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Lipoprotein (a) and fibrinolytic system in liver cirrhosis. Coagulation Abnormalities in Liver Cirrhosis (CALC) Study
C Cimminiello1, M Soncini, M C Gerosa
1Department of Internal Medicine, San Carlo Borromeo General Hospital, Milan, Italy.
Insights
Lipoprotein (a) levels decrease with worsening liver cirrhosis, correlating with plasminogen. It appears unlikely to cause hyperfibrinolysis in advanced liver disease.
Area of Science:
- Cardiology
- Hepatology
- Hematology
Background:
- Lipoprotein (a) [Lp(a)] is a known risk factor for coronary artery disease.
- Its role in liver cirrhosis and the fibrinolytic system is not well understood.
- Few studies have investigated Lp(a) in the context of liver cirrhosis.
Purpose of the Study:
- To elucidate the relationship between lipoprotein (a) and the fibrinolytic system in patients with liver cirrhosis.
- To investigate how Lp(a) levels change with the severity of liver cirrhosis.
- To assess the potential involvement of Lp(a) in the hyperfibrinolytic state of advanced liver cirrhosis.
Main Methods:
- Plasma levels of Lp(a) and fibrinolytic parameters were measured in 95 liver cirrhosis patients.
- Patients were categorized by Child-Pugh class (A, B, C) to assess disease severity.
- Correlations between Lp(a), plasminogen, and other fibrinolytic markers were analyzed.
Main Results:
- Lipoprotein (a) levels progressively decreased with increasing severity of liver cirrhosis (Child-Pugh C < B < A).
- A significant positive correlation was observed between Lp(a) and plasminogen levels (r = 0.43; p = 0.001).
- Patients with systemic hyperfibrinolysis exhibited lower Lp(a) levels compared to those without.
Conclusions:
- Lipoprotein (a) levels decline as liver cirrhosis progresses.
- Lp(a) is unlikely to be a primary cause of hyperfibrinolysis in advanced liver cirrhosis.
- Abnormalities in other fibrinolytic parameters, such as increased tissue plasminogen activator (t-PA), are more likely responsible for hyperfibrinolysis.
Abstract:
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.