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)

In the present study, the first case of ruptured hepatoma followed by disseminated intravascular coagulation is reported. An elastase-like enzyme which possessed elastolytic and caseinolytic activities was confirmed from patient plasma. On the other hand, no elastase activity was detected in the plasma of patients with hepatitis, liver cirrhosis or hepatoma without disseminated intravascular coagulation. The patient plasma did not possess H-D-Val-Leu-Lys-p-nitroanilide hydrochloride, succinyl-L-alanyl-L-alanyl-p-nitroanilide, and pyro-Glu-Pro-Val-p-nitroanilide amidolytic activities. However, when chromatographed on Sephadex G-200, the presence of low-molecular weight plasminogen was confirmed. Its molecular weight was approximately 52,000. A slight decrease of alpha 2-plasmin inhibitor was noted, but no decrease of alpha 2-macroglobulin was detected.
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PMID:A case of ruptured hepatoma followed by elastase-induced disseminated intravascular coagulation. 241 97

Hepatic arterial infusion chemotherapy with cisplatin (CDDP) and adriamycin (ADR) in combination with angiotensin-II (AT-II) was performed in 19 cases of hepatocellular carcinoma (HCC), 16 cases of metastatic liver tumor (MLT) and one case of cholangiocellular carcinoma. CDDP (60-120 mg) and ADR (20-50 mg) were infused into the hepatic artery with intra-arterial instillation of AT-II (0.5-1.5 microgram/min). Transcatheter arterial embolization (TAE) was additionally performed in 10 cases of HCC and 3 cases of MLT. The response rates for infusion chemotherapy combined with TAE were 44% in HCC and 67% in MLT. On the other hand, the response rates without TAE were 0% in HCC and 42% in MLT. In some cases of HCC, however, a marked decrease in serum alpha-fetoprotein levels was observed despite the lack of effectiveness evaluated by CT scan and angiography. Although minor side effects were noted such as a mild degree of leukocytopenia and/or thrombocytopenia and hepatic and/or renal dysfunction, they were only temporary with a duration of less than 3 or 4 weeks. In 4 patients with HCC without TAE treatment, however, lethal side effects occurred including pancytopenia, hepatic failure and disseminated intravascular coagulation, and they died within 2 months after infusion chemotherapy. Renal failure was not seen in either group.
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PMID:[Hepatic artery infusion chemotherapy with cisplatin and adriamycin in combination with angiotensin-II in the treatment of malignant liver tumors]. 245 73

Six cases of unresectable hepatic cancer in infant were treated with intra-arterial infusion therapy. The histological types were hepatoblastoma and hepatocellular carcinoma, 3 cases respectively. The clinical stages were 1 recurrent case in I, 1 in IIIA, 2 in IIIB and 2 in IV. Seldinger method and cannulation at laparotomy were employed in 4 cases and 2 cases, respectively. In the eldest case, a catheter with dual lumen reservoir developed in our department was inserted, making it possible to infuse drugs into hepatic artery and cutting off hepatic arterial blood flow temporarily. The anticancer drug used was ADM, CDDP, 5-FU, THP-ADM, and MMC; antiAFP-anticancer drug conjugate missile therapy was employed in 4 cases. According to image diagnosis, reduction or necrosis of tumor was observed in 5 cases. In all cases, AFP scores decreased. In 5 dead cases, 4 cases died of tumor enlargement (average survival time 16.3 months); 1 case died of DIC during chemotherapy. The other case could eventually undergo complete resection and is now alive. Intra-arterial infusion therapy seemed to be useful for patients of infant unresectable hepatic cancer.
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PMID:[Clinical study of intrahepatic arterial infusion of unresectable hepatoblastoma and hepatocarcinoma in children]. 247 63

Inhibition of Factor VIIa-tissue factor activity by a plasma component(s) that requires factor Xa has been described recently. In this communication, we have developed a specific radiometric assay (which utilizes 3H-Factor IX and is sensitive to less than 1% of plasma level) for this inhibitor and have measured its activity in various disease states. Strikingly, the levels of this inhibitor were found to be normal in patients with advanced chronic hepatocellular disease but low in patients with disseminated intravascular coagulation (DIC). When endotoxin was used to induce DIC in rabbits, the levels of this inhibitor fell by 25-90%. Human umbilical vein endothelial cells (HUVE), bovine pulmonary artery endothelial cells, and a human hepatoma cell line (HepG2) all synthesized and secreted this inhibitor, whereas a promyelocytic cell line (HL-60) did not and a monocytic cell line (U937) appears to synthesize only small amounts. When ammonium sulfate-fractionated human plasma and serum-free conditioned media from both HUVE and HepG2 cells were electrophoresed on sodium dodecyl sulfate acrylamide gels, two activity peaks corresponding to Mr approximately 45,000 and Mr approximately 33,000 were eluted in each case. These observations suggest that (a) the inhibitor is consumed in DIC and that (b) endothelial cells (or other cells) synthesize sufficient amounts of this inhibitor in vivo to compensate for any decreased production by liver cells.
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PMID:Inhibitor of the factor VIIa-tissue factor complex is reduced in patients with disseminated intravascular coagulation but not in patients with severe hepatocellular disease. 303 84

We describe the simple and rapid enzyme immunoassay of protein C in human plasma with use of a Cobas Fara centrifugal analyzer. The antibody, labeled with horseradish peroxidase, is reacted with antigen (protein C) for 15 min. The peroxidase activity of the resulting antigen-antibody conjugate is measured at 500 nm for 5 min in the presence of excess H2O2, phenol, and 4-aminoantipyrine, as compared with that of free conjugates. Results are calculated from a stored standard curve and expressed as a percentage of the value determined for a pooled specimen of normal adult plasma. The standard curve is linear from 0% to 200%. The CV is generally less than 4% for different concentrations of protein C. In liver cirrhosis, hepatocellular carcinoma, therapy with warfarin, thrombosis, and disseminated intravascular coagulation, protein C concentrations are about 40-70% of normal. Results obtained with the present homogeneous enzyme immunoassay correlated well with those by enzyme-labeled immunosorbent assay (r = 0.97).
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PMID:Protein C in human plasma determined by homogeneous enzyme immunoassay with use of a centrifugal analyzer. 304 78

Coagulation studies were performed in patients who underwent abdominal surgery. One hundred and twenty six patients with cholelithiasis, peptic ulcer and gastric cancer were examined. Although fibrinogen increased up to 560 mg/dl postoperatively, DIC did not occur among these patients, at all. For 30 patients who underwent hepatectomy, esophageal transection or pancreatoduodenectomy, HPT, PT, fibrinogen, platelet count, alpha 2-PI, AT-III, plasminogen and DIC score were investigated until 10 postoperative days. As for 13 patients without liver cirrhosis in this group, deterioration of HPT, PT and AT-III was noted on the second postoperative day, however these parameters improved on the fifth postoperative day and all patients recovered uneventfully. On the contrary, as to patients with liver cirrhosis, changes of coagulation parameters were drastic. Significant decrease of HPT, PT, AT-III, plasminogen and increase of FDP and DIC score were noted after operation and these values deteriorated with time in certain cases. Seven patients out of 17 died of DIC and multiple organ failure. More than half of these patients received Gabexate Mesilate (GM) injection in a dose of 1200 mg/day postoperatively for more than 5 days to prevent DIC. In patients who underwent hepatectomy due to hepatocellular carcinoma with liver cirrhosis, the increase of FDP and DIC score seemed to be inhibited by GM on the fifth postoperative day.
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PMID:[Coagulation studies in patients after abdominal surgery]. 308 4

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

The hemorrhagic disposition of patients with hepatic cirrhosis and hepatoma may be associated with DIC. Thus, elucidation of the role of coagulation and fibrinolysis inhibition factors as hemostatic mechanisms in living organisms and in the growth or metastasis of neoplasms is important. Therefore, we measured the levels of serum protease inhibitor and plasminogen in hepatoma patients and compared them with those of patients with other hepatic diseases. Hepatoma was found to induce a marked increase in the alpha 1 AT, alpha 1X and C1 INA levels and a marked decreased in the I alpha I and Pmg levels. The alpha 2 M and AT III levels showed a wide distribution; no significant difference was observed between the hepatoma group and the normal control group. However, hepatoma patients with the DIC syndrome showed a marked decrease in their AT III, Pmg, alpha 2M and I alpha I levels and an increase in their alpha 1 AT and alpha 1X levels. Moreover, the serum protease inhibitor levels corresponded closely with the clinical course.
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PMID:[Clinical studies of serum protease inhibitors in hepatoma]. 630

The blood coagulation and fibrinolysis of 33 patients with compensated liver cirrhosis and 31 patients with hepatocellular carcinoma were examined using several markers, namely thrombin-antithrombin III complex (TAT), plasmin-alpha 2 plasmin inhibitor complex (PIC), antithrombin-III (AT-III) and prothrombin time, and the relationship between these markers, endotoxemia, and TNF-alpha was examined. These patients had no complications due to hepatic failure, such as infections, encephalopathy, ascites, G-I bleeding and clinical DIC. PIC was not elevated, but TAT tended to be elevated in LC and significantly elevated in HCC. AT-III was decreased in LC and HCC, and the blood endotoxin was partly positive in LC and HCC, but was not correlated with AT-III or PT. The TAT level in the blood-endotoxin-positive patients measured by endospecy methods was higher than that in the negative patients, and was significantly correlated with the blood endotoxin level in the LC and HCC patients (r = 0.57, r = 0.88, p < 0.01). No relationship was observed between TNF-alpha and blood endotoxin. In conclusion, (1) blood coagulability was activated already in compensated LC and HCC, but was not connected with fibrinolysis, (2) the activation of coagulability was closely related with endotoxemia, and (3) TNF-alpha was not correlated with blood endotoxin or TAT.
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PMID:[Blood coagulation and fibrinolysis in relation to endotoxemia in liver cirrhosis and hepatocellular carcinoma]. 756 21

To investigate the pathogenesis of fibrinolysis in liver disease, antithrombin III (AT III) activity, prothrombin fragment (F1 + 2) and d-dimer (D-DI) were measured in 50 patients with liver disease and in 17 healthy controls. Moreover, 4 patients with cirrhosis were randomly assigned to receive either an intravenous infusion of AT III (at two different dosages) or placebo, with a crossover design. Increased levels of D-DI were detected in patients with cirrhosis and hepatocellular carcinoma in comparison both with control subjects and with patients with acute hepatitis or mild chronic liver disease. An inverse correlation was observed between AT III and D-DI (r = -0.755, P < 0.001, simple linear regression), while no correlation was found between D-DI or AT III and F1 + 2. The correlation of the deficiency of AT III activity by infusion of human AT III did not result in any significant change (P0.10, analysis of variance for repeated measures) of the plasma concentration of either D-DI or F1 + 2, in comparison to placebo. Thus, advanced forms of chronic liver disease, but not acute hepatitis and mild forms of chronic liver disease, are associated with increased plasma concentrations of markers of fibrinolysis, which are inversely correlated with AT III activity. However, the correction of the deficient AT III activity does not affect the plasma concentration of either D-DI or F1 + 2, thence not supporting the hypothesis that enhanced fibrinolysis in advanced liver disease is the result of low-grade disseminated intravascular coagulation.
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PMID:Deficient antithrombin III activity and enhanced fibrinolysis in patients with liver disease: evidence against a cause-effect relationship. 757 84


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