PB0486 - Decompensated cirrhosis with bacterial infections shows a peculiar derangement of the hemostatic balance

Monday, July 11, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Presenting Author(s)

EC

Elena Campello

Assistant Professor
Department of Medicine, University of Padova, Italy
Padova, Veneto, Italy

Co-Author(s)

AZ

Alberto Zanetto

Postdoc
Unviersity of Padova
Padova, Veneto, Italy
CB

Cristiana Bulato

PhD
Department of Medicine, Thrombotic and Haemorrhagic Diseases Unit, University of Padua Medical School, Padua (Italy)
Padova, Veneto, Italy
SG

Sabrina Gavasso

Laboratory technician
Unviersity of Padova
Padova, Veneto, Italy
GS

Graziella Saggiorato

Biologist
Unviersity of Padova
Padova, Veneto, Italy
NP

Nicola Perin

Resident in internal MEedicine
Department of Medicine, University of Padova, Italy
Padova, Veneto, Italy
SS

Sarah Shalaby

PhD student
Unviersity of Padova
Padova, Veneto, Italy
PB

Patrizia Burra

Full Professor
Unviersity of Padova
Padova, Veneto, Italy
MS

Marco Senzolo

MD
Multivisceral Transplant Unit, University Hospital of Padua, Padua, Italy
Padova, Veneto, Italy
Paolo Simioni, MD, PhD

Full Professor
Department of Medicine, Thrombotic and Haemorrhagic Diseases Unit, University of Padua Medical School, Padua (Italy)
Padua, Veneto, Italy

Background: Decompensated cirrhosis with bacterial infections shows a peculiar derangement of the hemostatic balance.

Aims: To assess the factors responsible for bleeding tendency in BIs, we conducted a prospective study comparing all components of hemostasis (platelets, coagulation, and fibrinolysis) in hospitalized patients with decompensated cirrhosis with vs. without BIs.

Methods: Primary hemostasis assessment included whole blood platelet aggregation and von Willebrand factor (VWF). Coagulation assessment included procoagulant factors (fibrinogen, factor II, V, VII, VIII, IX, X, XI, XII, XIII), natural anticoagulants (protein C, protein S, antithrombin) and thrombomodulin-modified thrombin generation test. Fibrinolysis assessment included fibrinolytic factors (plasminogen, t-PA, PAI-1, α2-AP, TAFIa/ai) and plasmin-antiplasmin complex (PAP).

Results: Eighty patients with decompensated cirrhosis were included (40 with and 40 without BIs). Severity of cirrhosis and platelet count were comparable between groups. At baseline, patients with cirrhosis and BIs had a significantly lower whole blood platelet aggregation, consistent with impaired platelet function, without significant differences in VWF. Regarding coagulation, BIs were associated with reduced procoagulant factors VII and XII, and a marked reduction of all natural anticoagulants. Thrombomodulin-modified thrombin generation, however, was comparable between groups. Finally, although mixed potentially hypo-fibrinolytic (low plasminogen) and hyper-fibrinolytic (high t-PA) changes were present in BIs, comparable levels of PAP were detected in both groups (Table 1). Upon resolution of infection (n=29/40), platelet aggregation further deteriorated whereas coagulation and fibrinolysis factors returned to levels observed in patients without BIs (Figure 1).

Conclusion(s): In hospitalized patients with decompensated cirrhosis, BIs are associated with reduced whole blood platelet aggregation and a marked decrease of all natural anticoagulants, which may unbalance hemostasis and potentially increase the risk of bleeding and thrombosis.