not differ in subgroups with normal FPA.
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PMID:alpha 2 Antiplasmin and disseminated intravascular coagulation in liver cirrhosis. 397 73

Heparin cofactor II (HCII) is a glycoprotein in human plasma which inactivates thrombin rapidly in the presence of heparin or dermatan sulfate. We have developed a functional assay for HCII in which inhibition of thrombin by plasma is determined in the presence of dermatan sulfate. The assay is specific for HCII by the following criteria: (a) under the conditions of the assay, 125I-thrombin forms complexes in plasma which comigrate with the thrombin-HCII complex during sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE); (b) activity detected by the assay is decreased in plasma absorbed with monospecific antibodies against HCII; and (c) purified antithrombin III (ATIII) is unreactive in the assay system. Addition of Polybrene to the assay permits determination of HCII activity in samples containing less than or equal to 12 U/mL of heparin. The range of HCII concentrations in normal individuals is 1.2 +/- 0.4 mumol/L (mean +/- 2 SD, n = 34). HCII activity was determined in 54 consecutive patients undergoing evaluation for the possibility of disseminated intravascular coagulation (DIC). Ten of the 11 patients with documented DIC had decreased HCII activity as compared with only 7 of the 43 patients without DIC (chi 2 = 19.3, P less than .0001). The concentrations of HCII and ATIII varied in parallel in most of the patients tested. A significant correlation between decreased HCII activity and decreased serum albumin concentration was also observed in these patients and in eight additional patients with hepatic failure in the absence of DIC. We conclude that HCII activity is decreased in many patients with DIC and hepatic failure.
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PMID:Heparin cofactor II activity in patients with disseminated intravascular coagulation and hepatic failure. 404 18

We have developed a radioimmunoassay (RIA) for the dodecapeptide that is liberated from protein C when this zymogen is activated by thrombin bound to thrombomodulin present on the vascular endothelium. The protein C activation peptide (PCP) was synthesized using the solid-phase method of Merrifield. Antisera were raised in rabbits to the synthetic analogue coupled to bovine serum albumin with glutaraldehyde. The antibody population obtained was used together with a 125I-labeled tyrosinated ligand and various concentrations of unlabeled PCP to construct a double antibody RIA capable of measuring as little as 10 pM of this component. We have established that the synthetic dodecapeptide has the same immunoreactivity as the native peptide and that the reactivity of protein C is less than 1/2,000 that of PCP on a molar basis. The extremely low levels of peptide in normal individuals as well as the nonspecific contributions of plasma constituents to the immunoreactive signal, necessitated the development of a procedure by which the PCP could be reproducibly extracted from plasma and concentrated approximately 20-fold. This methodology permitted us to demonstrate that the plasma PCP levels in 17 normal donors averaged 6.47 pM, and that elevations up to 180 pM were observed in individuals with evidence of disseminated intravascular coagulation. The validity of these measurements of protein C activation is supported by the fact that, in both of these situations, the RIA signal migrates on reverse-phase high pressure liquid chromatography in a manner identical to that of the native dodecapeptide. We have also noted that the mean PCP concentration in seven patients fully anticoagulated with warfarin averaged 2.61 pM. Our studies also show that PCP is cleared from the plasma of primates with a t1/2 of approximately 5 min. Given that the t1/2 of activated protein C is estimated to be 10-15 min, the latter enzyme appears to exert its effects on the activated cofactors of the coagulation system at concentrations considerably less than 1.0 nM.
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PMID:Detection of protein C activation in humans. 654 15

A coagulopathy resembling disseminated intravascular coagulation may occur in systemic juvenile rheumatoid arthritis. We have seen this in seven patients with three different circumstances of disease activity or drug treatment. In one patient, a coagulopathy was not associated with drug therapy, and required corticosteroid therapy for control. A second group of patients was receiving orally nonsteroidal anti-inflammatory drugs during an acute flare-up of disease associated with low serum albumin concentrations. Coagulopathy in these patients may be a result of reduced vascular endothelial cell cyclooxygenase activity secondary to increased levels of unbound nonsteroidal anti-inflammatory drug. In these children, corticosteroid therapy was required for control. A third form of coagulopathy was seen in patients receiving a second injection of aurothiomalate. This form appears to be idiosyncratic, self-limiting, and relatively benign.
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PMID:Consumption coagulopathy associated with systemic juvenile rheumatoid arthritis. 664 21

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.
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PMID:Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis. 725 99

A study based on clinical analysis was conducted regarding the 125 episodes in the elderly 112 patients of sepsis who were 70 (average 83.8 +/- 7.5) years old at Nagoyashi-Koseiin Geriatric Hospital from 1985 through 1994. 1) The backgrounds of the elderly patients with sepsis were as follows: bedridden (72.8%), urinary catheter in place (61.2%), central venous catheter in place (48.8%), and prior antibiotic use (40.8%). All patients had an underlying disease. 2) Organisms isolated were Escherichia coli (21.2%), Staphylococcus aureus (18.4%); Coagulase-negative staphylococci (CNS) (17.4%) and Candida albicans (6.1%). Chronologically, the quantity of gram-positive cocci increased while that of gram-negative bacilli decreased. As the age of the patients increased, the frequency of infections by Methicillin-resistant Staphylococcus aureus (MRSA), E. coli, and/or multiple bacteria increased, while that of infections by CNS and gram-negative bacilli excluding E. coli decreased. 3) The primary infected sites were the urinary tract system (24.8%), central venous catheter (21.6%) and unknown (31.2%). 4) The primary clinical observations were fever exceeding 38.0 degrees C (88.0%), tachycardia (60.8%), shivering (44.0%) and cyanosis (32.8%). 5) Complications were multiple organ failure (33.6%), septic shock (26.4%) and disseminated intravascular coagulation (22.4%). 6) The prognosis indicated that 65.6% were survivors, and 34.4% were nonsurvivors. At the onset of sepsis, weight, blood pressure, serum albumin, and total cholesterol in the nonsurvivors were significantly lower than those in the survivors, whereas heart rate, GOT, LDH, and BUN in the nonsurvivors were significantly higher than those in the survivors.
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PMID:[Study on sepsis in the elderly at Nagoyashi-Koseiin Geriatric Hospital]. 749 17

Patients infected with the human immunodeficiency virus (HIV) appear to have a high risk of ischaemic cerebral events. We observed two cases of cerebral infarction in patients with acquired immune deficiency syndrome (AIDS). In the first case, a 38-year-old homosexual with no cardiovascular risk other than smoking presented with rapidly progressive hemiparesia. Brain CT-scan visualized two infarcts in the territory of the right sylvian artery and the arteriography an occlusion of the internal carotid artery. In the second, a 37-year-old homosexual, hospitalization was required for a left-sided pure sensitive epilepsy seizure. There was no cardiovascular risk other than smoking. Magnetic resonance imaging showed parietal ischaemia and thrombus in the left atrium without atrial hypertrophy was seen at transoesophageal echocardiography. In both cases, there was no evidence of endocarditis, dissection of the neck vessels or disseminated intravascular coagulation nor of associated viral or bacterial infectious complication of AIDS. Angiographic findings eliminated cerebral vascularitis. Among the perturbed haemostasis factors previously reported in HIV+ patients, we observed free proteins S deficiency (68 and 43%) and heparin cofactor II deficiency (54 and 40%). Serum albumin was 33 and 32 g/l respectively. Outcome was favourable in both cases with anticoagulant therapy. These coagulation anomalies would not appear sufficient to explain cerebral infarction. Other mechanisms including immune complexed deposition, direct HIV toxicity for endothelial cells or the effect of cytokines on smooth muscles fibres and fibroblasts are probably more important causal factors.
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PMID:[Cerebral infarction in human immunodeficiency virus infection]. 763 44

The objective of this study, based on a series of 148 transplants performed in 131 children, was to evaluate the frequency, complications and predisposing factors of ascites occurring after liver transplantation (LT). The diagnosis of post-LT ascites was defined as a drainage rate greater than 25 ml/kg/day (or- > 500 ml/day) persisting for at least 72 hours after removal of the drains. Among the 123 transplants analysed, 31 (25.2%) were complicated by ascites (group I). Group II consisted of 92 LT without ascites. This ascites was predominantly lymphocytic (669 +/- 1,104/mm3), rich in proteins (32 +/- 13 g/l), with a low triglyceride concentration. The mean duration of ascites was 25 +/- 19 days. Complications of ascites included: infection of ascitic liquid (35%), respiratory complications (65%), parietal complications (50%), consumption coagulopathy (35%), functional renal failure (Creat > 130 mumol/l, 35%). There were 9 deaths (29%) in group I versus 8 in group II (p < 0.02). The predictive factors, pre-LT, of postoperative ascites included: serum bilirubin > 300 mumol/l (p < 0.02); PT < 30% (p < 0.05); and serum albumin < 30 g/l (p < 0.05). Intraoperative factors favouring the development of ascites were end-to-side cavo-caval implantation of the graft when it was reduced (p < 0.02) and a volume of transfused blood after unclamping greater than 60 ml/kg (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ascites after liver transplantation in children]. 799 26

Pichinde virus infection of inbred guinea-pigs is a model for arenaviral infections in humans. Infected animals experience reduced levels of multiple coagulation factors caused by either consumption coagulopathy or impaired factor synthesis. A radioimmunoassay (RIA) of guinea-pig fibrinopeptide A (gFPA) has been developed to measure the degree of thrombin action in vivo. gFPA was synthesized via the solid-phase method and conjugated to bovine serum albumin (BSA). A double antibody RIA was established employing goat anti-rabbit IgG to precipitate the primary complex composed of either 125I-5-Tyr-gFPA or 125I-12-Tyr-gFPA and rabbit anti-gFPA-BSA. The cross-reaching material was removed by mixing the plasma with 3 vol of ethanol. The supernatant was filtered through a hollow fibre apparatus by centrifugation. Plasma gFPA immunoreactivities of outbred guinea-pigs averaged 6.56 ng/ml. The gFPA-RIA was validated by determining the quantity of gFPA released from thrombin-degraded fibrinogen. A transient elevation of gFPA levels was detected in Pichinde-infected animals by the gFPA-RIA using 125I-12-Tyr-gFPA as a tracer. The pathogenic mechanism by which the increased gFPA levels may lead to the lethality of Pichinde virus infection remains to be elucidated. It is possible that the coagulopathy triggers changes in immune and inflammatory pathways that induces high cytokine concentrations, with deleterious effects on organs such as the heart and lungs.
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PMID:Haemostatic derangements associated with arenavirus infection in the guinea-pig: radioimmunoassay of fibrinopeptide A to assess thrombin action in infected animals. 838 97

A fatal case of hepatic actinomycosis with portal vein thrombosis is reported. The diagnosis of actinomycosis was delayed because of its rarity in Taiwan. This 63-year-old man was admitted due to body weight loss and poor appetite. No fever was noted before admission. Liver biochemical test showed a decreased serum albumin level with elevated serum levels of globulin and alkaline phosphatase. He was not a hepatitis B carrier and his serum level of alfafetoprotein was within normal range. Image studies (abdominal sonography and computed tomography) showed a hepatic mass over the medial segment of the left lobe with involvement of right lobe of the liver. Main portal vein thrombosis was also seen. Because of profound cachexia, he died of aspiration pneumonia and disseminated intravascular coagulation on the 11th day after admission. An autopsy revealed hepatic actinomycosis. High index of suspicion for early diagnosis and treatment is emphasized.
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PMID:Hepatic actinomycosis with portal vein thrombosis mimicking hepatocellular carcinoma: a case report. 839 99


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