Related Experiment Video
Updated: Mar 21, 2026
Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy
Published on: June 18, 2020
Emerging therapies for portal hypertension in cirrhosis
Harikumar Nair1, Annalisa Berzigotti1, Jaime Bosch1,2
1a Inselspital Universitatsspital Bern , Bern , Switzerland.
Insights
New treatments targeting liver microvascular dysfunction show promise for reducing portal hypertension (PH). Combining early-stage antifibrotic therapies with existing PH treatments offers a future strategy.
Area of Science:
- Hepatology
- Vascular Biology
- Pharmacology
Background:
- Portal hypertension (PH) management has focused on splanchnic vasodilatation and portal-collateral blood flow for decades.
- Despite advancements, significant room for improvement exists in treating PH.
- Increased hepatic vascular resistance due to cirrhosis and elevated hepatic vascular tone are key mechanisms in PH.
Purpose of the Study:
- To summarize molecules modulating microvascular dysfunction in PH.
- To address drug development challenges and clinical trial design considerations.
- To explore future therapeutic strategies for PH.
Main Methods:
- Review of preclinical and clinical trial data for molecules targeting microvascular dysfunction.
- Analysis of drug development issues.
- Consideration of clinical trial design for PH therapies.
Main Results:
- Molecules modulating liver microvascular dysfunction may reduce portal pressure by 30-40%.
- Early-stage cirrhosis treatments (antifibrotics, antiangiogenics, etiological therapies) can reduce fibrosis and halt PH progression.
Conclusions:
- A 'nip at the bud' policy combining early-stage and advanced-phase PH therapies is the future strategy.
- Novel agents for early-stage cirrhosis are expected soon.
- Integrated therapeutic approaches will enhance PH management.
Introduction:
Counteracting splanchnic vasodilatation and increased portal-collateral blood flow has been the mainstay for the treatment of portal hypertension (PH) over the past three decades. However, there is still large room for improvement in the treatment of PH.
Areas Covered:
The basic mechanism leading to portal hypertension is the increased hepatic vascular resistance to portal blood flow caused by liver structural abnormalities inherent to cirrhosis and increased hepatic vascular tone. Molecules modulating microvascular dysfunction which have undergone preclinical and clinical trials are summarized, potential drug development issues are addressed, and situations relevant to design of clinical trials are considered.
Expert Opinion:
Experimental and clinical evidence indicates that molecules modulating liver microvascular dysfunction may allow for 30-40% reduction in portal pressure. Several agents could be utilized in the earlier stages of cirrhosis (antifibrotics, antiangiogenics, etiological therapies) may allow reduction of fibrosis and halt progression of PH. This 'nip at the bud' policy, by combining therapies with existing agents used in advanced phase of cirrhosis and novel agents which could be used in early phase of cirrhotic spectrum, which are likely to hit the market soon would be the future strategy for PH therapy.
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