SummaryCirrhotic patients with decompensated state and high serum levels of fibrin(ogen) degradation products are at high risk of bleeding. The aim of this study was to further analyse the relationship between hyperfibrinolysis and bleeding in cirrhosis by measuring plasma values of D-dimer and tissue plasminogen activator (t-PA) activity. One-hundred-twelve cirrhotic patients with oesophageal varices and without previous upper-gastrointestinal bleeding entered the study and were followed-up for 3 years. Patients were considered to have hyperfibrinolysis if they concomitantly had high values of D-dimer and t-PA activity. During the follow-up 34 (30%) patients bled. They had more severe liver failure (p = 0.0001) and variceal size (p = 0.0031) and higher prevalence of ascites (p = 0.0003), varices with red signs and hyperfibrinolysis (p = 0.0001) than patients who did not bleed. Multivariate analysis disclosed hyperfibrinolysis as the only marker predictive of bleeding (Hazard Ratio = 42.5, p <0.001). Our findings suggest that screening for hyperfibrinolysis may be useful to identify cirrhotic patients at risk of bleeding.

Dipyridamole incubated in vitro in systems which peroxidize fatty acids inhibited arachidonic acid, gammalinolenic acid and linoleic acid peroxidation. In the xanthine-xanthine-oxidase system, which produces superoxide anion, dipyridamole inhibited the reduction of cytochrome-C in a dose-dependent fashion. In systems generating hydroxyl radicals, dipyridamole reduced deoxyribose degradation in a dose-dependent manner. The study suggests that dipyridamole inhibits lipid peroxidation, probably by scavening oxygen free radicals. Lipids 24, 430-433 (1989).