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PubMed1998

Liver cirrhosis.

Liver fibrosis and its related complications continue to represent a significant worldwide healthcare burden. Over the past decade there has been considerable improvement in our understanding of the cellular mechanisms and pathophysiology underlying hepatic fibrosis. This greater insight into the relevant basic sciences may lead to the development of novel treatment strategies designed to block the fibrogenic cascade or even enhance matrix degradation. In addition, there have been significant advances in the management of the complications of cirrhosis, with specific treatments now available for some conditions. Perhaps most notably, liver transplantation is now a highly successful treatment for end-stage liver disease and should be considered in all patients with chronic liver disease.

Esophageal and Gastric Varices↗
PubMed1995

Lipoprotein (a) and fibrinolytic system in liver cirrhosis. Coagulation Abnormalities in Liver Cirrhosis (CALC) Study Group.

Several observations have suggested that lipoprotein (a) (Lp(a)) is a risk factor for coronary artery disease because of potential interference with fibrinolysis secondary to its activation of plasminogen. However, there are few data on the possible role of Lp(a) in liver cirrhosis. The present study was carried out, to better elucidate its relationship to the fibrinolytic system in liver cirrhosis. We studied the plasma levels of Lp(a) and the fibrinolytic parameters of 95 patients with liver cirrhosis (57 men, 38 women, aged 26-81). Patients in Child-Pugh class C (n = 32) had significantly lower levels of Lp(a) than those in class B (n = 45), and the class B had lower Lp(a) values than class A (n = 18) (1.4 (0.0-3.7) vs 2.9 (0.0-6.1) vs 3.4 (1.8-5.5); the data are log-transformed). Alpha-2-antiplasmin and plasminogen, had patterns similar to those of Lp(a), tissue plasminogen activator (t-PA) was significantly increased only in class C (class A: 7.5 +/- 5.8 ng/ml; class B: 10.8 +/- 7.7 ng/ml; class C: 19.1 +/- 11.3 ng/ml). Patients with systemic hyperfibrinolysis (cross-linked fibrin degradation products, XDP > 200 ng/ml) also had lower levels of Lp(a) than those without 1.6 (0.0-4.4) vs (0.0-6.1); p = 0.0002. There was a significant correlation between Lp(a) and plasminogen (r = 0.43; p = 0.001). Lipoprotein (a) progressively decreases as liver cirrhosis worsens but it appears unlikely to be involved in causing the hyperfibrinolytic state often observed in advanced liver cirrhosis, in which there are marked abnormalities of several other fibrinolytic parameters, also including increased t-PA and decreased inhibitors.

Adult↗
PubMed2002

Human fetuin/alpha2HS-glycoprotein level as a novel indicator of liver cell function and short-term mortality in patients with liver cirrhosis and liver cancer.

OBJECTIVE: Human fetuin/alpha2HS-glycoprotein (AHSG) is synthesized by hepatocytes. We intended to determine whether liver dysfunction or acute phase reaction is dominant in the regulation of its serum concentrations and to see if decreased AHGS levels are associated with short-term mortality. DESIGN: We determined the serum AHSG levels in patients with acute alcoholic, acute A, B, and Epstein-Barr virus hepatitis, alcoholic cirrhosis, and hepatocellular cancer and correlated them to conventional laboratory parameters of inflammation and liver function. Patients were followed for 1 month. METHODS: Serum AHSG was determined by radial immunodiffusion. RESULTS: Compared to controls, significantly lower AHSG levels were found in patients with liver cirrhosis and hepatocellular cancer but not the acute viral hepatitides. Strong positive correlation with serum transferrin, albumin and prothrombin was found. Febrile episodes were not associated with significantly decreased AHSG levels. Concentrations below 300 microg/ml were associated with high mortality rate (52.0%; relative risk, 5.497; 95% confidence interval, 2.472-12.23; P < 0.0001). Of all laboratory parameters studied serum AHSG levels showed the greatest difference between deceased and survived patients with cirrhosis and cancer. Moreover, other acute phase reactants did not differ significantly. The multiple logistic regression analysis indicated that the decrease of serum AHSG is independent of all other variables that were found decreased in deceased patients. CONCLUSIONS: Decreased serum AHSG concentration is due rather to hepatocellular dysfunction than the acute phase reaction and is an outstanding predictor of short-term mortality in patients with liver cirrhosis and liver cancer.

Acute-Phase Reaction↗
PubMedDate not supplied

Variations of serum sialic acid level in liver cirrhosis.

BACKGROUND: Cirrhosis liver claims many lives in our country. However early diagnosis carries good prognosis and prevents complications. Estimation of serum sialic acid level may be helpful in the diagnosis of liver cirrhosis and following the dynamics of the disease especially during treatment and follow up to see the prognosis. METHODS: Sialic acid level of 82 confirmed liver cirrhosis patients of age between 18-60 years and admitted in Khyber Teaching Hospital Peshawar was determined and compared with 40 normal controls. The patients were studied in three groups according to the stage of the disease, i.e. the patients in early stages, in advancing stage, and those in terminal stage of liver cirrhosis. Sialic acid level was determined on HPLC (Hitachi) with D-2500 chromatographer. RESULT: Significantly high levels of sialic acid were recorded in patients as compared to controls. It was normal in early stage of liver cirrhosis (667 +/- 8.06 nmol/ml), markedly increased in advancing cirrhosis (952 +/- 3.29 nmol/ml) (P<0.05) and very high levels were observed in terminal stage (1058 +/- 7.50 nmol/ml). CONCLUSION: Serum Sialic acid level was high in advancing and terminal stages of disease as compared to early stage and controls that showed normal levels.

Adolescent↗
PubMed1995

[Studies on the mechanism of hyperfibrinolysis in liver cirrhosis--changes of plasma t-PA, PAI-1 and active PAI-1 levels in liver cirrhosis].

Liver cirrhosis is known to have abnormal fibrinolysis. In order to investigate the changes of fibrinolytic system in liver cirrhosis, plasma levels of various fibrinolytic molecular markers were measured in patients with different stages of liver cirrhosis, 20 compensated liver cirrhosis (c-LC) and 14 decompensated liver cirrhosis (d-LC) and were compared with those in normal subjects. Both the plasma levels of plasmin alpha 2-plasmin inhibitor complex (PIC) and the plasma levels of total fibrin/fibrinogen degradation products (T-FDP) were significantly elevated in patients with both c-LC and d-LC as compared with normal controls. Moreover, both factors in d-LC were significantly higher than those in c-LC. These findings indicate that patients with liver cirrhosis have hyperfibrinolysis. Then, in order to investigate the mechanisms of hyperfibrinolysis in liver cirrhosis, plasma levels of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) were determined in these patients. The plasma levels of t-PA significantly increased in both c-LC and d-LC as compared with normal controls. Its levels were higher in patients with LC at their decompensated stage than at their compensated stage. In patients with LC, plasma PAI-1 levels showed significantly higher values than those in normal controls. However, the plasma levels of active PAI-1 in patients with LC were similar to those in normal controls. These results suggest that hyperfibrinolysis in patients with LC is mainly due to increased concentrations of t-PA, without increased active PAI-1 levels.

Fibrinolysis↗