John Libbey Eurotext

Hépato-Gastro & Oncologie Digestive

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New therapeutic targets for portal hypertension in cirrhotic patients Volume 27, issue 3, Mars 2020

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Authors
Hôpitaux Universitaire de Strasbourg, Hôpital de Hautepierre, 1 Avenue Molière, 67200 Strasbourg
* Correspondance

Portal hypertension (PHT) and its complications are major determinants of the prognosis of the cirrhotic patient, especially when the porto-systemic gradient pressure is greater than 12 mmHg. The pathophysiology of PHT in cirrhotics is based on several mechanisms involving both an increase in intrahepatic vascular resistance, of functional origin through a deficit of NO, or structural through hepatic modeling secondary to fibrogenesis and microthrombosis, and increased splanchnic flow through systemic NO hyperproduction, leading to activation of the renin-angiotensin system and neo-angiogenesis. The local and systemic pro-inflammatory state secondary to bacterial translocation also seems to play a role in PHT in cirrhotic patients. Apart from the etiological treatment of cirrhosis, the pharmacological treatment of PHT currently relies on non-cardio-selective beta-blockers and splanchnic vasoconstrictors allowing a reduction in portal flow. The suboptimal efficacy, even the toxicity of these treatments justifies the development of new therapeutic strategies. A better understanding of the physiopathogenic mechanisms of PHT has enabled the identification of new therapeutic targets, several of which have already been the subject of clinical trials, which will be discussed in this review.