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)

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.
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PMID:Lipoprotein (a) and fibrinolytic system in liver cirrhosis. Coagulation Abnormalities in Liver Cirrhosis (CALC) Study Group. 856 64

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.
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PMID:[Studies on the mechanism of hyperfibrinolysis in liver cirrhosis--changes of plasma t-PA, PAI-1 and active PAI-1 levels in liver cirrhosis]. 856 37


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