Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Prothrombin antigen concentration was evaluated by means of laser nephelometry in 10 patients on coumarin therapy, in 17 patients with cirrhosis of the liver, and in four patients with congenital hypo- or dysprothrombinemias. The average values obtained were 46.4, 37.7, and 35.6%, respectively, for anticoagulated, cirrhotic, and congenitally abnormal patients. These values correlated well with those obtained by means of electroimmunoassay (Laurell) and immunodiffusion (Mancini) methods. Similarly, satisfactory results were obtained in eight normal subjects. Multiple evaluations at different incubation times, also allowed the authors to construct kinetic curves of the interaction between antigen and antibody. However, an abnormal kinetic curve was demonstrated only for coumarin-treated patients.
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PMID:Prothrombin antigen evaluation by means of laser nephelometry in health and disease. 713 21

Twenty patients with severe hepatic failure and fatal evolution, in whom hemostatic parameters were studied are presented. Eleven had fulminant acute viral hepatitis (FVH) and nine had liver cirrhosis. Hepatic parenchymal failure was followed by altered coagulation factors. In FVH major disturbances were detected in factors II, V, VII - X. In our cirrhotic patients factor alterations were moderated. In spite of these differences the percentage of bleeding patients was similar in both groups. Prothrombin time plus tromboplastine partial time (KPTT) are useful prognostic complements for these two entities.
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PMID:[Comparative study of hemostatic changes in acute viral hepatitis and terminal cirrhosis]. 718 33

The functional reserve of the liver should be estimated prior to hepatectomy. While the experienced liver surgeon often relies on the findings of manual palpation intra-operatively, this approach remains a subjective one. In 22 of our patients scheduled for hepatectomy, we measured intra-operatively hepatic consistency as well as the parameters of liver function. Hepatic consistency is augmented during progression from non-fibrosis to cirrhosis. We found a statistically significant correlation between liver consistency and the indocyanine green retention rate at 15 minutes (r = 0.682; p = 0.0009) and portal vein pressure (r = 0.733; p = 0.0008). Prothrombin time, the hepaplastin test, total bilirubin and glutamic pyruvic transaminase showed no significant correlation with hepatic consistency. The safety limits of the hepatic blood circulation for the performance of hepatectomy can be estimated using parameters of consistency in this organ.
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PMID:Significance of intraoperative measurement of liver consistency prior to hepatic resection. 778 35

To assess the contribution of naturally occurring portal-systemic shunts to the coagulopathy of patients with liver disease, we studied laboratory parameters of hemostasis in 20 adult patients with extrahepatic portal hypertension, secondary to portal vein thrombosis, that had resulted in variceal bleeding. All extrahepatic portal hypertension patients had normal liver function and histological appearance. None had any evidence of preexisting coagulation disorders, and none had bled or undergone sclerotherapy in the 6 mo before study. Age- and gender-matched groups of 20 healthy individuals and 20 stable patients with cirrhosis and portal hypertension who had a history of variceal bleeding served as controls. Both patient groups had thrombocytopenia consistent with hypersplenism and portal hypertension. Prothrombin international normalized ratio (extrahepatic portal hypertension, 1.3 +/- 0.12; cirrhosis, 1.7 +/- 0.2; control, 1.02 +/- 0.06; p < 0.05) and partial thromboplastin time ratios (extrahepatic portal hypertension, 1.12 +/- 0.1; cirrhosis, 1.26 +/- 0.2; controls, 1.01 +/- 0.03; p < 0.05) were significantly prolonged in both patient groups. Extrahepatic portal hypertension and cirrhotic patient groups had significantly increased levels of serum total fibrin(ogen)-related antigen (extrahepatic portal hypertension, 818 +/- 150 ng/ml; cirrhosis, 454 +/- 52 ng/ml; controls, 124 +/- 7.3 ng/ml; p < 0.05), fibrin monomer (extrahepatic portal hypertension, 168.8 +/- 16.9 ng/ml; cirrhosis, 115.6 +/- 11.1 ng/ml; controls, 19.7 +/- 0.4 ng/ml; p < 0.05) and D-dimer (extrahepatic portal hypertension, 118 +/- 9.6 ng/ml; cirrhosis, 129 +/- 10 ng/ml; controls, 53.2 +/- 1.6 ng/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disordered hemostasis in extrahepatic portal hypertension. 840 59

Ischaemic hepatitis, a condition to be distinguished from cardiac liver or stasis cirrhosis, can occur as an acute episode in patients with advanced stage congestive heart failure. The mechanism is massive necrosis in the central lobules resulting from acute hypoxia when low cardiac output reduces oxygen supply further aggravating the underlying condition of congestion due to poor venous outflow. We report 4 cases which illustrate the difficulties in diagnosis and treatment. All four patients (age range 79-86 years) were seen in an emergency situation caused by an acute drop in cardiac output aggravating their underlying heart failure. Clinical signs included jaundice, oligouria, abdominal pain and cardiovascular shock. The first element suggesting the diagnosis of ischaemic hepatitis was a sudden and massive peak in transaminase levels (> 20 times normal) which rapidly returned to normal. Prothrombin and fibrinogen levels fell rapidly and functional renal failure was present in all cases. Viral serology was negative and no hepatotoxic drugs could be incriminated. Despite symptomatic intensive care one patient died on day 15 due to cardiovascular shock. Enzyme movements, together with the lack of evidence for another cause, is the key to diagnosis of acute ischaemic hepatitis which thus is often established after the emergency situation has been controlled. Initially, viral hepatitis or drug-induced hepatotoxicity may be suspected, especially if the episode of low cardiac output goes unrecognized. Cases with signs of encephalopathy may also be difficult to distinguish from fulminating hepatitis and would be the only indication for needle biopsy in this acute situation. Outcome is generally unfavourable with mortality at 6 months estimated at 50%.
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PMID:[Acute ischemic liver]. 854 28

The purpose of our study was to evaluate the clinical impact of reperfusion injury after normothermic ischemia during major liver resections and the effect of an intraoperative antioxidant infusion. This prospective randomized study comprised 50 patients; half of them (treatment group) were given an antioxidant infusion containing tocopherol and ascorbate immediately prior to reperfusion onset. Venous blood samples for the determination of MDA-TBARS (malondialdehyde-thiobarbituric acid reactive substances) by a HPLC-based test as a marker of lipid peroxidation were taken prior to ischemia, 30 min after reperfusion onset and at the end of the operation. In the control group there was a significant increase of MDA-TBARS (p = 0.001) at 30 min after reperfusion onset. At the end of the operation the values had returned to the initial level. The treatment group showed only a marginal increase (p-value for the difference between the two groups: 0.007). After exclusion of the patients with histologically proven advanced cirrhosis the increase in the control group (p < 0.001) and the difference between the increase in the two groups (p = 0.001) became more significant. Prothrombin time was also significantly better in the treatment group (p = 0.003). Postoperative complications such as prolonged liver failure, bleeding disorders and infections were seen more often in the control group. In our study MDA-TBARS was increased after liver ischemia, but in patients with advanced cirrhosis the effect was smaller or even absent. This increase and possible clinical consequences of reperfusion injury could be reduced by intraoperative administration of an antioxidant infusion.
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PMID:Normothermic liver ischemia and antioxidant treatment during hepatic resections. 1040 Apr 58

Hepatocyte transplantation improves the survival of laboratory animals with experimentally induced acute liver failure and the physiological abnormalities associated with liver-based metabolic deficiencies. The role of hepatocyte transplantation in treating decompensated liver cirrhosis, however, has not been studied in depth. To address this issue, cirrhosis was induced using phenobarbital and carbon tetrachloride (CCL(4)) and animals were studied only when evidence of liver failure did not improve when CCL(4) was held for 4 weeks. Animals received intrasplenic transplantation of syngeneic rat hepatocytes (G1); intraperitoneal transplantation of syngeneic rat hepatocytes (G2); intraperitoneal transplantation of a cellular homogenate of syngeneic rat hepatocytes (G3); intraperitoneal transplantation of syngeneic rat bone marrow cells (G4); or intrasplenic injection of Dulbecco's modified Eagle medium (DMEM) (G5). After transplantation, body weight and serum albumin levels deteriorated over time in all control (G2-G5) animals but did not deteriorate in animals receiving intrasplenic hepatocyte transplantation (G1) (P <.01). Prothrombin time (PT), total bilirubin, serum ammonia, and hepatic encephalopathy score were also significantly improved toward normal in animals receiving intrasplenic hepatocyte transplantation (P <. 01). More importantly, survival was prolonged after a single infusion of hepatocytes and a second infusion prolonged survival from 15 to 128 days (P <.01). Thus, hepatocyte transplantation can improve liver function and prolong the survival of rats with irreversible, decompensated cirrhosis and may be useful in the treatment of cirrhosis in humans.
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PMID:Hepatocyte transplantation in rats with decompensated cirrhosis. 1073 39

We have shown, in animal models as well as in retrospective human study, that some degree of decreased thyroid function is beneficial for subjects with liver damage of various etiologies. Therefore, we herein present the results of a cohort population study. Between 1991 and 1994, 18 patients (12 women and 6 men; mean age, 59 +/- 24 years) with both biopsy-proven active cirrhosis (5 hepatitis C virus, 4 hepatitis B virus, 1 immunocompromised host, 2 primary biliary cirrhosis, 1 alcoholic, and 5 cryptogenic; Child's-Pugh criteria: A-8, B-8, C-2) and primary or induced (by either drug or surgery) thyroxine-treated hypothyroidism were prospectively followed. Each patient was examined at least twice yearly and served as their own control. The thyroid of the profiled patients ranged between euthyroidism and subclinical hypothyroidism. Liver function tests were evaluated and compared in states of normal versus increased thyroid-stimulating hormone (TSH) blood levels. A significant improvement in alanine aminotransferase (p < 0.001), alkaline phosphatase (p < 0.0001), albumin (p < 0.001), and bilirubin (p < 0.01) was found in the increased TSH group. Prothrombin time was also found to be significantly better (p < 0.001). We conclude that euthyroid patients with liver cirrhosis might benefit from a controlled hypothyroidism.
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PMID:The effects of hypothyroidism on liver status of cirrhotic patients. 1099 36

In this study, IgG was partially purified from rabbit antisera against human normal prothrombin. The presence of antibodies against prothrombin was shown by Ouchterlony's double immunodiffusion method. This IgG was adsorbed to microwells and an enzyme-linked immunosorbent assay (ELISA) method was developed by using biotinylated prothrombin. We used alkaline phosphatase as the labeling enzyme. Plasma prothrombin concentrations in 30 healthy individuals and 15 patients with liver cirrhosis were measured using this ELISA method. Prothrombin levels of the cirrhotic patients (61+/-36 microg/ml) were significantly lower than those of the control values (117+/-43 microg/ml) (P<.001). In addition to the ELISA method in the same samples, we assayed prothrombin levels by nephelometry and prothrombin activities using staphylocoagulase and chromogenic substrate. With nephelometry, in healthy individuals, a mean value of 104+/-17 microg/ml and, in cirrhotic patients, a mean value of 51+/-26 microg/ml of prothrombin levels were detected. The prothrombin activities were 10532+/-2429 and 2433+/-330 U/l, respectively. In both methods, the prothrombin values of cirrhotic patients were also significantly lower than those of the healthy individuals (P<.001). The correlation coefficient between ELISA and nephelometry was r=.90, P<.01, and between ELISA and the amidolytic assay was r=.69, P<.01. Prothrombin times (PT) of cirrhotic patients (18.5+/-2.3 s) were significantly longer and albumin (2.4+/-0.5 g/dl) levels were significantly lower than those of normal values (P<.001). PT were negatively correlated with prothrombin levels assayed by ELISA (r=-.59, P<.01). This enzyme immunoassay technique can be used to measure prothrombin levels in plasma.
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PMID:Avidin-biotin ELISA for measurement of prothrombin in human plasma. 1136 15

COACH syndrome is a disorder with cerebellar vermis hypoplasia, oligophrenia, ataxia, coloboma, and hepatic fibrosis. Sixteen cases with certain COACH diagnosis have been reported so far. Neurologic abnormalities are the first symptoms in most cases. The majority of cases were diagnosed late in childhood or adolescence. Complications of the hepatopathy contribute extensively to the morbidity and lethality in the course of the disease. Major complications are portal hypertension, esophageal varices, and gastrointestinal bleeding. We report of a child with only mild neurologic symptoms, but severe hepatic fibrosis with cholangiopathy, and review the literature. This is the first description of profound cholestatic hepatopathy in a very young child with COACH syndrome. The patient was found to have cerebellar vermis hypoplasia, unilateral optical nerve coloboma, mild dysmorphic signs, and a ventricular septum defect. Routine laboratory investigations eventually revealed elevated liver enzymes. Prothrombin time was abnormal. Ultrasound scan of the liver was normal. Hepatotropic viral infections were excluded. We performed a liver biopsy at the age of 16 months, confirming an early stage of cirrhosis with septal fibrosis and pseudolobules, inflammatory infiltrates, signs of cholestasis, and reduced numbers of intrahepatic bile ducts. Early detection and differentiation of liver pathology are important in COACH syndrome. Progressive destructive cholangiopathy may contribute to hepatic fibrosis in COACH syndrome. Liver disease can be severe even in cases with mild neurologic deficits.
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PMID:Early detection of severe cholestatic hepatopathy in COACH syndrome. 1221 Mar 5


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