Work

Abnormal lipid profiles are associated with markers of impaired fibrinolysis in patients with cirrhosis

Year: 2026

Type: article

Abstract: Background: Patients with liver cirrhosis exhibit abnormalities in lipid metabolism and in circulating proteins of clot breakdown. Recent studies have shown relationships between dyslipidemia and fibrinolytic abnormalities in noncirrhotic populations. Objectives: We investigated associations between lipid profiles and fibrinolytic markers in patients with cirrhosis. Methods: This observational study analyzed samples from 147 patients with stable cirrhosis, decompensated cirrhosis, acute-on-chronic liver failure, and sepsis without pre-existing chronic liver disease, and from 38 healthy controls. We studied fibrinolysis by clot lysis time (CLT), plasminogen, plasminogen activator inhibitor-1 (PAI-1), and tissue-type plasminogen activator (tPA), and lipid profiles by apolipoproteins A1 and B, common lipoproteins, triglycerides, and total cholesterol. Results: CLT was slightly enhanced in stable and decompensated cirrhosis, but prolonged in acute-on-chronic liver failure and sepsis. Plasminogen levels decreased, whereas PAI-1 and tPA increased with cirrhosis severity. All lipid parameters decreased with cirrhosis severity, besides triglyceride levels, which were preserved. In an analysis of all patients with cirrhosis combined, apolipoprotein A1 correlated inversely with CLT, levels of PAI-1 and tPA, and positively with plasminogen. Apolipoprotein B, low-density lipoprotein, and lipoprotein(a) correlated positively with plasminogen. Triglycerides correlated positively with CLT. Conclusion: Cirrhosis is characterized by decreased (apo)lipoprotein levels, preserved triglyceride levels, and a shift from enhanced to impaired fibrinolysis with increasing disease severity. Lower apolipoprotein A1 levels and higher triglyceride levels are associated with impaired fibrinolysis, which may reflect biological interactions between lipid metabolism and fibrinolysis or parallel alterations secondary to hepatic dysfunction.

Source: Research and Practice in Thrombosis and Haemostasis

DOI: 10.1016/j.rpth.2026.106975

Authors: Fynn L. Elvers, Jelle Adelmeijer, Marilena Stamouli, William Bernal, Vishal C. Patel, Ton Lisman