Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In liver disorders alterations of the coagulation system are mainly due to a reduced synthesis of coagulation proteins. In addition, an enhanced intravascular consumption of coagulation factors is discussed controversely in liver diseases. By measuring factor IXiAT- and TAT-complexes we tried to find out, whether coagulation activation in liver patients leads to activation of the complete coagulation cascade followed by DIC or whether in some diseases a futile partial coagulation activation develops. In all liver diseases examined, elevated factor IXiAT-complexes were demonstrated, while TAT-complexes were only elevated in chronic active hepatitis, metabolic decompensated liver cirrhosis and in patients suffering from end stage liver disease. We conclude that all liver diseases examined lead to an activation of the coagulation cascade. A complete activation followed by DIC only occurs in patients with very severe liver disorders.
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PMID:Coagulation activation in liver diseases. 181 43

Thrombomodulin (TM) is a constituent glycoprotein of endothelial cell membrane, and soluble TM is present also in plasma and urine. It was revealed by experiments using cultured HUVEC in vitro that TM is released from endothelial cell membrane not with monensin, thrombin, fibroblast growth factor, interleukin-1 or endotoxin, but with H2O2 or endotoxin-treated granulocytes. And the release was suppressed by the coexistence of gabexate mesilate or superoxide dismutase. It was suggested that soluble TM was released from endothelial cell membrane by its injury and digested to multiple molecular forms by endogenous and granulocytic protease(s). TM level in circulation is increased in cases of SLE, MCLS, diabetic angiopathy. It was increased in cases of overt DIC and decreased to the normal level when the patient was recovered from DIC. TM level in circulation was also increased in cases of decompensated liver cirrhosis and markedly in cases of renal insufficiency. It was concluded that plasma TM is a parameter reflecting endothelial injury due to inflammation or metabolic disorders of vascular system. But the interpretation of increased plasma TM was difficult when renal insufficiency was complicated.
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PMID:[Soluble thrombomodulin: a specific parameter of endothelial injury]. 185 Dec 35

In patients with liver cirrhosis, especially in the advanced stage, the coexistence of low clotting factor levels, hypofibrinogenemia, thrombocytopenia and elevated fibrin(ogen) degradation product (FDP) and D-dimer levels may suggest the presence of disseminated intravascular coagulation (DIC). In this study we evaluated, in 21 patients with decompensated liver cirrhosis and elevated FDP and D-dimer levels, the time sequence of their coagulation data during a follow-up period of 15 days after the first observation; our aim was to clarify if these patients tend to develop during this time interval a severe consumption coagulopathy as an expression of overt DIC. We evaluated serum fibrinogen, platelet count, prothrombin activity, serum FDP and plasma D-dimer levels at days 1, 3, 6, 10 and 15. The coagulation data were fairly stable during the study period in all patients, even in the two patients who had upper digestive tract bleeding during the study time. Only two patients affected by infectious diseases showed a decrease of D-dimer and FDP levels after healing. Our data suggest that in decompensated liver cirrhosis the detection of elevated FDP and D-dimer levels is seldom related to the occurrence of an overt DIC, at least during a short time interval; in this condition heparin therapy seems therefore not advisable and even potentially dangerous.
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PMID:Time sequence of coagulation data in patients with decompensated liver cirrhosis and suspected disseminated intravascular coagulation. 186 73

New trends in tests for coagulation and fibrinolysis and advances in diagnosis for the hypercoagulable state and utilization of immunological techniques such as various polyclonal and monoclonal antibodies are reported. We discussed (1) the new markers for hypercoagulable states, (2) differential diagnosis of disseminated intravascular coagulation (DIC) and abnormalities of coagulation in liver cirrhosis (LC), and (3) new markers for fibrinolysis and vascular function. Thrombin-antithrombin III complex (TAT) levels were higher in thrombotic diseases than in healthy controls. Therefore, TAT should be a good marker for hypercoagulation as fibrinopeptide A (FPA) and soluble fibrin monomer complex (SFMC). Measurement of TAT, plasma-alpha 2 plasmin inhibitor complex (PIC), and D dimer were useful for differential diagnosis of DIC and liver cirrhosis. t-PA-PAI complex correlated well with t-PA, but not with fibrinolytic parameters such as PIC. The t-PA-PAI complex may be a good marker for the function of the vascular endothelium.
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PMID:[A new advance in theory of blood coagulation and fibrinolysis and its practical application]. 190 12

The respective roles of intravascular coagulation (DIC) and fibrinolysis were assessed in severe chronic liver disease by measuring thrombin-antithrombin (TAT) complexes, tissue-type plasminogen activator antigen (tPA Ag) and fibrinogen and fibrin degradation products (FgDP and FbDP respectively) in 66 patients with liver disease caused by cirrhosis (n = 34) or chronic hepatitis (n = 32) as compared to findings in a control group (n = 30). There was a significant increase of TAT complexes (P less than 0.01), tPA Ag (P less than 0.002), FDP and FbDP (P less than 0.001) in patients as compared to controls. FbDP increase was more evident in patients with cirrhosis than in those with hepatitis (P less than 0.01). Significant correlations between these parameters with some liver function tests were also demonstrated. Thus, in patients with severe liver disease, an increased thrombin activity, as demonstrated by high TAT levels; followed by hyperfibrinolysis suggest that a low grade DIC may occur.
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PMID:Thrombin activation and increased fibrinolysis in patients with chronic liver disease. 190 1

To evaluate the activation of the extrinsic pathway of coagulation in disseminated intravascular coagulation (DIC), plasma factor VII coagulant activity (FVIIc) and antigen levels (FVIIag) were measured in 81 blood samples obtained from the 56 patients with DIC together with various hemostatic parameters. Plasma FVIIc (77 +/- 40%, range: 11-200%) and FVIIag (76 +/- 43%, range: 16-175%) were significantly lower in DIC subjects than in age-matched controls (FVIIc: 128 +/- 28%, FVII: 128 +/- 31%, p less than 0.01) and correlated significantly with both the antithrombin III and plasminogen activities (p less than 0.001). These results indicated that a decrease in factor VII levels is due to the consumption. However, there were several exceptions which showed elevated factor VII levels. This seems to be due to enhanced liver synthesis of factor VII compensating for the consumption. The level of tPA-PAI-I complex, a marker of pathologic endothelial stimulation, was negatively correlated with FVIIag (r = 0.45, p less than 0.05). Thus, the more the endothelium is pathologically stimulated, the more the extrinsic pathway is activated in DIC. The FVIIc/FVIIag ratio, an index of activation of factor VII zymogen, correlated with FDP and fibrin monomer levels (p less than 0.01). There were no correlations between the thrombin-antithrombin III complex. D-dimer, and alpha 2 antiplasmin-plasmin complex levels and factor VII levels. Considering the underlying diseases. the FVIIc and FVIIag levels were markedly lower in liver cirrhosis, but not significantly different in other diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Plasma factor VII levels in disseminated intravascular coagulation]. 192 Aug 59

We performed 93 sclerotherapy sessions on liver cirrhosis patients with recurrent variceal bleedings. In each session, hypertonic glucose, thrombin and 1% polidocanol were consecutively injected into the varices, and changes in the hemostatic system were examined in relation to the symptoms observed during the treatment. Patients underwent sclerotherapy with no complaints in 62 (67%) sessions, and complained of slight symptoms of general fatigue and headache in 19 (20%). In the other 12 (13%) sessions, the procedure was discontinued due to marked manifestations of these symptoms. All symptoms were temporary and disappeared completely after the procedure. These temporary symptoms were closely related to changes in coagulation tests similar to those of disseminated intravascular coagulation, which were observed just after the treatment. Possible activation of the renal kallikrein-kinin system following injection sclerotherapy was also demonstrated.
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PMID:Manifestations of temporary symptoms during endoscopic variceal sclerotherapy using thrombin as a sclerosant. 192 Sep 57

We analyze retrospectively all bacteremic episodes seen between January and December, 1987 in our institution. From a total number of blood cultures performed of 897, 145 were positive (16%), and 67 of them considered as contamination (7.5%). There were 78 episodes of bacteremia in 74 patients, 38 males and 36 females. Forty-eight episodes were community-acquired and 30 were nosocomial bacteremia episodes. Aerobic bacteria were isolated in 64 cases, anaerobic bacteria in 9 cases and polymicrobial bacteremia in 5 cases. The most commonly isolated microorganism was S. epidermidis in nosocomial cases and E. coli in community-acquired cases. Predisposing conditions registered were diabetes mellitus in 16 cases (20%), cirrhosis of the liver in 3 (4%), corticosteroid therapy in 7 (9%) and surgical procedures in 19 (24%). Shock was seen in 16 cases (20%), DIC in 8 cases (10%) and ARDS in 5 (6.5%). Appropriate antibiotic treatment was used in 60 episodes (77%). Seventeen patients (22%) died. Prognostic factors identified were: nosocomial bacteremia (p less than 0.05), corticosteroid prior therapy (p less than 0.05), underlying disease UF or RF (p less than 0.0001) and the presence of shock (p less than 0.0001). Mean hospital stay was 20.1 days in bacteremic patients vs. 7.6 days in non bacteremic patients (p less than 0.00001).
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PMID:[Bacteremia in a community hospital. Review of 78 cases]. 193 41

We prospectively evaluated 61 episodes of bacteremia in 54 patients with hepatic cirrhosis, representing 9% of the overall number of bacteremic episodes in adult patients seen in our center during the study period. Spontaneous bacteremia represented 46% of all episodes (virtually always in patients with ascites), followed by the urinary origin (30%). Gram negative organisms were isolated in 71% of episodes. 43% of these were hospital-acquired 25% of patients had spontaneous peritonitis. Among other complications of bacteremia there were shock (28%), renal failure (24%), and disseminated intravascular coagulation (6%). The mortality rate due to sepsis was 28%, that due to complications of cirrhosis by itself was 20%, and that of nonrelated diseases was 8%. Shock and renal failure secondary to bacteremia were independent predictors of a poor prognosis.
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PMID:[Bacteremia in the patient with liver cirrhosis. Prospective study of 61 episodes]. 209 53

Tissue plasminogen activator (t-PA) in plasma obtained from patients with acute hepatitis, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, drug-induced intrahepatic cholestasis, obstructive jaundice, fulminant hepatitis or disseminated intravascular coagulation (DIC), was analysed chromatographically. Liver disease cases showed a new peak (peak C) on HPLC fractionation. The protein of peak C had a lower molecular weight than ovalbumin. Lysine- and zinc- chelating affinity chromatography revealed that the peak C consist with the light chain (L-chain) of t-PA. The L-chain was also found in patients with DIC, but disappeared after improvement of DIC. Therefore, it was suggested that appearance of the L-chain would be related to acceleration of secondary fibrinolysis in plasma. The L-chain was especially high in plasma obtained from patients with decompensated liver cirrhosis. These results indicated that high increase of the L-chain in cases of severe liver disease may be due to either impaired clearance of t-PA in the liver or secondary hyperfibrinolysis accompanied by DIC. We concluded that determination of the L-chain of t-PA may contribute to clarify the mechanism of hyperfibrinolysis in liver diseases.
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PMID:[Qualitative analysis of tissue plasminogen activator in plasma obtained from various liver diseases by gel filtration and affinity chromatography]. 210 95


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