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)

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
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PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

Three cases of disseminated intravascular coagulation following infusion of ascitic fluid from the peritoneal cavity to the vascular system are reported in patients with hepatic cirrhosis. One of these was treated with intermittent drainage and infusion, and in the other two a LeVeen shunt was used. Studies on the ascitic fluid indicate the presence of a procoagulant material which would appear to be an activator of factor X. Preactivated factor X (Xa) from the fluid and/or a tissue factor activator of factor VII are additional possibilities.
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PMID:Procoagulant activity of ascitic fluid in hepatic cirrhosis: in vivo and in vitro. 49 63

The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.
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PMID:Association of abnormal fibrin polymerisation with severe liver disease. 59 Aug 52

Factor VII levels have been measured in 100 patients with liver disease following parenteral vitamin K1 therapy. There was good agreement between specific factor VII measurements and the one-stage prothrombin time apart from six patients with compensated cirrhosis in whom the prothrombin time was prolonged despite the presence of normal factor VII levels. A mean activity of 58% was found in patients with cirrhosis. Cirrhotic patients with features of hepatic decompensation had a significantly lower mean level of activity (40%) than the "contrast" patients with surgical obstruction of the major bile ducts (93%). Patients with chronic active liver disease had moderate depression of factor VII levels and those with non-cirrhotic liver damage had mean activities similar to the contrast group. Factor VII levels could not be correlated with BSP retention but there was a correlation with serum albumin concentration. It is concluded that the prothrombin time using Quick test with a standardized thromboplastin showing good sensitivity to factor VII, eg, the Manchester reagent (BCT), provides a reliable index of coagulability in chronic liver disease, and specific factor VII assays are not indicated.
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PMID:Factor VII as a marker of hepatocellular synthetic function in liver disease. 100 40

The relation between coagulation indexes and survival rate was studied and analyzed in 46 patients with advanced liver cirrhosis (grade B and C Child-Pugh Classification), during a follow-up of 1 year. Twenty-four patients (52%) died of liver failure or fatal haemorrhage within 12 months of follow-up. Prothrombin activity, fibrinogen, fibrin(ogen) degradation products, prekallikrein and factor VII, serum bilirubin, and the degree of liver insufficiency, scored by Child-Pugh classification, proved to be significantly correlated with survival by univariate analysis. A multivariate survival analysis (Cox regression model) disclosed two variables, prekallikrein and factor VII, that predicted survival. The rate ratios of death increased to 2.8 and 7.6 with values of prekallikrein < 26% and factor VII < 39%, respectively. This study shows that some simple laboratory tests exploring the clotting system may identify patients with poor prognosis in severe liver failure.
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PMID:1-year survey of patients with advanced liver cirrhosis. Prognostic value of clinical and laboratory indexes identified by the Cox regression model. 143 38

An enzyme-linked immunoassay (ELISA) was developed for measuring human factor VII antigen using two monoclonal antibodies, one of them reacting only with fully carboxylated factor VII. This assay permits to measure factor VII antigen in concentrations ranging from 0.78 to 100 ng/ml, with within- and between-assay coefficients of variation of less than 7%. In 53 normal subjects, 32 patients with liver cirrhosis, 21 pregnant women and 53 patients on oral anticoagulant therapy the plasma levels of FVII antigen were very similar to those of factor VII coagulant activity measured with a bioassay. The ELISA also gave very similar values of factor VII antigen in plasma and in serum, and in plasma before and after exposure to cold, indicating that the assay is not affected by factor VII activation. In five of 8 patients with severe congenital deficiency of factor VII values of factor VII antigen were higher than those of factor VII activity. The close concordance of factor VII values obtained by ELISA and bioassay in the majority of plasmas, including those from patients on oral anticoagulant therapy, indicates that the assay measures native factor VII and can perhaps replace the bioassay systems in clinical conditions associated with normal or high levels of factor VII.
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PMID:Enzyme-linked immunosorbent assay of human factor VII based upon a monoclonal antibody that recognizes the native conformation of the protein. 147 Oct 74

Twenty-seven patients suffering from congenital coagulation defects of the prothrombin complex factors were investigated: six had haemophilia B; 14, factor VII defect; four, factor X defect; and three, factor II defect. Nineteen patients (70.3%) had previously received plasma and/or clotting factors concentrates. Among these, markers of hepatitis B infection (HBV) were present in five cases (26.3%) and hepatitis C (HCV) antibodies were found in seven cases (36.8%). The HIV1 prevalence was similarly high. In fact, five patients (26.3%), previously infused with factor IX or prothrombin complex factors concentrates, developed HIV1 infection. No patient with factor VII deficiency became HIV1 positive, despite the administration of unheated factor VII concentrates and the consequent HBV and HCV contamination. In the HIV1 positive group, three patients showed a false positivity for HIV2 antibodies. Five years after seroconversion, three patients developed AIDS (stage IV) and died, one had persistent generalized lymphadenopathy (stage III), and one with post-hepatitis liver cirrhosis was asymptomatic (stage II) for HIV infection. The significant decrease in total white cells, T4 lymphocytes and platelet counts and increase of beta 2-microglobulin and neopterin levels confirmed the prognostic value of these markers for the progression of HIV1 disease. Only one HIV1 negative transfused patient developed anti-HTLV-I p19 antibodies.
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PMID:Prevalence of HIV infection in a cohort of patients with congenital coagulation defects of the prothrombin complex factors. 178 37

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

A 38-year-old man with severe factor IX and mild factor VIII deficiencies complicated by cirrhosis secondary to chronic non-A non-B hepatitis underwent orthotopic liver transplantation as treatment for both the cirrhosis and his congenital coagulopathy. Intraoperative hemostasis was obtained with factor VII-depleted prothrombin complex concentrate and fresh frozen plasma. Factor VIII and factor IX levels were assayed frequently in the perioperative period, and both returned to normal within 24 hr and remained normal postoperatively. Liver transplantation can be considered as definitive therapy for hemophilia A and/or B with transfusion-related liver disease.
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PMID:Orthotopic liver transplantation in a patient with combined hemophilia A and B. 210 34

In 100 adult patients with severe haemophilia A (78 patients) and B (22 patients) sera were screened for the presence of serological markers of hepatitis B virus (HBV) and of cytomegalovirus (CMV) and liver function tests were performed which included measurement of serum aminotransferase AST and ALT activities, total bilirubin concentration and plasma levels of factor VII and X. In all the patients at least one out of five determined HBV markers (HBsAg. HBeAg, anti-HBs, anti-HBc and anti-HBe) was detected. HBsAg was found in 10% of the patients, and its prevalence in haemophiliacs B was higher than than observed in haemophiliacs A (22.7% and 6.4%, respectively). HBsAg appeared more frequently in patients receiving factor VIII concentrates (16.7%) than in those treated with cryoprecipitate (4.5%). Anti-CMV antibody was detected in sera of 98% of the patients. In 1/3 samples of cryoprecipitate anti-HBc or anti-HBs were present, and in the half of samples anti-CMV occurred. Abnormal liver function tests indicating chronic hepatitis or liver cirrhosis were obtained in 8 patients. Raised ALT activity which could suggest chronic infection with non-A, non-B virus occurred in 6 cases. The present study indicates that haemophiliacs frequently transfused with plasma products are at high risk for viral infections leading to liver dysfunction.
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PMID:[Serological markers of hepatitis B virus and cytomegalovirus in patients with hemophilia]. 217 33


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