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Updated: Nov 4, 2025

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Portal hypertension and hepatocellular carcinoma: Des liaisons dangereuses…
Manon Allaire1,2, Marika Rudler1,3, Dominique Thabut1,3
1Service d'Hépatolo-gastroentérologie, Hôpitaux Universitaires Pitié Salpêtrière - Charles Foix, AP-HP, Sorbonne Université, Paris, France.
Insights
Portal hypertension (PHT) and hepatocellular carcinoma (HCC) are serious cirrhosis complications. This review explores their shared pathogenesis, focusing on angiogenesis and inflammation, and the challenges in treating coexisting PHT and HCC.
Area of Science:
- Hepatology
- Oncology
- Vascular Biology
Background:
- Portal hypertension (PHT) and hepatocellular carcinoma (HCC) are significant complications of cirrhosis, leading to high morbidity and mortality.
- Both PHT and HCC share common pathogenic pathways involving angiogenesis and inflammation.
- The coexistence of PHT and HCC presents complex therapeutic challenges.
Purpose of the Study:
- To review the roles of angiogenesis and inflammation in the pathogenesis of PHT and HCC.
- To discuss the difficulties in managing patients with both PHT and HCC.
- To highlight the need for effective treatment strategies for coexisting PHT and HCC.
Main Methods:
- Literature search of PubMed database for studies published in English until March 2021.
- Review of existing research on the pathogenesis and treatment of PHT and HCC.
Main Results:
- PHT involves increased intrahepatic vascular resistance, portosystemic collaterals, and neovascularization driven by VEGF.
- Bacterial translocation-mediated inflammation is a key contributor to PHT.
- VEGF and chronic inflammation are implicated in HCC development, and their interplay complicates management when PHT and HCC coexist.
Conclusions:
- Effective management of PHT is crucial for improving outcomes in HCC patients.
- Current treatment strategies for advanced HCC, such as Atezolizumab and Bevacizumab, may influence PHT, but real-world data are lacking.
- Further research is needed to address the complexities of treating coexisting PHT and HCC.
Background And Aims:
Portal hypertension (PHT) and hepatocellular carcinoma (HCC) are major complication of cirrhosis which significantly contribute to morbidity and mortality. In this review, we aim to describe the consequences of both angiogenesis and inflammation in the pathogenesis of PHT and HCC, but also the difficulty to propose adapted treatment when PHT and HCC coexist in the same patients.
Methods:
Studies for review in this article were retrieved from the PubMed database using literature published in English until March 2021.
Results:
Portal hypertension occurs secondary to an increase of intrahepatic vascular resistances, the opening of portosystemic collateral vessels and the formation of neovessels, related to vascular endothelial growth factor (VEGF). Recently, bacterial translocation-mediated inflammation was also identified as a major contributor to PHT. Interestingly, VEGF and chronic inflammation also contribute to HCC occurrence. As PHT and HCC often coexist in the same patient, management of PHT and its related complications as well as HCC treatment appear more complex. Indeed, PHT-related complications such as significant ascites may hamper the access to HCC treatment and the presence of HCC is also independently associated with poor prognosis in patients with acute variceal bleeding related to PHT. Due to their respective mechanism of action, the combination of Atezolizumab and Bevacizumab for advanced HCC may impact the level of PHT and its related complications and to date, no real-life data are available.
Conslusions:
Appropriate evaluation and treatment of PHT remains a major issue in order to improve the outcome of HCC patients.
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