Background: Hepatocellular carcinoma (HCC) increases the risk of non-neoplastic portal vein thrombosis (PVT) in cirrhosis. However, data on its natural history and prognostic role in HCC patients are lacking. Materials and methods: Cirrhotic HCC patients undergoing laparoscopic ablation were consecutively enrolled and followed-up to 36 months. HCC and PVT characteristics and evolution were reviewed. PVT evolution was categorized according to changes in occlusion (cut-off 20%) and extension to other segments and classified as ‘complete/progressive’ or ‘partial/ameliorated’. Variables associated with the presence of PVT and evolution patterns were analyzed, as well as their impact on survival. Results: Seven-hundreds-fifty patients were included, 88 with PVT. On multivariate analysis, the presence of PVT at HCC diagnosis was associated with pre-treatment total tumor volume (TTV) (p<.001) and clinically-significant portal hypertension (p=.005). During follow-up, 46 de novo PVT occurred, 27/46 (58.7%) in presence of viable tumor. Among 115 PVT diagnosed in presence of HCC, 83 had available radiological follow-up, and 22 were anticoagulated. The 'complete/progressive' evolution pattern was associated with occlusive PVT at diagnosis and absence of anticoagulation in all PVT, whereas to Child-C score and non-response to HCC treatment in untreated patients. Overall survival was lower in the presence of PVT, specifically for 'complete/progressive' PVT (p<0.001). A higher competing risk of death emerged for ‘complete/progressive’ PVT, both for HCC-related (p<0.001) and non-HCC-related (p<0.001) death. Conclusions: Non-neoplastic PVT in HCC is characterized by a higher risk of progression, correlated with the HCC activity, when not treated. Complete/progressive PVT is an independent factor associated with mortality, both HCC and non-HCC related.

Ruolo prognostico della trombosi portale non neoplastica nel paziente cirrotico con epatocarcinoma

SHALABY, SARAH
2024

Abstract

Background: Hepatocellular carcinoma (HCC) increases the risk of non-neoplastic portal vein thrombosis (PVT) in cirrhosis. However, data on its natural history and prognostic role in HCC patients are lacking. Materials and methods: Cirrhotic HCC patients undergoing laparoscopic ablation were consecutively enrolled and followed-up to 36 months. HCC and PVT characteristics and evolution were reviewed. PVT evolution was categorized according to changes in occlusion (cut-off 20%) and extension to other segments and classified as ‘complete/progressive’ or ‘partial/ameliorated’. Variables associated with the presence of PVT and evolution patterns were analyzed, as well as their impact on survival. Results: Seven-hundreds-fifty patients were included, 88 with PVT. On multivariate analysis, the presence of PVT at HCC diagnosis was associated with pre-treatment total tumor volume (TTV) (p<.001) and clinically-significant portal hypertension (p=.005). During follow-up, 46 de novo PVT occurred, 27/46 (58.7%) in presence of viable tumor. Among 115 PVT diagnosed in presence of HCC, 83 had available radiological follow-up, and 22 were anticoagulated. The 'complete/progressive' evolution pattern was associated with occlusive PVT at diagnosis and absence of anticoagulation in all PVT, whereas to Child-C score and non-response to HCC treatment in untreated patients. Overall survival was lower in the presence of PVT, specifically for 'complete/progressive' PVT (p<0.001). A higher competing risk of death emerged for ‘complete/progressive’ PVT, both for HCC-related (p<0.001) and non-HCC-related (p<0.001) death. Conclusions: Non-neoplastic PVT in HCC is characterized by a higher risk of progression, correlated with the HCC activity, when not treated. Complete/progressive PVT is an independent factor associated with mortality, both HCC and non-HCC related.
14-mag-2024
Inglese
BURRA, PATRIZIA
Università degli studi di Padova
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14242/160860
Il codice NBN di questa tesi è URN:NBN:IT:UNIPD-160860