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Cited by 337

The DOI matches its Crossref record; 132 of the 132 references it cites were found in a registry or an index.

Pathophysiology of Portal Hypertension

Open access
Iwakiri, Yasuko·2014·Clinics in Liver Disease

Abstract

Portal hypertension is a major complication of liver disease, which results from a variety of pathological conditions that increase the resistance to the portal blood flow into the liver. The primary cause of portal hypertension in cirrhosis is an increase in intrahepatic vascular resistance due to massive structural changes associated with fibrosis and increased vascular tone in the hepatic microcirculation. As portal hypertension develops, the formation of collateral vessels and arterial vasodilation progress, which results in increased blood flow to the portal circulation. Eventually the hyperdynamic circulatory syndrome develops, leading to esophageal varices or ascites. This review article will summarize the factors that increase 1) intrahepatic vascular resistance and 2) the blood flow in the splanchnic and systemic circulations in liver cirrhosis. Finally, the future directions of basic/clinical research in portal hypertension will be discussed.

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Crossref · 10.1016/j.cld.2013.12.001

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Metadata

Authors
Iwakiri, Y.
Venue
Clinics in Liver Disease
Publisher
Elsevier BV
Published
2014-05
Volume
18
Issue
2
Pages
281-291
ISSN
1089-3261 (ISSN-L)
OpenAlex
W2048951077
Cited by
337
References
132
FWCI
6.40
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Pathophysiology of Portal Hypertension. https://app.cochat.ai/papers/10.1016/j.cld.2013.12.001
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Iwakiri, Y. (2014). Pathophysiology of Portal Hypertension. Clinics in Liver Disease. https://doi.org/10.1016/j.cld.2013.12.001

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.