Background aims: Hepatocellular carcinoma (HCC) can increase the risk of non-neoplastic portal vein thrombosis (PVT) in cirrhosis. However, natural history of PVT and its prognostic role in HCC patients are unknown. Approach results: Consecutive cirrhotic HCC patients undergoing laparoscopic ablation were retrospectively evaluated and followed-up to 36 months. HCC and PVT characteristics and evolution were reviewed. PVT was categorized according to lumen occupancy (≤ 50%, > 50% < 100% and = 100%) and extension to other veins. Evolution of thrombosis was considered at 1 year from diagnosis. Variables associated with presence of PVT and evolution patterns were analyzed, as well as their impact on survival. Seven-hundreds-fifty patients were included, 88 with PVT. On multivariate analysis, the occurrence of PVT at HCC diagnosis was associated with pre-treatment total tumor volume (p < 0.001) and clinically-significant portal hypertension (p = 0.005). 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 non-response to HCC treatment in non-anticoagulated patients. The presence of PVT was independently associated with lower overall survival, particularly when progressive or occlusive (p < 0.001). A higher competing risk of death emerged for 'complete and progressive' PVT, both for HCC-related (p < 0.001) and non-HCC-related (p = 0.002) death. Conclusions: HCC represents an independent risk factor for the occurrence and progression of PVT in cirrhosis. Since progressive and occlusive PVT seems to be an independent factor associated with mortality, screening and prompt treatment of this complication should be considered.

Role of non-neoplastic portal vein thrombosis in the natural history of patients with cirrhosis and first diagnosis of hepatocellular carcinoma

Shalaby, Sarah;Vitale, Alessandro;Zanetto, Alberto;Feltracco, Paolo;Simioni, Paolo;Burra, Patrizia;Cillo, Umberto
2023

Abstract

Background aims: Hepatocellular carcinoma (HCC) can increase the risk of non-neoplastic portal vein thrombosis (PVT) in cirrhosis. However, natural history of PVT and its prognostic role in HCC patients are unknown. Approach results: Consecutive cirrhotic HCC patients undergoing laparoscopic ablation were retrospectively evaluated and followed-up to 36 months. HCC and PVT characteristics and evolution were reviewed. PVT was categorized according to lumen occupancy (≤ 50%, > 50% < 100% and = 100%) and extension to other veins. Evolution of thrombosis was considered at 1 year from diagnosis. Variables associated with presence of PVT and evolution patterns were analyzed, as well as their impact on survival. Seven-hundreds-fifty patients were included, 88 with PVT. On multivariate analysis, the occurrence of PVT at HCC diagnosis was associated with pre-treatment total tumor volume (p < 0.001) and clinically-significant portal hypertension (p = 0.005). 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 non-response to HCC treatment in non-anticoagulated patients. The presence of PVT was independently associated with lower overall survival, particularly when progressive or occlusive (p < 0.001). A higher competing risk of death emerged for 'complete and progressive' PVT, both for HCC-related (p < 0.001) and non-HCC-related (p = 0.002) death. Conclusions: HCC represents an independent risk factor for the occurrence and progression of PVT in cirrhosis. Since progressive and occlusive PVT seems to be an independent factor associated with mortality, screening and prompt treatment of this complication should be considered.
2023
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3489560
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