PB1228 - Increased platelet aggregation in patients with decompensated cirrhosis indicates higher risk of further decompensation and death.

Tuesday, July 12, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Co-Author(s)

EC

Elena Campello

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

Fabio Farinati

Full Professor
Unviersity of Padova
Padova, Veneto, Italy
FR

Francesco Paolo Russo

Associate Professor
Unviersity of Padova
Padova, Veneto, Italy
DT

Daniela Tormene

MD, PhD
University 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

Presenting Author(s)

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: Studies on platelet aggregation in cirrhosis are controversial because interpretation of platelet function is challenged by thrombocytopenia.

Aims: We conducted a prospective study to investigate whole blood platelet aggregation in cirrhosis and its association with liver-related outcomes.

Methods: Platelet aggregation was assessed by whole blood aggregometry (Multiplate®). To overcome the influence of platelet count and compare cirrhosis with thrombocytopenia versus controls with normal platelet count, we calculated a ratio between platelet aggregation and platelet count (PLT ratio). Then, we prospectively followed patients with cirrhosis and ascertained predictors of decompensation, transplantation, and death. Informed consent was obtained and the study was approved by the local medical ethics committee.

Results: Two-hundred and three cirrhosis patients were prospectively recruited (77% decompensated). PLT ratio was significantly higher in cirrhosis than in chronic hepatitis and healthy subjects (0.44 vs. 0.25 and 0.26, respectively; p< 0.0001). In cirrhosis, the ratio increased with disease severity (Child-Pugh class C>B>A) and was particularly elevated in decompensated patients with severe thrombocytopenia. Among decompensated patients, 65 had further decompensation, underwent transplantation, or died during a 6-month follow-up. On multivariate analysis, PLT ratio (OR: 1.87, 95%CI: 1.23-2.84; p=0.003) and MELD score (OR: 1.05, 95%CI: 1.01-1.08; p=0.01) were independently associated with outcome. The relative risk of events was 7.5-fold higher in patients with PLT ratio >0.75 versus patients with PLT ratio < 0.25 (RR: 7.5, 95% CI: 2.5-21.9; p=0.003) (Figure 1). The increased PLT ratio, its discriminative ability for composite outcome, and the prognostic value of PLT ratio >0.75 were validated in an independent cohort of hospitalized patients with decompensated cirrhosis (n=41).

Conclusion(s): Patients with cirrhosis, particularly when decompensated, exhibit significantly increased whole blood platelet aggregation. Decompensated patients with PLT ratio >0.75 have >80% probability of further decompensation, transplantation, or liver-related death within 6 months.