Low Levels of Thrombin Activatable Fibrinolysis Inhibitor (TAFI) in Patients with Chronic Liver Disease

2001 ◽  
Vol 85 (04) ◽  
pp. 667-670 ◽  
Author(s):  
Magdalene George ◽  
Jawed Fareed ◽  
David Van Thiel
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Degradation Products ◽  
Chronic Liver ◽  
Low Grade ◽  
Thrombin Activatable Fibrinolysis Inhibitor ◽  
Disseminated Intravascular Coagulopathy ◽  
Fibrinolysis Inhibitor ◽  
Intravascular Coagulopathy ◽  
Low Levels

SummaryThrombin Activatable Fibrinolysis Inhibitor (TAFI) is a 60 κD glycoprotein present in plasma that regulates fibrinolysis by limiting the amount of fibrin available for fibrinolysis by tissue plasminogen activator (t-PA). Chronic liver disease is well-known to be associated with a low-grade fibrinolytic syndrome that under the appropriate stimulus proceeds to an overt disseminated intravascular coagulopathy (DIC) with demonstrable bleeding. In the present study, TAFI activity was measured in the plasma of 74 patients with advanced liver disease, and the levels of TAFI were related to those of other important coagulation and fibrinolytic factors. TAFI levels were very low and essentially undetectable in the plasma of patients with advanced hepatocellular liver disease. No relationship with the degradation products of fibrin was evident.

Heparin Response and Clearance in Acute and Chronic Liver Disease

1985 ◽  
Vol 54 (03) ◽  
pp. 591-594 ◽  
Author(s):  
H Sette ◽  
R D Hughes ◽  
P G Langley ◽  
A E S Gimson ◽  
R Williams
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Peak Level ◽  
Chronic Liver ◽  
Clotting System ◽  
Activated Clotting Time ◽  
At Iii ◽  
Increased Sensitivity ◽  
Low Levels ◽  
Normal Controls

SummaryPatients with liver disease are at risk of bleeding due to abnormalities of the clotting system although they must be anticoagulated if they require haemodialysis or haemoperfusion. The anticoagulant of choice is heparin.In this study we have investigated heparin kinetics in patients with fulminant hepatic failure (FHF) after a single intravenous dose of heparin (2,500 units) and found there was an increased clearance of heparin whether measured by its anti-Xa effect (t1/2 = 27.8 ± 2.9 min compared to t1/2 = 50.2 ± 2.7 min in normal controls p <0.001) or by the whole blood activated clotting time (t1/2 = 23.7 ± 2.2 min compared to t1/2 = 37.0 ± 2.0 min p <0.001). There was a decreased peak level of heparin measured by anti-Xa effect (peak level in FHF = 0.48 ± 0.05 u/ml and in controls = 0.69 ± 0.04 u/ml, p <0.02), but an increased sensitivity to heparin (sensitivity in FHF = 0.072 ± 0.011 sec/unit, in controls 0.033 ± 0.003 sec/unit, p <0.001). Patients with FHF had very low levels of antithrombin III (AT III), but there was no correlation between this and any parameters of heparin effect or clearance. In a group of patients with chronic liver disease heparin kinetics did not differ from controls despite low levels of AT III.The changes in heparin kinetics in FHF are likely to be complex with the balance between the proteins that act as cofactors, (e.g. AT III) and the proteins that have heparin neutralising activity, controlling the response of added heparin.

Hepatic encephalopathy in chronic liver disease: a clinical manifestation of astrocyte swelling and low-grade cerebral edema?

2000 ◽  
Vol 32 (6) ◽  
pp. 1035-1038 ◽  
Author(s):  
Dieter Häussinger ◽  
Gerald Kircheis ◽  
Richard Fischer ◽  
Freimut Schliess ◽  
Stephan vom Dahl
Keyword(s):  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Chronic Liver Disease ◽  
Clinical Manifestation ◽  
Cerebral Edema ◽  
Chronic Liver ◽  
Low Grade ◽  
Astrocyte Swelling

scholarly journals TRACE ELEMENTS IN PLASMA AND NUTRITIONAL ASSESSMENT IN PATIENTS WITH COMPENSATED CIRRHOSIS ON A LIVER TRANSPLANT LIST

2016 ◽  
Vol 53 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Thays Santana GUERRA ◽  
Nelci Fenalt HOEHR ◽  
Ilka de Fátima Santana Ferreira BOIN ◽  
Raquel Silveira Bello STUCCHI
Keyword(s):  
Trace Elements ◽  
Liver Disease ◽  
Nutritional Status ◽  
Liver Transplant ◽  
Trace Element ◽  
Chronic Liver Disease ◽  
Disease Severity ◽  
Nutritional Assessment ◽  
Chronic Liver ◽  
Low Levels

ABSTRACT Background - In chronic liver disease, trace element levels in plasma are usually low. However, the specific cause and functional implications of this abnormality are yet not well understood. These element levels may decrease as a result of abnormal liver function in patients with cirrhosis and/or malnutrition. Objective - To evaluate the nutritional status and the profile of trace elements in plasma of patients with cirrhosis on a liver transplant list and to correlate them with disease severity. Methods - This cross-sectional study evaluated 31 male patients diagnosed with compensated liver cirrhosis on a waiting list for liver transplant. Nutritional status was objectively evaluated through anthropometry using Mendenhall score and Blackburn classification, subjectively through the Detsky questionnaire and severity of the disease by MELD and CTP score. Trace elements (Zn, Se, Cu, Ca, Fe, Mg and Mn) in plasma were analyzed by inductively coupled plasma mass spectrometry (ICP-MS). Statistical analysis was performed using Mann-Whitney test. Results - According to the nutritional assessment 19 (61.3%) were malnourished and 12 (38.7%) were overweight. Regarding disease severity 12 (39%) were classified as Child A, 17 (55%), Child B and 2 (6%) Child C, with 46.9% of patients with MELD score >17. The trace element analysis indicated that 31 (100%) had Mn levels above the reference range, 23 (74.2%) low levels of Cu, 29 (93.5%) with deficiency of Se, and 31 (100%) low levels of Ca and Mg. Disease severity did not show statistical difference between the studied trace elements, in contrast to the nutritional status, in which the malnourished group showed higher levels of Mn (P=0.01) and Fe (P=0.01) and low levels of Zn (P=0.03) when compared to the overweight group. Conclusion - The results showed that the trace elements in plasma are altered in chronic liver disease; without significant correlation to disease severity, but correlated to nutritional status. Malnutrition is present in the patients studied, nonetheless a new scenario with an increase in the prevalence of overweight was verified regardless of the degree of hepatic decompensation.

scholarly journals Acquired Dysfibrinogenemia in Acute and Chronic Liver Disease

1977 ◽  
Author(s):  
D.A. Lane ◽  
V.V. Kakkar ◽  
I.L. Woolf ◽  
R. Williams
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Polypeptide Chain ◽  
Degradation Products ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Chronic Liver ◽  
Polypeptide Chains ◽  
Fibrin Monomers

Recent work with the thrombin-like snake venom Reptilase has suggested that the incidence of dysfibrinogenemia in liver disease may be much higher than has been recognised previously. In the present study, nine patients with fulminant hepatic failure and three with chronic liver disease, all exhibiting prolonged thrombin and ancrod clotting times, were examined for evidence of dysfibrinogenemia with a variety of physiochemical and clotting techniques. Sodium dodecyl sulphate Polyacrylamide gel electrophoresis revealed normal fibrinogen polypeptide chains, polypeptide chain crosslinking by Factor XIII, and in vitro generated plasmin degradation products of fibrinogen (FDP) in the plasma of these patients. Isolated and purified fibrin monomers were prepared by clotting plasma with Reptilase (Reptilase monomer) and thrombin (thrombin monomers). This enabled fibrin monomer polymerisation to be studied free of interference from plasma inhibitors such as FDP, and independent of any abnormal fibrinopeptide release. Delayed polymerisation of both Reptilase and thrombin monomers was demonstrated, providing an explanation for the observed prolonged clotting times. These results confirm that an abnormal fibrinogen may be produced during acute and chronic liver disease.

scholarly journals The Interstitial Lymphatic Peritoneal Mesothelium Axis in Portal Hypertensive Ascites: When in Danger, Go Back to the Sea

2010 ◽  
Vol 2010 ◽  
pp. 1-18 ◽  
Author(s):  
M. A. Aller ◽  
I. Prieto ◽  
S. Argudo ◽  
F. de Vicente ◽  
L. Santamaría ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Ischemia Reperfusion ◽  
Lymph Flow ◽  
Point Of View ◽  
Chronic Liver ◽  
Low Grade ◽  
Extrahepatic Cholestasis ◽  
Peritoneal Mesothelium

Portal hypertension induces a splanchnic and systemic low-grade inflammatory response that could induce the expression of three phenotypes, named ischemia-reperfusion, leukocytic, and angiogenic phenotypes.During the splanchnic expression of these phenotypes, interstitial edema, increased lymph flow, and lymphangiogenesis are produced in the gastrointestinal tract. Associated liver disease increases intestinal bacterial translocation, splanchnic lymph flow, and induces ascites and hepatorenal syndrome. Extrahepatic cholestasis in the rat allows to study the worsening of the portal hypertensive syndrome when associated with chronic liver disease. The splanchnic interstitium, the mesenteric lymphatics, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of the portal hypertension syndrome complications. The hypothetical comparison between the ascitic and the amniotic fluids allows for translational investigation. From a phylogenetic point of view, the ancestral mechanisms for amniotic fluid production were essential for animal survival out of the aquatic environment. However, their hypothetical appearance in the cirrhotic patient is considered pathological since ultimately they lead to ascites development. But, the adult human being would take advantage of the potential beneficial effects of this “amniotic-like fluid” to manage the interstitial fluids without adverse effects when chronic liver disease aggravates.

scholarly journals The Gut–Liver Axis in Chronic Liver Disease: A Macrophage Perspective

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2959
Author(s):  
Kevin De Muynck ◽  
Bart Vanderborght ◽  
Hans Van Vlierberghe ◽  
Lindsey Devisscher
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Intestinal Barrier ◽  
Chronic Liver ◽  
Health Concern ◽  
Low Grade ◽  
Intestinal Dysbiosis ◽  
Health And Disease ◽  
Intestinal Macrophage ◽  
End Stage

Chronic liver disease (CLD) is a growing health concern which accounts for two million deaths per year. Obesity, alcohol overconsumption, and progressive cholestasis are commonly characterized by persistent low-grade inflammation and advancing fibrosis, which form the basis for development of end-stage liver disease complications, including hepatocellular carcinoma. CLD pathophysiology extends to the intestinal tract and is characterized by intestinal dysbiosis, bile acid dysregulation, and gut barrier disruption. In addition, macrophages are key players in CLD progression and intestinal barrier breakdown. Emerging studies are unveiling macrophage heterogeneity and driving factors of their plasticity in health and disease. To date, in-depth investigation of how gut–liver axis disruption impacts the hepatic and intestinal macrophage pool in CLD pathogenesis is scarce. In this review, we give an overview of the role of intestinal and hepatic macrophages in homeostasis and gut–liver axis disruption in progressive stages of CLD.

Genetic predictors of spontaneous viral elimination or chronic liver disease in hepatitis C infection

2001 ◽  
Vol 120 (5) ◽  
pp. A7-A7
Author(s):  
S ROSS ◽  
S MASCHERETTI ◽  
H HINRICHSEN ◽  
P BUGGISCH ◽  
U FOELSCH ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Hepatitis C Infection ◽  
Genetic Predictors
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