Medical Management of Portal Hypertension and Its Complications

AbstractPortal hypertension, most commonly caused by cirrhosis, is defined as an elevated hepatic venous pressure gradient that can lead to complications including ascites, hepatic, esophageal/gastric varices, hepatic encephalopathy, and hepatorenal syndrome. While these complications are initially managed by medical and endoscopic treatments, progressive decompensation of liver disease may lead to liver transplantation.

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Per‐rectal portal scintigraphy as an alternative measure of hepatic venous pressure gradient in chronic liver disease: a preliminary report

Clinical Physiology and Functional Imaging ◽

10.1111/cpf.12703 ◽

2021 ◽

Author(s):

Kohei Kotani ◽

Sawako Uchida‐Kobayashi ◽

Akira Yamamoto ◽

Etsushi Kawamura ◽

Masaru Enomoto ◽

...

Keyword(s):

Liver Disease ◽

Pressure Gradient ◽

Chronic Liver Disease ◽

Preliminary Report ◽

Venous Pressure ◽

Chronic Liver ◽

Hepatic Venous Pressure Gradient ◽

Alternative Measure

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Portal Angiogenesis in Chronic Liver Disease Patients Correlates with Portal Pressure and Collateral Formation

Digestive Diseases ◽

10.1159/000500115 ◽

2019 ◽

Vol 37 (6) ◽

pp. 498-508 ◽

Cited By ~ 1

Author(s):

Carolina A. Serrano ◽

Simon C. Ling ◽

Sofia Verdaguer ◽

Miguel León ◽

Nicolás Jarufe ◽

...

Keyword(s):

Liver Transplantation ◽

Portal Hypertension ◽

Liver Disease ◽

Chronic Liver Disease ◽

Venous Pressure ◽

Portal Pressure ◽

Peripheral Circulation ◽

Chronic Liver ◽

Noninvasive Markers ◽

Collateral Formation

Background/Aims: One hallmark of chronic liver disease in patients with portal hypertension is the formation of portal-systemic collaterals in which angiogenesis has a fundamental role. We studied patients with chronic liver disease undergoing liver transplantation to correlate levels of circulating angiogenic factors in portal and peripheral circulation with portal pressure and portal-systemic collaterals. Methods: Sixteen patients who underwent liver transplantation were enrolled. During transplant surgery, we determined portal venous pressure and portal-systemic collateral formation. We determined angiogenics mediator levels in systemic and portal plasma. Peripheral plasma from healthy donors was measured as controls. Results: Vascular endothelial growth factor (VEGF)-R1 and 2, Ang-1 and 2, Tie2, FGF- 1 and 2, CD163, PDGFR-β, PDGFsRα, PDGF-AB and BB, CD163, TGF-β VASH-1 levels were significantly different in the controls in comparison to cases. Significantly decreased portal venous levels of Ang-1, FGF-1, PDGF-AB/BB, and CC were observed in patients with higher portal pressure. Peripheral VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation. While peripheral VEGF-R1 was higher in patients with severe collateral formation. For portal circulation, VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation Conclusions: Angiogenesis factors correlated with portal pressure and collateral formation and different patterns of circulating angiogenesis mediators were found in peripheral and portal blood of patients with chronic liver disease. These results support the importance of angiogenic pathways in cirrhosis and portal hypertension and highlight areas for further study to identify clinically useful noninvasive markers of portal pressure and collateral formation.

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