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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Testing for soluble fibrin complexes was performed using a sensitive and reliable haemagglutination assay, with red cells sensitized by fibrin monomers. The principle is based on the fact that the monomers linked to red cells and induce their agglutination. This test, used in clinical trials, has revealed the presence of soluble complexes in every confirmed case of acute DIC, but also in Chronic DIC where diagnosis is difficult to establish (negative ethanol gelation test, normal or sub-normal levels of fibrin breakdown products). In Cirrhosis of the liver, the test gives positive results in a non negligible number of cases. Several hypotheses are made to explain why in certain confirmed cases of DIC, low fibrin breakdown products levels are found.
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PMID:[The detection of soluble fibrin complexes by a haemagglutination test. Clinical applications (author's transl)]. 60 Jul 51

Affinity chromatographic studies using insolubilized fibrinogen (fibrinogen-agarose) revealed that fibrin monomer present in plasma is selectively adsorbed to fibrinogen-agarose and may be quantitatively estimated following desorption. Analysis of plasma samples from patients with myocardial infarction, cirrhosis of the liver malignant diseases and DIC confirmed the presence of considerable amounts of fibrin monomer revealing concentrations between 3 and 15 mg/100 m1 plasma as compared to normal plasma (1.96 +/- 0.37 mg/100 m1, = 27). The method is suitable for the assessment of hypercoagulable states. Standard conditions for the procedure were evaluated using 3H-labelled fibrinogen and fibrin monomer.
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PMID:Detection of thrombin-induced fibrinogen derivatives in thrombotic states. 61 80

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 case of Vibrio cholerae non-O1 septicemia is described in this paper. A 45-year-old male with a three year history of liver cirrhosis, was admitted to our division with hematemesis, abdominal pain, high fever and a loss of consciousness. Three days before onset of symptoms, he traveled to Ishigaki Island and ate a raw lobster. Two days after, his temperature rose to 39.7 degrees C and the blood pressure dropped to 36/- mmHg. By endoscopic examination, an ulcer was found in the stomach, and the bleeding was stopped by electrical coagulation. Blood culture showed growth of V. cholerae non-O1. The organism was found to be sensitive to OFLX, CZX, MINO, LMOX and CP. Although DIC, infections of fungus and MRSA occurred as complications, he recovered by adequate procedures. Subsequently, he left this division after eight weeks. There are various reports related to V. cholerae non-O1 septicemia in foreign countries, but few cases have been reported in Japan. And these cases had severe underlying diseases such as leukemia and liver cirrhosis.
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PMID:[A case of Vibrio cholerae non-O1 septicemia with liver cirrhosis]. 140 1

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

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

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

Since 1984 the peritoneovenous shunt has been installed in 33 patients (10 females - 30.3%; 23 males - 69.7%) of the average age of 54 +/- 8, all in the phase of therapeutically resistant ascites (alcoholic cirrhosis 28 - 84.85%; 4 - 12.12% posthepatitic cirrhosis; and 1 - 3.03% hepatic amyloidosis). The control group consisted of 39 patients (11 females - 28.2% and 28 males - 71.8%) treated in an identical time span with the strict conduction of medicament-diet therapy. The aim of this study was to check the value of this method on our own clinical-patient material, and therefore establish the incidence of complications. By the use of a unique protocol we followed mortality, morbidity, body weight, belly circumference, diuresis, the ultrasonographic finding of the abdominal cavity and the complications which appeared. Out of the group operated on 19 (57%) of the patients died, and so did all the control group patients as well. The average life duration was 275 +/- 810 days in the group operated on, and 44 +/- 29 (p less than 0.005) in the control group. All those alive (14.33-42.42%) lived longer than six months. Six patients lived longer than one year (42.85%), 4 (28.47%) longer than two years, and one (7.14%) longer than three years. There is a statistically significant decrease in body weight, belly circumference, diuresis increase and the consequent ascites withdrawal. DIC occurred in 2 patients, shunt malposition in 2, saccular dilatation in 1, plastic peritonitis in 6, and ileus in 1 patient. Not one of the listed complications resulted by death.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of resistant ascites using the peritoneojugular (Leveen shunt)]. 228 15

In order to detect even minimal fibrinolysis activation in liver cirrhosis, we measured fibrinopeptide B beta 15-42 (B beta 15-42), an indicator of plasmin activity in vivo and alpha 2-antiplasmin (alpha 2-AP) in a group of cirrhotic patients. The second goal of this study was to investigate whether an increased fibrinolytic activity is related to a chronic disseminated intravascular coagulation. For this purpose we concomitantly measured fibrinopeptide A (FPA), marker of thrombin activity in vivo. Results show significantly higher levels of B beta 15-42 in cirrhotic patients than in control (p less than 0.01). In patients with high FPA levels we found significantly higher values than in patients with normal FPA (p less than 0.01). alpha 2-AP was lower in patients with high FPA levels than in patients with normal FPA (p less than 0.05). A significant negative correlation was found between FPA and alpha 2-AP only in patients with high FPA (p less than 0.05). There was no relationship between B beta 15-42 and FPA nor between B beta 15-42 and alpha 2-AP when all patients were considered. These findings confirm that in liver cirrhosis fibrinolysis activation may occur. The primary pathogenetic role of DIC may be important in this respect. However the lack of correlation between FPA and B beta 15-42 suggests that other pathogenetic factors may be involved in determining fibrinolysis activation.
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PMID:Fibrinopeptide A and B beta 15-42 in liver cirrhosis. 245 43


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